Table of Content

05 March 2023, Volume 43 Issue 3

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Original Articles

Expression and clinical significance of ASH2L in human gastric carcinoma cell lines infected with Helicobacter pylori

XIE Xiaoting, ZHANG Lei, ZHANG Li, DONG Feng, LIU Ying, LI Guanghua, YANG Xing

2023, 43(3):  367-373.  doi:10.16352/j.issn.1001-6325.2023.03.367

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Objective To explore the expression and clinical significance of Drosophila protein Ash2 analogue(ASH2L)in gastric carcinoma cell lines infected with Helicobacter pylori(Hp). Methods The expression of ASH2L in various tumors, the relationship between ASH2L and pathological characteristics of stomach adenocarcinoma and the prognosis of the patients were analyzed by TIMER2.0, UALCAN and other software. Human gastric mucosal epithelial cell line GES, gastric carcinoma cell lines SGC-7901 and AGS were infected with Hp and the expression of ASH2L before and after Hp infection was detected by RT-qPCR and Western blot. Results The analysis showed that ASH2L was differentially expressed in 15 kinds of tumors and was highly expressed in stomach adenocarcinoma. The overall survival (OS) and post-progression survival (PPS) of patients with high ASH2L expression were lower than those with low ASH2L expression(P＜0.05). There were some differences in the expression of ASH2L in patients with stomach adenocarcinoma in different age groups, different races and different pathological grades, but not related to gender. The expression of ASH2L was significantly up-regulated in three human gastric epithelial cell lines infected with Hp(P＜0.05). Conclusions ASH2L may play an important role in tumorigenesis of gastric carcinoma caused by Hp infection, and its expression level is closely related to various pathological features and prognosis of the patients, and it is expected to be a molecular marker for prognosis.

Risperidone induces apoptosis of human osteoblast cell line hFob1.19 through Wnt/β-catenin signaling pathway

PANG Lan, LI Peifan, ZHENG Lei, WANG Yiming

2023, 43(3):  374-379.  doi:10.16352/j.issn.1001-6325.2023.03.374

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Objective To investigate the effect of risperidone on the apoptosis of human osteoblast cell line hFob1.19 and analyze potential molecular mechanism based on Wnt/β-catenin signaling pathway. Methods hFob1.19 cells were divided into control group and risperidone intervention group (0, 5, 20, 40, 60, 80, 100 and 120 μmol/L). Cell viability was detected by CCK-8 assay. The apoptosis rate was detected by flow cytometry. RT-qPCR and Western blot was used to detect the mRNA and protein expression of BCL-2, MCL-1, BAX, and β-catenin. Results 1)Compared with the control group, the cell viability of the risperidone group decreased in a dose- and time-dependent manner (P＜0.05), while the apoptosis rate increased in a dose-dependent manner(P＜0.05). 2)Compared with the control group, the expression of pro-apoptotic gene BAX in risperidone group increased, while the expression of anti-apoptotic genes BCL-2 and MCL-1 decreased, and the expression of β-catenin decreased (P＜0.01). 3)Compared with the control group, the levels of pro-apoptotic proteins BAX and cleaved caspase-3 were increased, the levels of anti-apoptotic proteins BCL-2 and MCL-1 were decreased, and the expression of β-catenin protein was decreased in risperidone group (P＜0.01). 4) Compared with the control group, the expression of β-catenin protein in the nucleus and cytoplasm of risperidone group decreased (P＜0.05). Conclusions Risperidone induces apoptosis of hFob1.19 cells, and the mechanism may be related to the inhibition of β-catenin expression and nuclear translocation of β-catenin by risperidone, which leads to the disruption of the balance between anti-apoptotic and pro-apoptotic proteins.

Activin A improves the outcomes of neurological function in mice with ischemic stroke through ACVR1C of oligodendrocytes

LI Yudie, WANG Hongyu, HAN Song, LI Junfa

2023, 43(3):  380-385.  doi:10.16352/j.issn.1001-6325.2023.03.380

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Objective The role of activin A receptor type 1C(ACVR1C) in white matter remyelination and neurological outcome of mice with ischemic stroke were investigated. Methods Mice were randomly divided into empty virus vector sham operation group, adeno-associated virus(AAV) sham operation group, empty virus vector model group, AAV model group, empty virus vector activin group A and AAV activin group A.Acvr1c^flox/flox mice with middle cerebral artery oclusion-reperfusion (MCAO/R) for 1 to 10 days were established. Adeno-associated virus AAV-PDGFRα-cre and AAV-PLP-cre with cre recombinase were injected into the lateral ventricles of the mice. Conditional knockout of Acvr1c on oligodendrocytes and oligodendrocytes. Neurological function score was used to observe the prognosis of neurological function. The expressions of ACVR1C protein and myelin basic protein (MBP) were detected by Western blot. Results With the extension of reperfusion time, activin A improved the behavioral outcome of mice by ACVR1C on oligodendrocytes at day 7 (P＜0.05), and significantly increased the expression of MBP protein in corpus callosum at day 10 (P＜0.05). Conclusions Activin A promotes white matter remyelination and improves outcomes of neurological function of ischemic stroke mice by acting on ACVR1C on oligodendrocytes.

Effects of Quanduzhong Jiaonang on microcirculatory blood perfusion of intestinal wall in spontaneously hypertensive rats

WANG Qin, ZHANG Xiaoyan, LIU Xueting, Li Bingwei, LI Hongwei, YANG Yili, HAN Jianqun

2023, 43(3):  386-392.  doi:10.16352/j.issn.1001-6325.2023.03.386

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Objective To investigate the effects of Quanduzhong Jiaonang(QDZJN) and pinoresinol diglucoside (PDG) on microcirculatory blood perfusion in intestinal wall and its spectral characteristics in spontaneously hypertensive rats (SHRs). Methods SHRs were randomly divided into SHR, SHR+QDZJN, SHR+PDG (L), SHR+PDG (M) and SHR+PDG (H) groups with 6 in each group. The control group consisted of 6 WKY rats. All treatment groups were given intragastric administration of QDZJN, PDG, or pure water. After 2 month continuous administration, rats' intestines were exposed by surgery. The wall microcirculatory blood perfusion of was measured by laser Doppler flowmetry (LDF) and laser Doppler perfusion imaging (LDPI). Wavelet transform analysis was performed, and the amplitudes of NO-independent endothelial and NO-dependent endothelial oscillators were compared among six groups. Results Compared with the control group, blood perfusion level of intestine wall was significantly decreased in SHRs group (P＜0.001). After two months of treatment with QDZJN and PDG, the blood perfusion level of SHRs was significantly elevated (P＜0.001). The amplitudes of NO-dependent and -independent endothelial activity in SHRs group were significantly lower than those in the control group (both P＜0.01). QDZJN and PDG significantly enhanced the amplitude of NO-dependent and -independent endothelial activity of intestine wall perfusion in SHRs (P＜0.0001 and P＜0.01). Conclusions Treatment with QDZJN and PDG for two months may significantly improve the microhemodynamics and endothelial function of intestine wall in SHRs.

miR-425-5p targets TGF-β1/Smad2 signaling pathway to attenuate collagen fiber deposition in hypertrophic scar tissue in mice

LIANG Yan, WANG Lijuan, WU Huilin

2023, 43(3):  393-401.  doi:10.16352/j.issn.1001-6325.2023.03.393

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Objective To investigate the role and mechanism of miR-425-5p in the formation of hypertrophic scar(HS).Methods The levels of miR-425-5p, transforming growth factor-β1 (TGF-β1) and SMAD family member 2 (Smad2) in 16 pairs of HS tissue and normal skin tissue were detected by RT-qPCR and Western blot. The fibroblast cells were divided into nine groups: control group, miR-425-5p-mimic group, NC-mimic group, miR-425-5p-inhibitor group, NC-inhibitor group, TGF-β1-pcDNA3.1 group, NC-pcDNA3.1 group, miR-425-5p-mimic+NC-pcDNA3.1 group and miR-425-5p-mimic+TGF-β1-pcDNA3.1 group. The cells were transfected with Lipofectamine 2000. The targeting relationship between miR-425-5p and TGF-β1 was verified by dual-luciferase reporter gene assay. Hypertrophic scars in mice were induced by bleomycin(BLM), and then the mice were randomly divided into 3 groups, control group (NC-agomir), model group (NC-agomir+BLM) and intervention model group transfected with miR-425-5p (miR-425-5p-agomir+BLM), mice were treated for 21 days. Collagen fiber deposition in HS tissue was detected by Masson's trichrome staining. The expressions of miR-425-5p, type Ⅰ collagen (Col-Ⅰ), type Ⅲ collagen (Col-Ⅲ), α-smooth muscle actin (α-SMA), TGF-β1 and Smad2 in tissues and cells were detected by RT-qPCR and Western blot. Results Compared with normal group, the expression of miR-425-5p in HS group was decreased (t=4.242, P＜0.001), while the mRNA and protein expression of TGF-β1 was increased(P＜0.001). Compared with control group, the mRNA and protein expression of Col-Ⅰ, Col-Ⅲ, α-SMA, TGF-β1 and Smad2 in miR-425-5p-mimic group were all decreased (P＜0.05). Compared with control group, mRNA and protein expression of Col-Ⅰ, Col-Ⅲ, α-SMA, TGF-β1 and Smad2 in miR-425-5p-inhibitor group was all increased(P＜0.05). After co-transfection with miR-425-5p-mimic, the relative luciferase activity of TGF-β1-3′-UTR-WT group was reduced as compared with TGF-β1-3′-UTR-MUT group (P＜0.05). Compared with miR-425-5p-mimic+NC-pcDNA3.1 group, mRNA and protein expression of Col-Ⅰ, Col-Ⅲ, α-SMA, TGF-β1 and Smad2 in miR-425-5p-mimic+TGF-β1-pcDNA3.1 group were all increased (P＜0.05). Compared with NC-agomir+BLM group, the relative collagen content of miR-425-5p-agomir+BLM group was decreased (P＜0.05) and the expression of miR-425-5p was increased (P＜0.05). The TGF-β1 mRNA and protein were decreased (P＜0.05).Conclusions The miR-425-5p is down-regulated in HS tissue, and up-regulated miR-425-5p inhibits collagen deposition and HS formation by inhibiting TGF-β1/Smad2 signaling pathway.

Dexamethasone attenuates airway inflammation in mouse models with allergic asthma

LIU Fen, HU Runfang, MAO Song, XU Min, SHI Wenjing, CHEN Ling

2023, 43(3):  402-407.  doi:10.16352/j.issn.1001-6325.2023.03.402

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Objective To observe the inhibitory effect and the relative mechanisms of dexamethasone(DEX) on airway inflammation in mouse models with allergic asthma. Methods BALB/c mice were randomly divided into control group, asthma group, and dexamethasone group. The mice in the asthma group were subcutaneously injected with ovalbumin (OVA)/aluminum hydroxide mixture on day 0, 7, 14 and nebulized with 1% OVA suspension for 20 minutes on day 21 and 22. The mice in the dexamethasone group were given intraperitoneal injection of dexamethasone 3 hours before each inhalation based on the asthma group. The airway resistance of mice was measured at the end of the last aerosol inhalation, the cells in bronchoalveolar lavage fluid (BALF) were counted by Wright-Giemsa staining. The concentration of inflammatory factors in BALF was measured by ELISA. The protein expression of NLRP3 and IL-1β were detected by immunohistochemistry (IHC), and lung histopathological analysis was performed. Results Compared with the control group, the airway hyperresponsiveness (AHR) of mice in the asthma group was significantly enhanced; The numbers of eosinophils and neutrophils in BALF were significantly increased (P＜0.01); IL-5, IL-6, IL-18 and IL-1β expression in BALF were significantly increased (P＜0.01); The expression of NLRP3 and IL-1β in lung tissue was enhanced as shown by IHC result. Compared with the asthma group, AHR of mice in the dexamethasone group was significantly reduced; The expression levels of IL-18 and IL-1β were also significantly decreased(P＜0.01); The protein expressions of NLRP3 and IL-1β in the lung tissue were decreased; The pathological histology analysis showed inflammatory infiltration in lung tissue from the dexamethasone group was significantly reduced (P＜0.01). Conclusions Dexamethasone suppresses NLRP3 inflammasome activation induced by OVA, decreases inflammatory factors expression and airway hyperresponsiveness, thereby effectively alleviates the airway inflammation of asthmatic mice.

miR-767-5p inhibits the invasion of ovarian cancer cell lines by regulating the expression of TBL1XR1 protein

LENG Haina, ZHANG Yan, WANG Xiaodong, ZHANG Xueyou, LI Hongli

2023, 43(3):  408-414.  doi:10.16352/j.issn.1001-6325.2023.03.408

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Objective To explore the effect and mechanism of miR-767-5P and transductin β1X linked receptor protein 1 (TBL1XR1) on the progression of ovarian cancer. Methods Database analysis: KEGG (Kyoto Encyclopedia of Genes and Genomes, Kyoto Encyclopedia) enrichment analysis of miR-767-5P using GEO, miRPATH database and RStudio TOP5 microRNAs with differential expression multiples were selected from low and high expression microRNAs in the GEO data set, then ranked from low to high in terms of differential multiples. The target genes for miR-767-5p were predicted by miRDB and other databases. The intersection was selected. The target genes were screened by the Open Target Platform, GEPIA and other databases. GEPIA and THPA databases were used to analyze the expression level of TBL1XR1 in human organs, immunohistochemical analysis and survival curve analysis. Experimental verification: Dual luciferase assay detected the binding target of miR-767-5P and TBL1XR1. Western blot was used to detect TBL1XR1 expression in ovarian cancer cell lines (OC3, SKOV-3, HO-8910) and normal ovarian epithelial cell line(IOSE80). After transferring into SKOV-3 cells with miR-767-5P over-expression plasmid and TBL1XR1 over-expression plasmid, Western blot was used to detect the expression level of TBL1XR1 and Tanswell cell assay was used to detect cell invasion. Results Database analysis: miR-767-5p with the highest differential ratio of low expression was selected as the target microRNA for follow-up research; miR-767-5p was involved in various cancer-related pathways, and miR-767-5p and TBL1XR1 were closely associated with breast cancer and ovarian cancer, etc. TBL1XR1 was highly expressed in ovarian cancer and was associated with poor prognosis. Experimental verification: miR-767-5p and TBL1XR1 could be targetly bound(P＜0.05); Compared with IOSE80, TBL1XR1 was significantly over-expressed in OC3, SKOV-3 and HO-8910 cells. After the transfection of miR-767-5p over-expressed plasmid, the expression level of TBL1XR1 was decreased and the aggressiveness of ovarian cancer cells was reduced(P＜0.05), while simultaneously transfection of TBL1XR1 over-expressed plasmid could reduce this effect to some extent. Conclusions miR-767-5p regulates TBL1XR1 expression and inhibits the invasion of human ovarian cancer cell lines.

Construction and genotype identification of Nrf2 knockout mouse model

WANG Minrong, ZHANG Feng, LU Liqun

2023, 43(3):  415-418.  doi:10.16352/j.issn.1001-6325.2023.03.415

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Objective To construct and identify Nrf2 knockout mouse model. Methods A pair of male and female heterozygous (Nrf2^-/+) mice were introduced to breed F1 mice. Male and female Nrf2^-/+ mice from F1 generation were bred to obtain F2 generation mice. DNA was extracted from the tail tissue of mice at 5 days of age and their genotype was determined by PCR and agarose gel electrophoresis. NRF2 protein was extracted and coding gene was knocked out from the lung tissues of mice. The expression of NRF2 protein was detected by Western blot, and the identification results were confirmed laterally. Results Homozygous (Nrf2^-/-) mice continued to mate and obtain homozygous mice. Three genotypes were identified when F1 was mated with F2 generation heterozygous mice: wild type (Nrf2^+/+), heterozygous (Nrf2^+/-) and homozygous (Nrf2^-/-). The genotypes of offspring mice were successfully identified by PCR. NRF2 protein expression in lung tissue of Nrf2 knockout mice was significantly lower than that of wild-type mice (P＜0.05). Conclusions The mouse model with Nrf2 knockout is successfully bred in this study, which provides a new experimental tool for further exploring the role and mechanism of NRF2.

CIRC_0044235 targeting miR-574-5p attenuates IL-1β-induced injury in human chondrocyte

WANG Bo, ZHANG Minghuan

2023, 43(3):  419-426.  doi:10.16352/j.issn.1001-6325.2023.03.419

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Objective To investigate whether CIRC_0044235 targeting miR-574-5p could affect the levels of chondro-cyte apoptosis, oxidative stress and inflammatory factor expression induced by interleukin (IL)-1β. Methods The cells were divided into control group, IL-1β group, transfected with pcDNA, pcDNA-CIRC_0044235, anti-miR-NC, anti-miR-574-5p, pcDNA-CIRC_0044235+miR-NC, pcDNA-CIRC_0044235+miR-574-5p, interfere with IL-1β. RT-qPCR was used to detect the expression of CIRC_0044235 and miR-574-5p in cell. Flow cytometry and Western blot were used to detect apoptosis and the expression of related proteins Bcl-2 and Bax, respectively. Colorimetry was used to superoxide dismutase (SOD) and lactate dehydrogenase (LDH) activity were detected, and ELISA was used to detect the levels of IL-6 and IL-10. A dual-luciferase reporter assay was used for examining the targeted binding of CIRC_0044235and miR-574-5p.Results Compared with the control group, the expression of CIRC_0044235, the expression of Bcl-2 protein, the activity of SOD and the content of IL-10 in chondrocytes in the IL-1β group were decreased (P＜0.05), while the expression of miR-574-5p and the rate of apoptosis were decreased (P＜0.05). Bax protein expression, LDH activity and IL-6 content all increased(P＜0.05). Compared with IL-1β group or pcDNA intervention group, CIRC_0044235 expression, Bcl-2 protein expression, SOD activity and IL-10 content in chondrocytes of pcDNA-CIRC_0044235 group increased, while miR-574-5p expression, apoptosis rate, Bax protein expression, LDH activity and IL-6 content decreased (P＜0.05). CIRC_0044235 targeted miR-574-5p. miR-574-5p expression, apoptosis rate, Bax protein expression, LDH activity and IL-6 content in chondrocytes of anti-miR-574-5p group were all lower than those found in anti-miR-NC group. Bcl-2 protein expression, SOD activity and IL-10 content were higher than those in anti-miR-NC group (P＜0.05). miR-574-5p expression, apoptosis rate, Bax protein expression, LDH activity and IL-6 content in chondrocytes of pcDNA-CIRC_0044235+miR-574-5p group were higher than those of pcDNA-CIRC_0044235+miR-NC group. The Bcl-2 protein expression, SOD activity and IL-10 content were lower than those in the pcDNA-CIRC_0044235+miR-NC group (P＜0.05).Conclusions CIRC_0044235 may inhibit IL-1β-induced apoptosis, oxidative stress and inflammatory factor expression in human articular chondrocytes by targeting miR-574-5p.

Dihydroartemisinin alleviates lung injury in rat models with chronic obstructive pulmonary disease(COPD)

QIN Yuchun, KUANG Xiangdong, CAI Linzai, XIE Jingchen, CHEN Shan

2023, 43(3):  427-432.  doi:10.16352/j.issn.1001-6325.2023.03.427

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Objective To investigate the impacts of dihydroartemisinin (DHA) on airway inflammation and lung injury in chronic obstructive pulmonary disease (COPD) rats by inhibiting interleukin (IL)-6/signal transducer and activator of transcription (STAT) 3 signaling pathway. Methods SD rats were randomly divided into control group, COPD group, low and high dose DHA (L-DHA, H-DHA) groups and neutralized IL-6 group. The inflammatory factors[IL-6, IL-1β, IL-17, tumor necrosis factor alpha (TNF-α)] in bronchoalveolar lavage fluid (BALF) were measured by ELISA; The total number of cells in BALF and the numbers of inflammatory cell types[eosinophils (Eos), neutrophils (Neu), lymphocytes (Lym)] were counted. The pathological changes of lung tissue were microscopied with HE staining and Masson staining; The expression of IL-6/STAT3 signaling pathway proteins in lung tissue was measured by Western blot. Results Compared with the control group, the level of IL-6, IL-1β, IL-17, TNF-α, the total number of cells, the numbers of Eos, Neu and Lym cells in the BALF of the COPD group all increased (P＜0.05); The lung tissue was obviously damaged, and the phosphorylation level of IL-6 protein and STAT3 in lung tissue increased (P＜0.05). After the intervention with L-DHA, H-DHA and neutralized IL-6, the above conditions were improved (P＜0.05). Conclusions DHA can reduce airway inflammation and lung tissue damage in COPD rat models, the potential mechanisms may be related to the inhibition of IL-6/STAT3 signaling pathway.

Puerarin attenuates the inflammatory response of vascular endothelial cells in KKAy mice

ZOU Jie, ZHANG Dede, TAO Yi, ZHAO Jing, WANG Qiong, XU Naijia

2023, 43(3):  433-437.  doi:10.16352/j.issn.1001-6325.2023.03.433

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Objective To explore the intervention mechanism of puerarin(PUR) on the inflammatory response of vascular endothelial cells with KKAy mouse models.Methods C57bL/6j mice were used as the control group. KKAy mice were randomly divided into diabetes group, metformin hydrochloride(MH)and puerarin(PUR) group with 10 in each. The indexes of glucose metabolism in each group were recorded. The contents of tumor necrosis factor-α (TNF-α), interferon-γ(IFN-γ), transforming growth factor-β1(TGF-β1), interleukin-1 (IL-1) and vascular endothelial growth factor (VEGF) were detected by ELISA; TUNEL method was used to detect apoptosis in vascular tissue; mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were detected by RT-qPCR and Western blot. Results Compared with the control group, the indexes of glucose metabolism and apoptosis in diabetes group increased significantly; The contents of TNF-α, IFN-γ, TGF-β1, IL-1 and VEGF in serum changed significantly (P＜0.05) and the mRNA and protein expressions of VCAM-1 and ICAM-1 in vascular tissue increased significantly(P＜0.05). Compared with diabetes group, MH group and PUR group significantly improved glucose metabolism and cell apoptosis; TNF-α, IFN-γ, TGF-β1, IL-1 and VEGF decreased significantly (P＜0.05); The mRNA and protein expressions of VCAM-1 and ICAM-1 were all significantly improved(P＜0.05). Conclusions PUR can effectively inhibit the expression of vascular endothelial inflammatory factors, VCAM-1 and ICAM-1 adhesion molecules in KKAy mice, and alleviate the vascular endothelial injury found in diabetes mice.

Antibodies to SARS-CoV-2-related linear epitopes induce neuroinflammation of mice

XU Jinming, HONG Yuxuan, WEI Hui, XU Qi

2023, 43(3):  438-443.  doi:10.16352/j.issn.1001-6325.2023.03.438

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Objective To evaluate the potential biological functions of non-viral neutralizing antibodies associated with linear epitopes of the SARS-CoV-2 spike protein. Methods The linear epitope S2-78 with the highest response frequency and longest antibody retention time in COVID-19 patients was selected according to previous reports. After immunizing mice with keyhole limpet hemocyain conjugated S2-78 polypeptide(KLH-S2-78), the serum anti-S2-78 IgG antibody level, mouse behavioral phenotype and the density of microglia in the brain were detected. Results KLH-S2-78 immunized mice developed high titers of anti-S2-78 IgG antibodies(the highest titer was 25 600, A₄₅₀=0.305 5), a psychomotor-like behavioral phenotype with defective sensorimotor gating, impaired olfactory function, and impaired spontaneity. The density of microglia significantly increased in the cortex and hippocampus(P＜0 .05), suggesting a state of central inflammatory stress. Conclusions Anti-S2-78 IgG antibody may cause neuroinflammatory damages in the brain tissue by stimulating the host inflammatory response.

Over-expression of miR-144-3p attenuates Ang Ⅱ-induced injury of HUVEC

YE Yuanzheng, FU Xiaoxiao, MA Xiaoyun, FAN Ping

2023, 43(3):  444-449.  doi:10.16352/j.issn.1001-6325.2023.03.444

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Objective To investigate the effect of miR-144-3p on the proliferation, invasion, apoptosis and ROS levels of human umbilical vein endothelial cell (HUVEC) induced by angiotensin Ⅱ(Ang Ⅱ). Methods The cells were divided into control group, model group (Ang Ⅱ), negative control group (Ang Ⅱ+ transfection miR-144-3p NC) and experimental group (Ang Ⅱ + transfection miR-144-3p mimic). RT-qPCR was used to detect the transfection efficiency. MTT method was used to detect cell proliferation. Cell invasion was examined by Transwell chamber. Apoptosis kit and flow cytometry were applied to detect apoptosis, and the flow cytometry was applied to detect intracellular reactive oxygen species(ROS) level. Results Compared with control group, the proliferation and invasion of the cells in the model group decreased significantly, but the apoptotic rate and intracellular ROS level increased significantly(P＜0.05). The above indicators found in the experimental group were all alleviated to a certain extent (P＜0.05). Conclusions Over-expression of miR-144-3p can effectively reduce the proliferation and invasion of HUVEC induced by Ang Ⅱ and reduce the apoptosis rate as well as ROS level.

Effect of IL-35 on the adhesion of human umbilical vein endothelial cells after sCD40L stimulation

GUO Weiwei, ZHAO Pingping, YU Lulu, LI Ming

2023, 43(3):  450-455.  doi:10.16352/j.issn.1001-6325.2023.03.450

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Objective To investigate the effect of interleukin (IL)-35 on vascular endothelial cell adhesion after stimulation with soluble CD40 ligand (sCD40L). Methods Thirty patients with lower extremity deep vein thrombosis in acute phase (DVT group) and 30 healthy subjects (HC group) were selected. Peripheral blood was collected, and the level of IL-35, sCD40L, VCAM-1, P-selectin and vWF in the serum was measured by ELISA. The human umbilical vein endothelial cells (HUVECs) were cultured and divided into three groups: control group, sCD40L group and IL-35 group. ELESA and Western blot were used to detect the expression of VCAM-1, ICAM-1, P-selectin and vWF. The adhesion of platelet and peripheral blood mononuclear cells to HUVECs was examined by immunofluorescence. Results Compared with control group, the level of IL-35 in serum of DVT group was significantly decreased(P＜0.05), and the levels of sCD40L, VCAM-1, ICAM-1, P-selectin and vWF were significantly increased(P＜0.05). In vitro, experiments showed that IL-35 significantly inhibited the expression of VCAM-1, ICAM-1, P-selectin and vWF in HUVECs stimulated by sCD40L(P＜0.05) and inhibited the adhesion of platelet and peripheral blood mononuclear cells to HUVECs. Conclusions IL-35 may reduce the adhesion function of HUVECs after sCD40L stimulation and inhibit thrombosis in DVT patients.

Herkinorin pretreatment alleviates cerebral injury in rat models with ischemic stroke

SONG Wanqing, LI Junfa, CUI Xu

2023, 43(3):  456-461.  doi:10.16352/j.issn.1001-6325.2023.03.456

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Objective To investigate the regulation and mechanism of Herkinorin preconditioning on NOD-like receptor protein 3 (NLRP3) in brain tissue of transient middle cerebral artery occlusion (tMCAO) rats. Methods Rats were randomly divided into sham operation group (sham), model group (tMCAO) and Herkinorin group (Herkinorin). Before modeling, rats in Herkinorin group were intraperitoneally given Herkinorin (10 mg/kg) once a day for a week. The rats were evaluated by neurologic score, TTC staining, TUNEL staining 24 h after reperfusion. The expression levels of IκBα, p65, p-p65, pro-IL-1β, IL-1β, pro-caspase1, caspase1 p20 and NLRP3 were detected by Western blot. The binding level of IκBα to β-arrestin2 was detected by co-immunoprecipitation (Co-IP). Results Compared with sham group, rats in tMCAO group had higher behavioral score (P＜0.01), increased cerebral infarction percentage and increased cerebral edema rate (P＜0.01). The level of cell apoptosis was increased in ischemic penumbra (P＜0.01). The expression levels of IκBα and p65 were decreased (P＜0.01) and the expression levels of p-p65, IL-1β, caspase1 p20 and NLRP3 were increased in ischemic penumbra (P＜0.01). The binding level of IκBα to β-arrestin2 was decreased in ischemic penumbra (P＜0.01). Compared with tMCAO group, rats in Herkinorin group had lower behavioral score (P＜0.01), lower cerebral infarction percentage and lower cerebral edema rate (P＜0.01). The level of cell apoptosis was decreased in ischemic penumbra(P＜0.01). The expression of IκBα and p65 was increased (P＜0.01) and the expression of p-p65, IL-1β, caspase1 p20 and NLRP3 was decreased in ischemic penumbra (P＜0.01). The binding of IκBα to β-arrestin2 was increased in ischemic penumbra (P＜0.01). Conclusions Herkinorin may negatively regulate NF-κB/NLRP3 pathway to alleviate cerebral ischemia-reperfusion injury of tMCAO rats.

Nitric oxide synthase inhibitor reduces airway inflammation in mouse models with asthma

WANG Fei, LI Wenxuan, DING Junqiong, LIU Zhen, WANG Xiaoming, YANG Ju, WANG Dalian

2023, 43(3):  462-467.  doi:10.16352/j.issn.1001-6325.2023.03.462

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Objective To explore the therapeutic effect of nitric oxide synthase (NOS) inhibitor in asthmatic mice. Methods BALB/c mice of 5 to 6 weeks were randomly divided into five groups with 10 in each: 1)control group; 2)asthma group: The asthma model was established by ovalbumin (OVA)-sensitized mice; 3)S-methyl isothiourea sulfate (SMT) group: OVA-sensitized asthmatic mice were stimulated and then given with SMT; 4)N-nitro-L-arginine methyl ester (L-NAME) group: OVA-sensitized asthmatic mice were stimulated and then given with L-NAME; 5) NG-monomethyl-L-arginine (L-NMMA) group: OVA-sensitized asthmatic mice were stimulated and then given with L-NMMA. HE staining was used for histopathological analysis. Airway reactivity was assessed using a methacholine challenge test. The levels of nitric oxide (NO) and cytokines in serum and bronchoalveolar lavage fluid(BALF) were detected by ELISA. Results Compared with the control group, goblet cell proliferation and increased mucus secretion were found in the asthma group, together with a large number of inflammatory cell infiltration around the trachea and blood vessels and significantly increased airway resistance, which were improved after the administration of NOS inhibitors, especially in the SMT group. Compared with the control group, the levels of NO in plasma, BALF and lung tissue homogenate were significantly increased in the asthma group (P＜0.05), while the level of IL-2, IL-4, IL-17 and TNF-α in plasma and BALF was significantly increased (P＜0.05). Compared with the asthma group, the level of NO in plasma, BALF and lung tissue homogenate was significantly decreased in SMT group (P＜0.05), while the level of IL-2, IL-4, IL-17 and TNF-α in plasma and BALF was significantly decreased in SMT group (P＜0.05). Compared with the asthma group, the level of plasma NO, IL-2, IL-17, and TNF-α in the L-NAME group was significantly decreased (P＜0.05). The level of NO, IL-2, IL-17, and TNF-α in BALF was significantly decreased (P＜0.05). Compared with the asthma group, the plasma level of NO, IL-2, IL-4, IL-17 and TNF-α in the L-NMMA group was significantly decreased (P＜0.05). The level of NO, IL-2, IL-4, IL-17 and TNF-α in BALF was significantly decreased(P＜0.05), and the level of NO in lung tissue homogenate was significantly decreased (P＜0.05). Conclusions NOS inhibitor, especially SMT may reduce airway inflammation of asthmatic mice.

Clinical Sciences

Prevalence and influencing factors of cognitive dysfunction among inpatients in Geriatrics Department of a hospital in Yunnan Province

DAI Jingrong, LI Jie, HE Xu, LI Yang, LI Yan

2023, 43(3):  468-475.  doi:10.16352/j.issn.1001-6325.2023.03.468

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Objective To investigate the prevalence of cognitive dysfunction among inpatients in Geriatrics Depart- ment of a hospital in Yunnan Province, and to analyze the influencing factors of cognitive dysfunction of the elderly.Methods A total of 2 216 admitted patients(≥60 years old) in the Department of Geriatrics of a hospital in Yunnan Province from September 2018 to August 2021 were recruited as the subjects. General data of the patients were collected. Comprehensive geriatric assessment was conducted by an internet-based platform of the Comprehensive Geriatric Assessment developed by the Department of Geriatrics of Yunnan First People's Hospital, among which cognitive function was assessed by the Mini-Mental State Examination(MMSE)phenotype. Results Among 2 216 patients, 1 087(49.1%) had normal cognitive function, 639(28.8%) had mild cognitive impairment, 285 (12.9%) had moderate cognitive impairment and 205 (9.3%) had severe cognitive impairment. According to multivariate Logistic regression analysis, increased age [OR=1.026,95% CI(1.015, 1.037),P＜ 0.001], vision decline[OR=1.290,95% CI(1.002, 1.662),P＜ 0.05], empty nest[OR=1.433,95% CI(1.009, 2.034),P＜ 0.05], family support disorder[OR=1.436,95% CI(1.120, 1.842),P＜ 0.05], insomnia [OR=1.380,95% CI(1.095, 1.740),P＜ 0.05] and suffered chronic obstructive pulmonary disease [OR=1.234,95% CI(1.008, 1.512),P＜ 0.05) were the risk factors for cognitive function in the elderly, while the individuals mainly engaged in mental activities[OR=0.678,95% CI(0.540,P＜ 0.05).0.852, P＜ 0.001], education experience of primary school[OR=0.613,95% CI(0.485,0.776,P＜0.001], secondary school[OR=0.670,95% CI(0.534, 0.839), P＜ 0.001) and university degree or above [OR=0.555,95% CI(0.410, 0.751),P＜ 0.001] were protective factors. Conclusions The prevalence of cognitive dysfunction in elderly hospitalized patients is high and closely related to a variety of factors. Specific intervention of related factors is of great significance for the early prevention of cognitive impairment in the elderly.

Mini Reviews

Research progress on the role of endoplasmic reticulum stress in osteoarthritis

JIN Tao, YANG Qingshan, WU Shujin, ZHU Xiaoyan, SHI Yucong, NIU Jianxiong, LIU Lin

2023, 43(3):  476-480.  doi:10.16352/j.issn.1001-6325.2023.03.476

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Osteoarthritis is a common degenerative disease in which endoplasmic reticulum stress(ER stress) plays an important role in the pathogenesis of chondrocyte apoptosis. To limit the adverse effects of endoplasmic reticulum stress, cells activate the unfolded protein response (UPR). However, when endoplasmic reticulum stress persists beyond the maximum tolerance of UPR, cells may trigger endoplasmic reticulum dysfunction through three pathways of UPR leading to chondrocyte apoptosis.

Research progress on the role of neutrophil extracellular traps in lung diseases

DING Yu, WU Yan, BIAN Tao

2023, 43(3):  481-485.  doi:10.16352/j.issn.1001-6325.2023.03.481

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Neutrophils are resident immune cells in the lung, which can release decondensed chromatin containing neutrophil elastases, myeloperoxidases, citrullinated histones and cytoskeletal proteins upon stimulation, namely neutrophil extracellular traps(NETs). NETs play an anti-infective role in lung diseases. But excessive NETs release potentially leads to cause lung tissue injury, enhances inflammatory response and promotes tumor metastasis. These results of research provide some new ideas for the development of potential drugs.

Recent progress of the role of ferroptosis in the pathogenesis of early brain injury after subarachnoid hemorrhage

QU Dapeng, SUN Huiyan, LI Qiang, WANG Hongquan

2023, 43(3):  486-489.  doi:10.16352/j.issn.1001-6325.2023.03.486

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Subarachnoid hemorrhage (SAH) leads to ferroptosis with clinical evidence like iron metabolism deregulation, increased lipid peroxitation(LPO) and the inhibition of glutathione/glutathione peroxides 4(GSH/GPX4). Ferroptosis mediated early brain injury (EBI) may occur in the 72-hour period following SAH (EBI-SAH) leads to the poor prognosis of SAH. Pharmacological targeting at ferroptosis mitigate EBI-SAH, provides a new target for future treatment and prevention of EBI-SAH through targeting at ferroptosis.

Advances in the study of the correlation between vitamin D-24-hydroxylase and thyroid carcinoma

CHEN Shijing, FU Jinglan, DENG Yuanyuan, ZHANG Ying, LIU Huixia

2023, 43(3):  490-494.  doi:10.16352/j.issn.1001-6325.2023.03.490

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Thyroid carcinoma(TC) is the most common malignant tumor of endocrine system. Patients with vitamin D deficiency have an increased risk of TC. Vitamin D-24-hydroxylase (CYP24A1) is main inactivating enzyme of active vitamin D which may inhibit the antiproliferative effect of vitamin D and promote the development of TC by inactivating 1,25-dihydroxyvitamin D₃.

Research progress on the correlation between polymorphism of immunoregulatory gene and susceptibility to Graves' disease

WANG Yujie, YANG Mengdi, HE Fengying, DING Yulu, SUN Linnan, ZHEN Donghu

2023, 43(3):  495-499.  doi:10.16352/j.issn.1001-6325.2023.03.495

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Graves' disease(GD)is an organ-specific autoimmune disease with genetic background. The core pathogenesis of GD is immune factors, but genetic factors also play an important role in it. The susceptibility genes of GD are mainly divided into immunoregulatory gene and thyroid specific gene. The polymorphism of immunoregulatory gene may have some impact on the susceptibility of GD through various mechanisms, which may provide new ideas for the further study of the susceptibility genes and pathogenesis of GD.

Research progress on biomarkers of irritable bowel syndrome

ZHENG Xingjian, RAN Xue, REN Ziyue, DAI Chibing

2023, 43(3):  500-504.  doi:10.16352/j.issn.1001-6325.2023.03.500

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Irritable bowel syndrome (IBS) is a functional gastrointestinal disease, and its diagnostic criteria has been based on clinical profile. There are various biomarkers associated with IBS.This paper reviews the relationship between IBS and those biomarkers like mean platelet volume (MPV), red blood cell distribution width (RDW), neutrophil/lymphocyte ratio (NLR), high-sensitivity C-reactive protein (HS-CRP), C-reactive protein (CRP), resolvin D1 (RvD1), interleukin 6 (IL-6), interleukin 8(IL-8), tumor necrosis factor-α(TNF-α), fecal calprotectin (FCP), fecal lactoferrin (LF).The research and clinical application of valuable biomarkers for the diagnosis of IBS may make the diagnosis of IBS more accurate and faster,with less application of colonoscopy.

Progress in evaluation of cervical metastatic lymph nodes of differentiated thyroid cancer with ultrasonography

TIAN Yan, MA Jiaojiao, XI Xuehua, ZHANG Bo

2023, 43(3):  505-508.  doi:10.16352/j.issn.1001-6325.2023.03.505

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Accurate evaluation of cervical metastatic lymph nodes is of great significance to the risk staging, treatment and prognosis of patients with differentiated thyroid cancer(DTC). Ultrasonography is the main examination method to evaluate cervical lymph nodes. In recent years, with the emergence and extensive application of new technologies such as elastic imaging, contrast-enhanced ultrasonography, fine needle aspiration cytology and artificial intelligence, the diagnostic effectiveness of cervical metastatic lymph nodes of DTC has been further improved.

Research progress on the role of IgG N-glycosylation modification in diabetic retinopathy

ZHANG Yixin, CAI Shanjun, LI Zhili, YU Weihong, ZHANG Hua

2023, 43(3):  509-513.  doi:10.16352/j.issn.1001-6325.2023.03.509

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Diabetic retinopathy (DR) is an immune-inflammatory disease and immunoglobulin G(IgG) N-glycosylation modifications are closely associated with DR. Among them, the modification of galactosylation, fucosylation, sialylation and bisecting N-acetylglucosamine of IgG changed has been proved to be predisposing factor to stimulate inflammation and related retinopathy.

Research progress on the role of DNA methylation in the occurrence and prognosis of lung cancer

XUE Jianchao, WANG Yadong, LI Bowen, LIU Xinyu, LIANG Naixin, LI Shanqing

2023, 43(3):  514-518.  doi:10.16352/j.issn.1001-6325.2023.03.514

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Lung cancer is a leading cause of cancer-related morbidity and mortality in China. Early recurrence is the main cause of poor prognosis. The existing prognostic indicators are insufficient. Thus, it is urgent to find reliable prognostic indicators. DNA methylation is the most important epigenetic change in the development of lung cancer. With the development of high-throughput sequencing technology, DNA methylation has shown its great clinical value in the prognosis prediction of lung cancer patients due to its stable and detectable features.

Medical Education

Probe into the clinical standardized training mode for refresher physicians in Rheumatic Immunology Department

ZHANG Shangzhu, LI Qingyang, LI Hailong, SU Jinmei, LI Mengtao, ZHANG Wen, ZENG Xiaofeng

2023, 43(3):  519-522.  doi:10.16352/j.issn.1001-6325.2023.03.519

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Objective To evaluate the training outcomes of refresher physicians in Department of Rheumatic Immunology, Peking Union Medical College Hospital, and to explore the standardized training mode. Methods In September 2021, twenty three intermediate-level refresher physicians from the Department of Rheumatology and Immunology, Peking Union Medical College Hospital participated in a comprehensive multi-scene training program including outpatient tutorials, case-based teaching of difficult and critical cases in wards, specialist lectures and multi-disciplinary lectures. After six months of training, the refresher physicians completed a questionnaire survey covering medical care, scientific research, teaching format, and advanced training duration, with 10 multiple-choice questions and 3 fill-in-the-blank questions. The results were analyzed descriptively. Results After six months of training in a multi-scene comprehensive training program, as shown by the results of the self-assessment by the trainees, the clinical skills and scientific research capacity improved by 55.7% and 50% respectively as compared to the pre-training period. The average improvement of standardized diagnosis and treatment was 60.9%, and the average improvement of diagnosis and treatment skills was 53.5%. The average improvement in the diagnosis and treatment level of difficult cases was 53.0%. The average improvement in the diagnosis and treatment level of rare diseases was 50.4%.There were 65.25% of the refresher physicians believed that the most rewarding learning was in the outpatient clinics, followed by discussion of difficult cases in wards and lectures by the fellowship physicians. 56.5% of the refresher physicians felt that the optimal duration of the advanced training was 12 months.Conclusions A comprehensive training system combining outpatient tutorials, case-based training of difficult cases in the ward, specialized lectures and multidisciplinary lectures for advanced refresher physicians is effective for training rheumatologists.