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Table of Content
05 October 2016, Volume 36 Issue 10
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Effects of mfn2 siRNA on vascular smooth muscle cells derived foam cells formation inhibited by testosterone
2016, 36(10): 1323-1328.
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Objective To evaluate the effects of mitofusin 2(mfn2) gene silencing by specific small interference RNA(siRNA) on vascular smooth muscle cells(VSMCs) derived foam cells formation inhibited by testosterone. Methods The three double-strand siRNAs targeting mfn2 gene were designed and synthesized, then transfected into rat VSMCs by positive ion liposome Lipofectamine 2000. The mRNA and protein expression levels of mfn2 in VSMCs were detected by real-time fluorescent quantitative PCR and Western blotting, respectively. Then, VSMCs were divided into control group, testosterone group, testosterone+control-siRNA group, and testosterone+mfn2-siRNA group. Effects of testosterone with or without siRNA on the quantity of intracellular lipid of the VSMCs were detected with Oil red O staining and enzymatic fluorometric method. The expression of the Mfn2 was analyzed with Western blotting. We also examined the effect of testosterone with or without siRNA on the cholesterol transport related protein(CD36 and ABCA1). Results After mfn2-siRNAs were successfully transfected into rat VSMCs, compared to the non-targeting siRNA,the mfn2 mRNA and protein expression levels in VSMCs were significantly decreased at 12, 24, 36, 48 h(P<0.05). Compared with the control group, lipid deposition was reduced significantly in the testosterone with or without control-siRNA groups(both P<0.05). Testosterone markedly increased the expression of Mfn2 and ABCA1(both P<0.05), while suppressed the expression of CD36(P<0.05) in ox-LDL stimulated VSMCs. Moreover, such suppressive effects of testosterone on foam cells formation could partly been reversed by the mfn2-siRNA(P<0.05), suggesting an involvement of mfn2 in the mechanism. Conclusions Testosterone inhibited the formation of VSMCs derived foam cells induced by ox-LDL partly via the Mfn2 dependent manner by down-regulation of CD36 and up-regulation of ABCA1 expression.
miR-221 promotes N-MYC expression and cell proliferation in neuroblastoma SH-SY5Y cells
2016, 36(10): 1329-1334.
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Objective To explore the impact of miR-221 overexpression on the expression of N-MYC level and the cell proliferation in neuroblastoma SH-SY5Y cells. Methods miR-221 overexpression lentiviral vector was constructed and its stable transfection cells were established. Untreated group, control group and miR-221 group were set up. The expression of miR-221 was detected by RT-qPCR. The N-MYC mRNA and protein expression level were analyzed by RT-qPCR and Western blot, respectively. The distribution of cell cycle was tested by flow cytometry. The cell proliferation was measured by CCK8 assay. Results The recombinant vectors were verified by DNA Sanger sequencing. The results of RT-qPCR indicated that the miR-221 expression in cells transfected with miR-221 lentiviral vector as seven times as SH-SY5Y cells (P<0.01), with no difference between control and SH-SY5Y cells. Compared with SH-SY5Y cells, the mRNA and protein level of N-MYC were dramatically increased in cells transfected with miR-221 (P<0.01). The results of Flow cytometry demonstrated that miR-221 significantly decreased the G1-S checkpoint arrest (P<0.05). The results from CCK8 assay showed that overexpression of miR-221 promoted cell proliferation (P<0.01). Conclusion miR-221 may contribute to the enhancement of N-MYC and cell proliferation by rescue of G1-S checkpoint arrest in neuroblastoma SH-SY5Y cells.
Influence of miR-26a on proliferation and migration in human hepatic carcinoma cell lineSMMC-7721
2016, 36(10): 1335-1340.
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Objective To observe the expression level of miR-26a in human hepatic carcinoma and the influence of high expressed miR-26a on the proliferation and migration in human hepatic carcinoma cell lineSMMC-7721. MethodsThe miR-26a expression level was analyzed by bioinformatic analysis in human hepatic carcinoma and normal hepatic tissue. The miR-26a oligonucleotide was chemically synthesized and confirmed by sequencing. The miR-26a eukaryon expression system was constructed by pcDNA6.2-GW/Em-GFP-miR plasmid. The miR-26a was transfected into the SMMC-7721 cells transiently by pcDNA6.2-GW/Em-GFP -miR-15a plasmid, and quantified by quantitative real-time PCR on mRNA level. The proliferation and migration ability of SMMC-7721 cell with high-expressed miR-26a were detected by CCK8 assay and Wound Healing assay, respectively. Results The miR-26a was remarkable lower in the hepatic carcinoma tissues than in the normal hepatic tissues, the difference was statistically significant(P<0.0001). The sequence of miR-26a oligonucleotide wasmatched withthe designed sequence in 100%. The miR-26a expression was increased statistically (P<0.05) in SMMC-7721 cell transfected by pcDNA6.2-GW/Em-GFP-miR plasmid than control groups. The proliferation velocity of SMMC-7721 was decreased in high expressed miR-26a group than control groups with statistically difference (P<0.05). The migration velocity of SMMC-7721 was also decreased in high expressed miR-26a group than control groups with statistically difference (P<0.05). ConclusionsMiR-26a is low expressed in hepatic carcinoma tissue. High expressed miR-26a could decrease the capability of proliferation and migration in human hepatic carcinoma cell lineSMMC-7721.
Overexpression of CXCR4 /CXCR7 affects migration and proliferation of human umbilical cord mesenchymal stem cells
2016, 36(10): 1341-1347.
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Objective: To investigate the effect of SDF-1 / CXCR4 and SDF-1/ CXCR7 on the migration and proliferation of human umbilical cord mesenchymal stem cell. Methods: Using Ad-EASY adenoviral vector systems to construct recombinant adenovirus with overexpression of CXCR4 and CXCR7,hUC-MSCs was infected with Ad-CXCR4 or Ad-CXCR7 respectively, FCM was used to detect the expression of CXCR4 and CXCR7 as membrane receptors, Transwell assay was carried out to evaluate the SDF-1 induced migration ability of hUC-MSCs with CXCR4 or CXCR7 overexpression.MTT assay was performed to detect the cell proliferation activity for overexpression CXCR4 or CXCR7 of hUC-MSCs, as well as the cell survival after treated with H2O2. Results:The constructed adenovirus CXCR4 and CXCR7 successfully infected UC-MSCs, and the positive cell rate with membrane expression of CXCR4 or CXCR7 were 93.7% and 78.5%, respectively. Overexpression of CXCR4 and CXCR7 significantly enhanced SDF-1 induced cell migration of hUC-MSCs,which CXCR7 showed weaker effect, then CXCR7 but not CXCR4 was responsible for the SDF-1 induced cell viability and proliferation of hUC-MSCs. Conclusion: Both CXCR4 and CXCR7 mediated the SDF-1 induced migration of hUC-MSCs, in addition CXCR7 mediated the SDF-1 induced hUC-MSCs proliferation and cell viability under anti-oxidative stress.
Effect of 17β-estradiol on the expression of Hsp27 in papillary thyroid cancer BCPAP cells and its mechanism
2016, 36(10): 1348-1353.
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Objective To investigate the effect of 17β-estradiol on the expression of Hsp27 in papillary thyroid cancer BCPAP cells and its mechanism . Methods BCPAP cells were treated with 10-8 mol/L 17β-estradiol (E2) for different time periods , the expression of Hsp27 protein in cells was detected by Western blot; BCPAP cells were treated with E2, PPT and DPN, then detected the levels of Hsp27 byWestern blot ; RNA interference against ERα ( ERα siRNA ) and ERβ (ERβ siRNA ) was designed and synthesized, then transfected to BCPAP cells.The expression levels of Hsp27, ERα and ERβ in cells was analyzed by Western blot. The activity of Hsp27promoter was evaluated by chromatin immunoprecipitation analysis(CHIP). Results BCPAP cells were treated with 10-8 mol/L E2 for different time periods , the expression level of Hsp27 in BCPAP cells was increased gradually with the increasing hours for E2 treatment, and peaked at 24 h (P<0.05). Pretreatment with ERα siRNA obliterated the inductive effects of E2 on Hsp27 protein expression levels (P<0.05), but pretreatment with ERβ siRNA increased the inductive effects of E2 on Hsp27 protein expression levels in BCPAP cells (P<0.05). ChIP result has confirmed that ERα protein could bind to the region of Hsp27 gene promoter in BCPAP cells.Conclusion E2 can induced the the expression of Hsp27 in BCPAP cells by a ERα-dependent manner.
The value of differential diagnosis of combined detection of PTH, IL-6 and Cys-C in acute and chronic renal failure
2016, 36(10): 1354-1358.
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Objective To explore the value of combined detection parathyroid hormone,PTH, interleukin-6,IL-6,cystatinC,Cys-C in differentiating acute and chronic renal failure. Methods 72 patients who diagnosed with acute renal failure(ARF), 162 the chronic renal failure(CRF) ,and 114 kidneys disease with non-renal failure(NRF) and 117 healthy people were detected and compared the levels of PTH,IL-6 and Cys-c.Analyse the diagnostic efficiency of each combination , PTH+IL-6,PTH+Cys-C,IL-6+ Cys-C,PTH+IL-6+ Cys-C,and evaluation with decision matrix. Results 1 .PTH of ARF group were significantly lower than CRF group (P <0.01) ;IL-6 of ARF group were significantly higher than healthy controls ,NRF group and CRF group (P <0.01);Cys-C of ARF group were higher than healthy controls and NRF group,were lower than CRF group (P<0.01). PTH,IL-6 and Cys-C of CRF group than healthy controls and NRF group were all significantly higher (P<0.01). Combination IL-6+Cys-C could increase LR+,CCR and YI index of ARF.And combined detection of PTH and Cys-C could obviously improve LR+ CCR and YI index of CRF.Conclusion Combine detection of IL-6+Cys-C and PTH+Cys-C is useful in differential diagnosis of ARF and CRF.
Astragalus polysaccharide(APS) promote the proliferation of neural stem cells (NSCs) through the PI3K / AKT signaling pathway
2016, 36(10): 1359-1363.
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Objective To observe the effect of astragalus polysaccharide on the proliferation of neural stem cells through FLK-1/PI3K/AKT signaling pathway.Methods neural stem cells were randomly divided into control group, APS (5%) group, APS (5%) +LY294002 group, LY294002 group,we detected the expression of Nestin and Brdu;Testing the cell proliferation by CCK-8;the content of VEGF,Flk-1 by Elisa,and the protein expression of Flk-1、PI3K、p-Akt by Western blot. Results The proliferation of neural stem cells in APS group and LY294002 group were significantly different (P < 0.05), APS can improve the proliferation of neural stem cells after LY294002 intervention, and increase the content of VEGF, FLK-1 and FLK-1, P-Akt and PI3K protein expression (PC).Conclusion APS group can promote the proliferation of neural stem cells,maybe relation with improve the content of VEGF,FLK-1,promote the expression of FLK-1 protein expression, Akt phosphorylation, activate PI3K/AKT signaling pathway, regulate the downstream target genes of PI3K/AKT signaling pathway.
Prevalence of anemia in Han and Li people in Hainan province
2016, 36(10): 1364-1368.
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Objective To know and compare the prevalence of anemia in Han and Li adults in Hainan province. Methods The current study was a cross-sectional study. By cluster sampling method, adults aged over 20 from Haikou city, Danzhou city, Changjiang county, Ledong county and Baisha county in Hainan province were surveyed in 2014. Results Totally 4590 participants from these 5 regions were surveyed. The total prevalence of anemia was 9.28%, 4.61% for males and 12.06% for females respec-tively. The prevalence in Han adults were 3.09% and 7.98 for males and females.The prevalence in Li adults were 7.14% and 17.13% for males and females respectively. According to data of the national census 2010, standardization was conducted.The age adjusted prevalence in Han population were lower than Li population by sex (male: Han 2.67%, Li 6.24%, female: Han 7.96% Li 17.39%). The age adjusted rural and urban prevalence were not significantly different (p>0.05) by sex and race, except for the lower prevalence observed in Han urban females than in Han rural females (p<0.05). Conclusion Li people had higher prevalence than Han. Except nutrition status, Mediterranean anemiasusceptibility genecarrying rate should be further identified in adults to estimate is there a genetic effect in order to early prevention and intervention.
Effect of acetylpuerarin on expressions of caspase-8 and caspase-3 in BV-2 mousemicrogliacell lineinduced by Aβ25-35
2016, 36(10): 1369-1373.
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Objective To investigate the effect of acetylpuerarin on expression of caspase-8 andcaspase-3 in BV-2 mousemicrogliacell line induced by Aβ25-35. Methods BV-2 microglia cellswere divided into six groups: control group,model group(cells were activated with condensed Aβ25-35 as cell model),acetylpuerarininterventiongroups (low-dose group,moderate-dose group, high-dose group)andcaspase-3 inhibitor (Z-IETD-fmk) group. The protein expressionof caspase-8 andcaspase-3 was detected by Westernblot. ThemRNA expressionof caspase-8 andcaspase-3 was measured by real-time PCR. ResultsCompared with control group, protein expression ofcaspase-8 and caspase-3 in model groupwas significantly up-regulated (P<0.01), and gene expression ofcaspase-8 and caspase-3was markedlyincreased (P<0.01). Compared withmodel group,protein expressionof caspase-8 andcaspase-3in acetylpuerarin each dose groupwas significantly down-regulatedin different degrees (P<0.01),and gene expressionof caspase-8 andcaspase-3 was markedlydecreased(P<0.01).ConclusionsAcetylpuerarin can inhibit caspase-8 andcaspase-3expression ofBV-2 mouse microglia cell line induced by Aβ25-35in a dose-dependent manner.
microRNA expressionprofileanalysis of essential hypertension patients in Uyghur population
2016, 36(10): 1374-1380.
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Objective The aim of this study was to screen the microRNA expression file in Uighur population, which would supply research data for further exploring the relationship of microRNA and molecular mechanism of hypertension. Methods Whole blood samples were taken from 4 hypertension patients and 4 health people from Uighur population. MicroRNA expression profile was tested by using Agilent Human miRNA array. Clustering analysis and target gene annotation were performed on differentially expressed microRNAs. Another 30subjects were sampled independently (15 from hypertension patients and 15 from healthy people) andthe differentially expressed microRNAs were validated by quantitative PCR. Results Compared microRNA profiles of the two groups, 257 differentially expressed microRNAs were filtered, in which 161 were up-regulated and 97 were down-regulated. Target genes were predicted in three database, that is, TargetScan, PITA and microRNAorg. 6’580 target genes were obtained by computing the intersection of three databases.Hsa-miR-1183 was the most up-regulated and hsa-miR-30e-5p was the most down-regulated microRNA in hypertension patients. Conclusions microRNA expression profile of Experimentalgroup was different from the control group. Differentially expressed microRNAs would be potential biomarkers for diagnosis or therapy. This study supplied a foundation for exploring the mechanism of essential hypertension.
PKCα participates involves in highglucose-medaited bone morphogenetic protein-7 expression in renal tubular epithelial cells of rats
2016, 36(10): 1381-1387.
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Objective To observe the expression of Bone morphogenetic protein-7 (BMP-7) in renal tubular epithelial cells could be influenced by protein kinase Cα (PKCα) under diabetes mellitus(DM) and high-glucose cultivation. Methods Rats were randomly divided into control group(control) and diabetic group(DM). Rats were sacrificed after 12 weeks. primarily cultured renal tubular epithelial cells (RTECs) were divided into four groups: control group (control), high glucose group (HG), HG+PKCα specific inhibitor G?6976 1μmol/L (HG+G?6976) group and hyperosmosis group (HM). Immunohistochemical and Immunocytochemical analysis were used to examine the protein expression levels of BMP-7, PKCα, angiotensin II and fibronectin; RT-PCR was used to examine the mRNA levels of BMP-7, PKCα and fibronectin. Results In normal glucose group, BMP-7 protein and mRNA highly expressed in renal tubular epithelial cell in rat. The expression of BMP-7 protein and mRNA were down-regulated remarkably in diabetic rats or high glucose group compared control group(P<0.05). PKCα, angiotensin II and fibronectin were highly expressed compared control group(P<0.05). BMP-7 was negatively associated with PKCα. Compared with HG group, BMP-7 expression had significantly increased but angiotensin II and fibronectin expression decreased in HG+G?6976 group(P<0.05). Conclusions PKCα could involve in the regulation of BMP-7 expression under high glucose in renal tubular epithelial cell in rat.
Bufalin attenuates TGF-β1-induced epithelial-mesenchymal transition in HK2 cells
2016, 36(10): 1388-1392.
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Objective To investigate the preventive effects of bufalin on transforming growth factor-beta 1(TGF-β1) induced epithelial-mesenchymal transition of human kidney cells. Methods Human kidney proximal tubular cell line (HK-2)was used as the proximal tubular cell model. Cells were divided into five groups as follows:control group, TGF-β1 (5 μg /L) group, TGF-β1 (5 μg/L) plus bufalin (1×10-9、1×10-8 and 1×10-7mol/L) groups. Epithelial to mesenchymal transition(EMT) was induced with 5 μg/L of human TGF-β1. The effects of bufalin on cell morphology were observed by phase contrast microscopy, the expression of α-smooth muscle actin (α-SMA) and E-cadherin were measured by immunofluorescent staining, real-time reverse transcription-polymerase chain reaction and western blot. Results Our results revealed that bualin not only prevented α-SMA expression(P<0.05) but also prohibited the decrease of the epithelial marker E-cadherin(P<0.05) in HK-2 cells in a dose-dependent manner. Simultaneous incubation of bufalin with TGF-β1 could protect the change to the myofibroblast phenotype and restore the epithelial morphology of the HK-2 cells. Conclusion These observations strongly suggest that bufalin is a potent inhibitor of TGF-β1-induced EMT and may be a promising agent for treating tubulointerstitial fibrosis.
HBV promotes migration and invasion of hepatocellular carcinoma cell lines
2016, 36(10): 1393-1399.
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Objective To observe and compare the different migration and invasion activities between the HepG2 and HepG2.2.15 cells and to explore the influence and mechanism of HBV on the migration and invasion of hepatocellular carcinoma cells via the live cell imaging technology. Methods The three cell lines of HL-7702, HepG2 and HepG2.2.15 were planted on 96-well plates with a 30% degree of cell confluence. When the cells were in the 70% degree of confluence, the scratch-wound healing assay was performed to determine the relative wound density (RWD) via the live cell imaging technology. The EphA2 expression was examined via immunofluorescence staining and Western blotting and the relationship between the EphA2 expressions and the RWD levels in the HepG2 and HepG2.2.15 groups were analyzed. Results Cell migration assays showed that at 24~96 h after scratch, the RWD in the HL-7702 group was higher than that in the HepG2 and HepG2.2.15 groups (P<0.01). At 72~144 h after scratch, the RWD in the HepG2.2.15 group was higher than that in the HepG2 group (P<0.01). Cell invasion assays showed that there was no quantitative value of RWD in the HL-7702 group. At 72~144 h after scratch, the RWD in the HepG2.2.15 group was higher than that in the HepG2 group (P<0.05 or P<0.01). EphA2 expressions showed that comparing with that in the HL-7702 group, EphA2 expressions increased in the HepG2 and HepG2.2.15 groups (P<0.01), and the EphA2 levels in the HepG2.2.15 group were higher than that in the HepG2 group (P<0.01). Moreover, the EphA2 expression in the HepG2 and HepG2.2.15 groups was positively correlated with the RWD levels in cell migration assays (r=0.962, P=0.002) and cell invasion assays (r=0.980, P=0.001). Conclusions HBV might promote the migration and invasion of hepatocellular carcinoma cells and its mechanism might be associated with the up-regulation of EphA2 expressions.
Estrogen regulates ABCG2-mediated chemotherapy sensitivity of MCF-7
2016, 36(10): 1400-1406.
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Objective To explore the interaction between ER and GPER in the process of estradiol-mediated regulation of ABCG2 in MCF-7 cells. Methods Western blot and immunoflurescent were used to detect the expression and localization of ABCG2 treated with 17-β estradiol( E2 ), G1 respectively or combined with inhibitors. The intervented cells mentioned above was treated doxorubicin (Dox), then the change of drug sensitivity was test by flow cytometry analysis and CCK8 method. Results ABCG2 localizes at both of plasma membrane and cytoplasm. E2 upregulates the level of ABCG2 protein and translocates it from cytoplasm to plasma membrane, which result in inhibiting the effect of chemotherapy drugs Dox . The relative protein expression of ABCG2 in E2 treatment group was higher than those of the control group( P<0.05) . Above-mentioned changes were blocked by E2 antagonist (TAM) ( P<0.05). The expression of ABCG2 was both downregulated in TAM and GPER specific angonist (G1) treatment groups( P<0.05). Cytotoxic of Dox was improved in those groups as well( P<0.05). The relative protein expression of ABCG2 were lower, which were blocked by GPER specific antagonist (G15). Conclusion Estradiol upregulates the expression of ABCG2 and weakens the effect of chemotherapy drugs in the case of activate ER and GPER simultaneously. On the contrary, acivating GPER specifically have an opposite result which improves the efficacy of chemotherapy.
Expression and significance of C-erbB-2 and VEGF in sinonasal squamous cell carcinoma
2016, 36(10): 1407-1411.
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Objective:To explore the expression and significance of C-erbB-2 and vascular endothelial growth factor (VEGF) in sinonasal squamous cell carcinoma(SNSCC). Methods: Immuno -histochemical method and Western blot method was used to determine the expression of C-erbB-2 and VEGF in specimen of sixty-two cases of sinonasal squamous cell carcinoma(SNSCC) ,thirty cases of nasal polyps﹙NP﹚and twenty-five cases of normal nasal mucosa. Results:The expression of C-erbB-2 and VEGF in SNSCC significantly higher than that in nasal polyps﹙NP﹚and normal nasal mucosa(P﹤0.05). Furthermore,the expression of C-erbB-2 and VEGF correlated with tumor classification,clinicopathologic stage,lymph node involvement(P﹤0.05),but not with patient’s age and gender.Conclusion: C-erbB-2 and VEGF are closely related to the tumorigenesis,differentiation and proliferation of SNSCC.Detection of these protein combined helps to diagnose and treatment of SNSCC.
Impacts of blood glucose variation on the sciatic nerve injury of STZ-DM rats
GU Xin
2016, 36(10): 1412-1416.
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Objective To observe the impacts of blood glucose fluctuation on the sciatic nerve of diabetic rats and its possible mechanism. Methods Rats were randomly divided into control group (NS group), continuous high glucose group (DM group) and fluctuating blood glucose group (FDM group, Regular insulin and glucose were used to induce blood glucose fluctuation). After 12 weeks, the conduction velocity of sciatic nerve (MNCV) and HbA1C in rats were evaluated. HE staining was performed to observe the morphological changes of sciatic nerve. The expression of NGF, TrkA and p75 were determined by immunohistochemistry and Western blot. Results 1) Compared with the NS group, the HbA1C level of FDM group and DM group were increased (P<0.01); CV value of FDM group significantly higher than DM group and NS group (P<0.01) while with MNCV value was lower than DM group and NS group (P<0.05). 2) NGF and TrkA expression in FDM group was lower than that in DM group (P<0.05), while the expression of p75 was increased in DM group (P<0.05). Conclusions Blood glucose fluctuation may aggravate the progression of diabetic peripheral neuropathy at the same level of HbA1C, the mechanism of which may be related to the downregulation of NGF and TrkA expression, while the upregulation of p75 expression.
Geniposide attenuates airway inflammation and down-regulation TLR4/NF-κBactivity in infant asthma mice
2016, 36(10): 1417-1421.
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Objective To explore the protective effects of geniposide on airway inflammation and smooth muscle cells (ASMCs) injury in infant asthma mice. Methods BALA/c mice were divided into three groups,including control group, asthmagroup, and geniposide group(80 mg/kg) (10 in each group). The pathological changes in experimental lung tissues, including cells infiltrating, goblet mucus secretion were detected by H&E staining and AB-PAS staining.The number of inflammatory cells in bronchoalveolar lavage fluid (BALF), including Eosinophils, Neutrophils, and Macrophages, was also observed.The levels of TLR4 and Th2 type cytokines IL-4, IL-5 and IL-13 in the BALF were determined by ELISA assay. Then, ASMCs were isolated and cultured in vitro. Cultured cells were divided into five groups, control group, asthma group (Ova), low dose of geniposide group(20mg/L), medium dose of geniposide group (50mg/L) and high dose of geniposide group (100mg/L)(8 in each group). The expression of TLR4 and NF-κB p65 were detected by qRT-PCR and Western blot analyses.The cell proliferation ability of ASMCs was determined using the MTT assay. Results In vivo studies, the results indicated that geniposide induced the decrease of asthma lung cells infiltrating and goblet mucus cells secretion, and the increase of inflammation cells(P<0.01),as well as the reduction of TLR4 and Th2 type cytokines secretion(P<0.01).In vitro studies, the results demonstrated that geniposide inhibited TLR4/NF-κB activation, and restrained cell proliferation in asthma-derived ASMCs. Conclusions The effect of Geniposide reduces airway inflammation and ASMCs injury in infant asthma mice, which may be through the ability of inhibiting the TLR4/NF-κB activation.
The relationship between ALDH1 and C-myc expressions in gastric cancer tissue and Helicobacter pylori L infection in patients with gastric cancer
2016, 36(10): 1422-1424.
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Research progress of stanniocalcin-1 in cancer
2016, 36(10): 1425-1428.
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Stanniocalcin-1(STC1) was initially discovered as a glycoprotein hormone keeping the homeostasis of calcium and phosphate. In addition, STC1 also plays an important role in cancer. STC1 promotes proliferation, angiogenesis, invasion and metastasis and inhibits apoptosis and hypoxia. Emerging evidences show that STC1 may be the next new biomarker, which will be useful for the diagnosis, treatment and prognosis of cancer.
microRNA and hepatocellular carcinoma
2016, 36(10): 1429-1432.
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Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide and the third cause of cancer-related death. MicroRNA (miRNA), a class of noncoding single-stranded RNAs, posttranscriptional regulate gene expression by base pairing with the 3’untranslated regions (3UTRs) of target messenger RNAs (mRNAs).Recent studies show that miRNA play an important role in HCC, it has become a target diagnostic biomarkers and therapy of HCC.
Caveolae and vascular endothelial permeability
2016, 36(10): 1433-1436.
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Caveolae is the key molecular that regulates the permeability of vascular endothelial cells through Cav-1 expression and phosphorylation, Src kinase activation and paracellular permeability. Caveolae and Cav-1 participate in the process of LDL transport across the cell, regulate the blood-brain barrier, interpose the tumor pathological angiogenesis and the pulmonary endothelial barrier,and provide new therapeutic targets for atherosclerosis, stroke and other cardiovascular and cerebrovascular diseases and certain cancers.
Research progress of SWI/SNF chromatin remodeling in malignancies
2016, 36(10): 1437-1440.
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The mutations of SWI/SNF subunits genes, with about 20% high in human cancers, promote oncogenesis by inactivating the function of encoding proteins and further perturbing the whole function of SWI/SNF complexes. The main yet known mechanisms by which SWI/SNF suppress tumor development include its epigenetic antagonism with Polycomb complexes, as well as synergetic interaction with other oncogene signaling such as c-Myc and PIK3CA.
Research progress of long noncoding RNAs in autoimmune diseases
Li ZOU
2016, 36(10): 1441-1445.
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Long noncoding RNAs(LncRNAs)are RNA transcripts larger than 200 nucleotides, which do not encode proteins. LncRNAshave diverse important properties, such as gene transcription, protein transport and chromatin remodeling, which involve in pathogenesis, development and prognosis of various immune diseases. The LncRNAs play crucial role in autoimmune diseases.
Research progress in regulation of mTORC1 signaling pathway by amino acids
2016, 36(10): 1446-1449.
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Amino acids not only are materials for protein synthesis,but also are signaling molecules that activate Mammalian target of Rapamycin complex 1 (mTORC1).mTORC1 translocation to the lysosomal surface is the key step to regulation of mTORC1 activity by amino acids. Lysosome associated proteins including RagGTPase,Ragulator,v-ATPase and SLC38A9,and some cytoplasmic proteins,such as GATOR,Sestrins,have an important role in regulation of mTORC1 translocation to the lysosomal surface.
Progress of NVP-BEZ235 in combination antitumor therapy
2016, 36(10): 1450-1454.
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NVP-BEZ235, a novel dual PI3K/mTOR inhibitor, has exhibited significant anti-proliferative activity in a great variety of cancer types in vitro by inducing cell-cycle arrest and apoptosis. Disappointingly, NVP-BEZ235 monotherapy have not yielded satisfactory results in preclinical models. However, compared with every single agent alone, improved anti-tumor activity can often be achieved when NVP-BEZ235 combined with other cancer therapeutics. In this regard, NVP-BEZ235 in combination with chemotherapeutic drugs may present a new therapeutic strategy.
Advances on the structure, expressionand physiological functionof amphiregulin
2016, 36(10): 1455-1459.
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Amphiregulin is the ligand of epidermal growth factor receptor. The synthesis of amphiregulin is regulated by endogenous and exogenous stimuli. Amphiregulin is expressed in a variety of tissues and takes part in series of physiological process, including mammary gland development, embryo implantation, bone formation, axon growth, keratinocyte proliferation, female reproductive system development, the branching and tubulogenesis processes oflung, kidney, and prostate, spermatogenesis, development of neuronal and bonetissues, the maintenance of immune function.
How often and how long does normalizing standardized patient assessment spend
2016, 36(10): 1460-1463.
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Objective To explorehow often and how long does the SP-trainer to trainStandardizedpatients (SPs) to normalize their standardized assessments. Methods 2 SPs were included, one was senior and the other was junior. One senior SP trainer controlled the whole process. Results After 4 times standardized training, all SPs nearly well done the “sandwich”assessment completely. Conclusions It is at least 4 times (2 hours) in training the SPs who can use the standardized “sandwich” assessments style in assessing medical students’ inquisition smoothly.
Strengthening the role of the chief resident system in standardized training of residents in the department of internal medicine
2016, 36(10): 1464-1466.
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Chief resident system is an important link of personnel training in hospital. Chief residents of internal medicine department serve at first line of teaching and health care, andimprove quality of residents in aspects of health care, education and management. To insist on and strengthen the role ofchief resident system in the standardized training of residents of internal medicine department, is of great importance for the success of the standardized training.
Basic & Clinical Medicine
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CN 11-2652/R
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