Table of Content

    05 April 2018, Volume 38 Issue 4
    Limonin inhibits the PM2.5 inhalation-induced airway inflammation and mucus hypersecretion in rats
    Mei-Hua LIU Xiang-dong Zhou
    2018, 38(4):  433-438. 
    Asbtract ( 541 )   PDF (612KB) ( 468 )  
    Related Articles | Metrics
    Objective To investigate the inhibitory effect of limonin on airway inflammation and mucus hypersecretion. Methods The experiment was divided into three groups (n=10), namely blank control group, PM2.5 group (the rat models of chronic airway inflammation were established by aerosolized PM2.5 suspension ) and PM2.5+limonin group (intervening with the extract from tangerine peel). The levels of mRNA and protein of inflammatory cytokines, mucin (MUC) and TAS2Rs were measured by ELISA, RT-PCR and Western blot respectively. Results The mRNA and protein expression levels of IL-1β, CINC-1 and MUC5AC and MUC5B in PM2.5 group were significantly higher than those in control group (P<0.05), and then the expression of MUC5AC protein in broncho alveolar lavage fluid (BALF) was increased. Compared with PM2.5 stimulated group, the levels of mRNA and protein of TAS2R14 in PM2.5+limonin intervented group was significantly higher (P<0.05). Moreover, the expression of IL-1β, CINC-1 and MUC5AC, MUC5B was lower than PM2.5 group (P<0.05).While the expression of MUC5B was mainly increased in BALF. Conclusions The production of mucin can been inhibited by aerosolized limonin, meanwhile the secretion of mucin also can be promoted.This effect is achieved by activating the expression of TAS2Rs in the lungs, which enhances the anti-inflammatory effect of airway inflammation.
    Construction of dual luciferase reporter plasmid of HIPK3 3'UTR and verification its targeting miR-146
    2018, 38(4):  439-444. 
    Asbtract ( 1012 )   PDF (2068KB) ( 846 )  
    Related Articles | Metrics
    Objective To construct a dual luciferase reporter vector containing the 3'untranslated region(3'UTR) of HIPK3 gene and verify the relationship between HIPK3 and miR-146. Methods The binding sites of miR-146 and HIPK3 genes were predicted by miRDB database and DIANA TOOLS database. The 3'UTR region sequences of HIPK3 genes and its mutants were inserted respectively into the luciferase report plasmid psiCHECK-2 to construct a wild-type and a mutant recombinant dual luciferase report plasmid. The 293T cells were divided into 6 groups and transfected with 1) HIPK3-WT + NC negative control; 2) HIPK3 -WT + miR-146a mimics; 3) HIPK3-WT + miR-146b mimics; 4) HIPK3-MU + NC negative control; 5) HIPK3-MU + miR-146a mimics and 6) HIPK3-MU+ miR-146b mimics respectively. After 48 hours, the luciferase activity was detected. Results HIPK3-WT and HIPK3-MU recombinant plasmid were successfully constructed. When HIPK3-WT recombinant plasmids and miR-146b mimics were transfected into 293T cells, the luciferase activity was decreased (P<0.05). Conclusions miR-146a does not have a target relationship with HIPK3 gene, whereas miR-146b can regulate the 3'UTR of HIPK3 gene.
    Inhibitory effects of resveratrol on the proliferation, migration and angiogenesis of HUVECs through targeting mTORC2/Rictor
    2018, 38(4):  445-450. 
    Asbtract ( 461 )   PDF (4520KB) ( 404 )  
    Related Articles | Metrics
    Objective: To investigate the effect of resveratrol on the proliferation, migration and angiogenic ability of HUVECs mediated by Rictor over-expression adenovirus. Methods: The Rictor was obtained through PCR and cloned into GV314 plasmid to construct recombinant plasmid, then co-transfected 293T cells with helper plasmids to obtain Rictor overexpressing adenoviral particles (Ad-Rictor), the vector without target gene Ad-Null was set as the negative control group. Ad-Rictor and Ad-Null were infected HUVECs respectively, we also set up blank control group and resveratrol-intervention group (Ad-Rictor + Res). The expression of recombinant protein was detected by fluorescence microscopy and Western blot. CCK-8 assay, Wound Healing and Matrigel assay were performed to assess the proliferation, migration and tube formation of HUVECs. Result: We constructed Ad-Rictor and Ad-Null successfully, they could infect HUVECs and express Rictor protein efficiently. Ad-Rictor could significantly improve the proliferation, migration and lumen formation ability of HUVECs in vitro compared with control (P<0.05), resveratrol intervention could significantly inhibit these abilities induced by Ad-Rictor (P<0.05). Conclusions: Resveratrol inhibits the proliferation, migration and angiopoietic ability of HUVECs through targeting mTORC2/Rictor.
    TRIM11 promotes proliferation and invasion of breast cancer cell line MCF7 by targeting miR-24-3p
    2018, 38(4):  451-457. 
    Asbtract ( 481 )   PDF (2155KB) ( 433 )  
    Related Articles | Metrics
    Objective To investigate the effect of TRIM11 (tripartite motif-containing protein 11) target regulating MicroRNA-24-3p (miR-24-3p) on the proliferation and invasion of breast cancer cells, and the relation between TRIM11 high expression and the prognosis of breast cancer. Methods Immunohistochemical method was used to detect the expression of TRIM11 in 31 cases of breast cancer and 31 cases of adjacent breast cancer normal tissues. The siRNA TRIM11 lentivirus and miR-24-3p lentivirus was transfected into human breast cancer MCF7 cell lines, observe the correlation expression of TRIM11 and miR-24-3p mRNA and protein by using real-time fluorescence quantitative PCR (RT-qPCR) and Western bolt, luciferase reporter experiments was used to verify that the miR-24-3p as a direct target of TRIM11, MTT and Transwell were used to investigate the cells proliferation, activity and invasion. Results The expression of TRIM11 in breast cancer tissues or MCF7 cells was significantly higher (P < 0.05), and we found TRIM11 high expression predicts poor prognosis in breast cancer patients (P < 0.05). siRNA TRIM11 significantly inhibited the expression of TRIM11 in MCF7 cells, moreover, which inhibited the MCF7 cells proliferation, viability and invasion (P < 0.05). miR-24-3p significantly reduced 3,-UTR TRIM11 luciferase activity in wild-type (P < 0.05), however, no effect was found in mutant type. The expression of miR-24-3p was decreased, miR-24-3p and TRIM11 mRNA expression was negatively correlated in MCF7 cells (P < 0.05), miR-24-3p inhibition protein and mRNA expression of TRIM11 in MCF7 cells, and inhibit MCF7 cells proliferation, viability and invasion (P<0.05). Conclusions The expression of TRIM11 is up-regulated in breast cancer and cells, promote the proliferation and invasion of breast cancer cells though regulating miR-24-3p expression, TRIM11 high expression predicts poor prognosis in breast cancer, TRIM11/ miR-24-3p axis is expected to become a new target for treatment of breast cancer.
    Activation of M3-mAChR attenuates hypoxia injury induced by CoCl2 in rat myocardial cell line H9c2
    2018, 38(4):  458-463. 
    Asbtract ( 436 )   PDF (1839KB) ( 450 )  
    Related Articles | Metrics
    Objective To investigate the cytoprotection and mechanism of carbachol(CCH) stimulate M3 muscarinic acetylcholine receptor(M3-mAChR) against on hypoxia injury induced by Cobaltous chloride hexahydrate(CoCl2) in rat cardiomyocyte strain H9c2. Methods Select the normal rat cardiomyocyte strain H9c2 as the control group, rat cardiomyocyte strain H9c2 were managed with CoCl2 to establish hypoxia injury model, M3-mAChR specific agonist CCH and antagonist 4-diphenyl-acetoxy-N-methyl-piperidine methiodide(4-DAMP) were used for intervention. The cell viability was tested by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT); The apoptosis in cardiomyocyte was detected by flow cytomery(FCM); The expression levels of M3-mAChR, caspase-3, HIF-1α and HO-1 proteins were measured by Western blot assay. Results In hypoxia group, the apoptosis rate was significantly increased, cell proliferation was distinctly decreased, and the expression of HIF-1α, caspase-3 and HO-1 proteins were up-regulated obviously; After treated with CCH, the apoptosis rate of cardiomyocytes was significantly decreased, while the proliferation of cells was significantly increased, and the expression of M3-mAChR, HIF-1α and HO-1 proteins were increased, and the expression of caspase-3 protein was significantly decreased. Moreover, when applying 4-DAMP for intervention, these effects that mediated by CCH was abolished. Conclusions CCH stimulate M3-mAChR against on hypoxia injury induced by CoCl2 in rat cardiomyocyte strain H9c2, and the mechanism may be related to down-regulation of caspase-3 expression and up-regulation of HIF-1α and HO-1 protein expression.
    Prognostic value of Per2 in hepatocellular carcinoma and its effect on the growth and apoptosis of hepatocellular carcinoma cells
    2018, 38(4):  464-469. 
    Asbtract ( 486 )   PDF (1470KB) ( 553 )  
    Related Articles | Metrics
    Objective To explore the expression of Per2 in hepatocellular carcinoma (HCC) and its effect on the survival of HCC patients, and to analyze the effects of Per2 on the proliferation and apoptosis of SMMC-7721 cells. Methods The protein expression of Per2 in HCC patients was analyzed by immunohistochemical (IHC) staining. SMMC-7721 cells were transfected with Per2 eukaryotic expression plasmid. The protein expression of Per2 was detected by Western blot. The cell proliferation and apoptosis was detected by MTS and flow cytometry. Results In 117 HCC tissues, the Per2 positive expression rate was 70.94%, which was significantly lower than that of 87.18% in the adjacent HCC tissue. The Per2 staining score was 2.14±1.76, which was significantly lower than that of 6.39±3.84 in the adjacent HCC tissue (P<0.01). Per2 expression was related to tumor diameter, portal vein invasion and TNM staging (P<0.05) in 117 HCC patients. The overall survival (OS) and recurrence-free survival (RFS) of HCC patients with low expression of Per2 were shorter than those with Per2 high expression (P<0.05). The cell proliferation was significantly inhibited and the level of apoptosis was increased with the transfection of Per2 eukaryotic expression plasmid in SMMC-7721 cells (P<0.05). Conclusions The expression of Per2 in HCC was significantly reduced. Per2 inhibits the progression of HCC, possibly by inhibiting cell proliferation and promoting apoptosis.
    Detection of novel mutations related to maturity-onset diabetes of the young
    Yu-xiu LI, Yong-sheng CHANG
    2018, 38(4):  470-474. 
    Asbtract ( 556 )   PDF (1221KB) ( 585 )  
    Related Articles | Metrics
    Objective To find novel genes related to maturity-onset diabetes of the young(MODY)or novel mutations of known MODY related genes and provide the basis for MODY diagnosis. Methods Taking the known clinical features of MODY as screening criteria, we choose four patients from the Endocrine Department of Peking Union Medical College Hospital and extract their genomic DNA for whole exome sequencing. PCR and Sanger sequencing are used to validate the sequencing results. Results Two novel mutations of the GCK gene and HNF4α gene, c.1348G>T(p.Ala450Thr)and c.758G>A(p.Arg253Gln)were found in two patients. Conclusions These two patients are both MODY patients and this is the first time the novel mutations were found.
    siRNA-mediated antizyme inhibitor down-regulates the expression of ornithine decarboxylase of prostate cancer cell PC3
    2018, 38(4):  475-479. 
    Asbtract ( 400 )   PDF (652KB) ( 398 )  
    Related Articles | Metrics
    Objective To evaluate whether down-regulating antizyme inhibitor(AZIN) can regulate the expression of ornithine decarboxylase(ODC) and the proliferation of prostate cancer cell PC3 or not. Methods siRNA-AZIN transfected prostate cancer cell PC3, the level of antizyme(AZ), AZIN and ODC were measured by RT-PCR and westernblot. MTT was used to measure the proliferation of cells. Results The mRNA level of AZIN declined(P<0.01); the protein level of AZIN and ODC declined(P<0.05). Knockdown of AZIN significantly inhibited the proliferation of PC3(P<0.05). Conclusions Transfecting siRNA-AZIN can decrease the level of AZIN, then the decline level of ODC inhibits the proliferation of PC3.
    Hydroxysafflor yellow A reduces anoxia/reoxygenation-induced injury in rat cardiomyocytes
    2018, 38(4):  480-484. 
    Asbtract ( 452 )   PDF (1044KB) ( 390 )  
    Related Articles | Metrics
    Objective To observe the protective effect of Hydroxysafflor yellow A (HSYA) on anoxia/reoxygenation (A/R) injury of neonatal primary cardiomyocytes, and its relationship with phosphoinositide 3-kinase / protein kinase B / glycogen synthase kinase 3β (PI3K/Akt/GSK3β) signaling pathway. Methods The neonatal rats, primary cardiomyocytes were isolated from the rats and incubated for 48 hours. The cells were adhered to each other and then divided into five groups: control group (Con group) , anoxia / reoxygenation group (A/R group) , HSYA treatment group(A/R+H group), PI3K inhibitor (LY294002)treatment group(A/R+L group)and HSYA + LY294002 treatment group (A/R + H +L group). Collect the supernatant fluid of each group to measure LDH.The flow cytometry was used to measure the rate of apoptotic cells. The protein levels of Bcl-2, Bax, Akt,p-Akt (Ser473),GSK3β ,p-GSK3β (Ser9) was evalated by Western blot. Results A/R increased LDH release ,the apoptosis rate (P<0.001), and the expression of pro-apoptotic protein Bax (P <0.001) with the decrease of anti-apoptotic protein Bcl-2, p-Akt(Ser473), p-GSK3β(Ser9)(P<0.001) compared with the control group. HSYA treatment decreased LDH release ,the apoptosis rate (P<0.001), and the expression of Bax (P<0.001) and increase the expression of Bcl-2, p-Akt(Ser473), p-GSK3β(Ser9)(P<0.001) . Compared with the A/R+ H group, the expression of Bax was increased (P<0.001),while the expression of Bcl-2, p-Akt(Ser473), p-GSK3β(Ser9)was decreased (P<0.001) in the A/R + H + L group. Conclusions HSYA protects rats,cardiomyocytes from anoxia / reoxygenation injury by regulating PI3K/ Akt / GSK3β signaling pathway.
    Effects of Ursolic acid on activation of NOX2/ROS/NLRP3 inflammasome in liver fibrosis rats
    2018, 38(4):  485-491. 
    Asbtract ( 585 )   PDF (3663KB) ( 742 )  
    Related Articles | Metrics
    Objective To investigate the effect of Ursolic acid on NOX2/ROS/NLRP3 inflammasome activation in carbon tetrachloride(CCl4)-induced liver fibrosis SD rat,and observe the improvement of collagen deposition in liver tissues. Methods All rats were randomly divided into 3 group: control group, CCl4 model group, UA treatment group. Liver fibrosis models SD rats were established by the CCl4-induced method and half of them was used as UA treatment group. Serum ALT was detected by ALT detection kit. The liver pathology and collagen deposition were observed by HE and Sirius-red staining. The mRNA expression of Nox2, Nlrp3, Caspase1, Il1β in liver tissues was detected by RT-qPCR. The protein expression of NOX2, NLRP3, caspase-1 and IL-1β in liver tissues was detected by Western blot and immunohistochemistry and the ROS generation in liver tissues were detected by DCFH-DA fluorescence probe. Results Compared with control group, in the CCl4 model group, the serum ALT was much higher (P<0.05); the Ishak’s fibrosis score and collagen deposition was increased significantly(P<0.05) and Nox2, Nlrp3, Caspase1, Il1β mRNA expression were increased. In addition, both the NOX2, NLRP3, caspase-1 p10 and IL-1β protein expression and ROS level (P<0.05) of CCl4 model group were significant increased. Compared with CCl4 model group, the UA treatment group was found that the Ishak’s fibrosis score, collagen deposition and ALT decreased. Both mRNA expression of the Nox2, Nlrp3, Caspase1, Il1β and protein expression of NOX2, NLRP3, caspase-1 p10 and IL-1β as well as ROS were significant decreased, but the caspase-1 p45 protein level has no difference among all these groups (P>0.05). Conclusion Ursolic acid attenuates the liver injury and reduces the collagen deposition, which may relate to its inhibitory effects on NOX2/ROS/NLRP3 inflammasome activation to reduce and release of IL-1β.
    Crotonaldehyde inhibits myocardial contractile function in mice
    2018, 38(4):  492-496. 
    Asbtract ( 429 )   PDF (3198KB) ( 370 )  
    Related Articles | Metrics
    Objective To study the effect of an essential α,β-unsaturated aldehyde from cigarette smoke crotonaldehyde on myocardial contractile function and intracellular Ca2+ function in mouse. Methods Hearts were removed from male C57BL/6 mice were digested by Langendorff to islate the cardiomyocytes. The cardiomyocytes of mice were then incubated with crotonaldehyde (1, 10, 25 and 50 μmol/L) for 6 h, and the control group was treated without crotonaldehyde, then they were evaluated including peak shortening (PS), maximal velocity of shortening/relengthening (±dL/dt), time-to-PS (TPS), time-to-90% relengthening (TR90), fura-2 fluorescence intensity (FFI), intracellular Ca2+decay and SERCA 45Ca2+ uptake and the expression of Na+-Ca2+ exchanger were evaluated using Western blot analysis. Results Compared with the control group, the higher concentrations of the crotonaldehyde(25 and 50 μmol/L) groups significantly diminished the PS, ±dL/dt, ΔFFI, SERCA activity and Ca2+ decay (P<0.05), as well as prolonged the TR90 (P<0.05); however the crotonaldehyde with different concentrations had no effect on the expression of Na+-Ca2+ exchanger in cardiomyocytes. Conclusions Crotonaldehyde may inhibit cardiomyocyte contraction by suppressing SERCA activity and compromising intracellular Ca2+ handling.
    Increased expression of Hsp90 in pancreatic cancer and its clinical pathological significance
    2018, 38(4):  497-501. 
    Asbtract ( 533 )   PDF (2603KB) ( 382 )  
    Related Articles | Metrics
    Objective To explore the expression and meaning of heat shock protein 90 (Hsp90) in pancreatic cancer and its correlation with the occurrence, development and metastasis of the tumor tissues and its influence on prognosis. Methods Via immunohistochemical staining, this study used the commercial tissue chip to determine the expression of Hsp90 in 63 pancreatic cancer resection specimens and their para-cancerous counterparts, which were pathologically confirmed from January 2009 to August 2013. We also analyzed the correlation with patient's clinical parameters by using one-way ANOVA or t test. Results Hsp90 expression in pancreatic cancer tissues is significantly higher than tissue adjacent to carcinoma, and it is associated with histological grade, lymph node metastasis, clinical and TNM phase of pancreatic cancer (P < 0. 05). Conclusion Hsp90 is highly expressed in pancreatic cancer tissues, and its expression is associated with invasion and metastasis of pancreatic cancer. Therefore, Hsp90 may serves as a prognostic indicator of pancreatic cancer while its high expression may represent poor prognosis of pancreatic cancer patients.
    bFGF promotes blood spinal cord barrier recovery in rats
    2018, 38(4):  502-506. 
    Asbtract ( 415 )   PDF (2089KB) ( 558 )  
    Related Articles | Metrics
    Objective To investigate the mechanisms of basic fibroblast growth factor( bFGF) promoting blood spinal cord barrier(BSCB) recovery in rats with spinal cord injury(SCI).Methods Rats were randomly divided into sham group, SCI model group, bFGF intervention group( 80 μg/kg ). The nerve function of hind limb motor was evaluated by Basso, Beattie, and Bresnahan ( BBB) scores during the 14 days postoperative period.Neuron loss of injured spinal cords were observed by haematoxylin and eosin( HE) staining and NeuN staining.The integrity of BSCB was investigated with Evan’s Blue dye and fluorescein isothiocyanate (FITC)–dextran extravasation. The expression protein of adhesive connection protein (p120 - catenin, β- catenin) and tight junction protein expression (occludin, claudin - 5) were analysised by Western blot. Results Compared with SCI model group, bFGF intervention group neuron loss decreased significantly at 3d after injury(P<0.05); the permeability of blood spinal cord barrier was found obviously reduced at 1d after injury; the expressions of p120 - catenin, beta - catenin, occludin, claudin - 5 protein of bFGF intervention group were increased dramatically at 1d after injury(P<0.05). Conclusion bFGF improves the recovery of BSCB in an SCI model by reducing the loss of neurons and increasing the expressions of adhesion junction proteins and tight juction proteins.
    Morphine promotes glioblastoma cell proliferation through activating ERK1/2 signaling pathway
    2018, 38(4):  507-511. 
    Asbtract ( 485 )   PDF (1866KB) ( 519 )  
    Related Articles | Metrics
    Objective To observe the effect of Morphine on the proliferation of glioblastoma T98G and U118MG cells and to explore the possible mechanism. Methods Glioblastoma T98G and U118MG cells were cultured in plates for 24 h and randomly divided into five groups: control (con), Morphine 0.1 μmol/L(M1), 1.0 μmol/L (M2), 10.0 μmol/L (M3) and 100.0 μmol/L (M4). MTS and BrdU methods were used to detect the proliferation of glioblastoma T98G and U118MG cells-treated with Morphine for 24 h and 48 h. Western blot analysis was applied for determing the levels of p-ERK1/2 and cyclin D1 protein expression. Results Compared with control group, morphine in M3 and M4 groups significantly promoted the proliferation of T98G and U118MG cells (P <0.05) in a concentration-and time-dependent manner. In addition, the levels of ERK1/2 phosphorylation and cyclin D1 protein expression significantly increased in both M3 and M4 groups as compared with that of control group (P <0.05). Conclusions Morphine may promote the proliferation of glioblastoma T98G and U118MG cells through activating the ERK1/2 signaling pathway.
    Correlation between the expression of JARID1B/KDM5B in breast cancer tissues and the circulating tumor cells
    2018, 38(4):  512-515. 
    Asbtract ( 149 )   PDF (1521KB) ( 356 )  
    Related Articles | Metrics
    Objective To investigate the relation between expression of JARID1B/KDM5B in invasive breast cancer tissue and circulating tumor cells of invasive breast patients. Methods The S-P immunohistochemical method was used to observe the expression of JARID1B/KDM5B in lesions. ImFish method was used to detect circulation tumor cells. Results Twenty-seven cases of patients showed CTC positive (the number of CTC was more than or equal to 2) in 35 invasive breast cancer cases,The results of JARID1B/KDM5B expression were as follows: (-) (n = 0) and (+) in 1 case, (+ +) in 3 cases, (+ + +) in 23 cases, 8 cases of negative cases (the number of CTC < 2),JARID1B/KDM5B immune group of results: (-) (n=2), (+) in 2 cases, (+ +) in 1 case, (+++) in 3 cases,The positive relation was found in expression of JARID1B/KDM5B and circulating tumor cells(P<0.05). Conclusions JARID1B/KDM5B positive expression in tumor tissues has a certain significance in judging the recurrence and metastasis of tumor.
    Silencing Itch gene expression by ultrasound-targeted microbubble destruction to enhance the immune killing efficiency of T lymphocyte against lung neoplasms cells LA795
    2018, 38(4):  516-521. 
    Asbtract ( 177 )   PDF (2243KB) ( 330 )  
    Related Articles | Metrics
    Objective To silence the expression of Itch gene of T-Lymphocytes by ultrasound-targeted microbubble destruction (UTMD) and investigate the cytotoxicity activity of transfected T lymphocytes against LA795 Lung Neoplasms cells in vitro. Methods T lymphocyte were isolated by magnetic bead, and an targeted shRNA to silence Itch gene of T lymphocytes was established. 48 hours after transfection by UTMD, the transfection efficiency was detected and analyzed by fluorescence microscope and flow cytometry; the expression of Itch protein was measured with Western Blot; 72 hours after transfection, the secretion of IL-2 and IFN-γ in the cell supernatant were measured by enzyme-linked immunosorbent assay (ELISA) and the cytotoxicity activity changes against LA795 Lung Neoplasms cells were compared between transfected T lymphocytes and negative control or simplex T lymphocytes in vitro. Results The transfection rate to silence Itch gene of T lymphocytes by UTMD was (52.3±3.8)%. At 48 h after transfection, the Itch gene expression can be effectively suppressed by UTMD. 72 hours after transfection, the secretion level of cytokines, including IL-2 and IFN-γ, were significantly rise in the group of targeted shRNA to silence Itch gene of T lymphocytes by UTMD (p<0.05) and transfected T lymphocyte also showed more efficient killing ability against LA795 Lung Neoplasms cells than negative control or blank group at E:T of 10:1、20:1 and 40:1 (p<0.05). Conclusion Silencing the expression of Itch by UTMD can significantly promoted immune activity of T lymphocyte, enhanced the cytotoxicity activity of T lymphocyte against LA795 Lung Neoplasms cells in vitro.
    Effects of hypoxia on expression of autophagy-related molecules in human colon cancer cells
    2018, 38(4):  522-526. 
    Asbtract ( 144 )   PDF (2002KB) ( 384 )  
    Related Articles | Metrics
    Objective To explore the mechanism of hypoxia on SW480 cell autophagy.Methods We screened the CD133+ cell with the characteristics of stem cell by magnetic cell separation. Then the SW480 cell and CD133+ cell were cultivated under hypoxic conditions. Subsequently, we detected the HIF-1α expression by immunofluorescence (IF), LC3 expression by western blot and HIF-2α and Beclin 1 expression in 94 colon cancer tissue samples by immunohistochemistry. Results The results showed that hypoxia induced the activation of HIF-1α in SW480 cell. After hypoxia 24 h, compared with the normal, the LC3 expression was increased in both SW480 cell and CD133+ cell and increased as the processing time increased. The conversion from LC3Ⅰto LC3Ⅱwas increased in CD133+ cell, but decreased in SW480 cell. In olon cancer tissue samples, HIF-2α and Beclin 1 expression in poorly differentiated group were higher than well-differentiated group.HIF-2α expression in no lymph node metastasis group was higher than high lymphatic metastasis group. However the Beclin expression was in the opposite regulation. Conclusion Hypoxia can induce the SW480 apoptosis and a few of CD133+ cell autophagy that can protect the cell from apoptosis by inducing the HIF expression and increasing LC3.
    Comparison of clinical effects of PICC and TIVAP in malignant tumor chemotherapy
    2018, 38(4):  527-529. 
    Asbtract ( 195 )   PDF (385KB) ( 466 )  
    Related Articles | Metrics
    Objective To study the advantages and disadvantages of two different methods(the peripherally inserted central venous catheter (PICC) and the totally implantable venous-access ports (TIVAP) in the chemotherapy of tumor patients. Methods The clinical data of 160 patients treated with PICC or TIVAP from March 2016 to December 2016 were retrospectively analyzed, and the complications of the two groups were compared and analyzed. Results The catheter occlusion rate, catheter infection rate and the incidence of phlebitis in the TIVAP group were lower than that in the PICC group (P<0.05). Conclusion The patents treated with TIVAP have fewer complications. The indwelling time is prolonged, and the quality of life of patients with the tube has no significant difference.
    Isolation and culture of adult rat cardiac microvascular endothelial cells
    2018, 38(4):  530-534. 
    Asbtract ( 159 )   PDF (2517KB) ( 344 )  
    Related Articles | Metrics
    Objective To establish a simple and efficient method for isolation and culture of adult rat cardiac microvascular endothelial cells. Methods 7 to 8 weeks old Wistar rats were anesthetized and thoracotomy was performed. Cardiac microvascular endothelial cells were separated by heart perfusion and enzymatic digestion. The morphology and growth curve of the third generation cells were investigated by inverted microscope. Its molecular markers factor Ⅷ-related antigen and CD31 were detected by immunocytochemistry and immunofluoresence. The angiogenic ability was examined by matrigel. Results The primary cultured cardiac microvascular endothelial cells in vitro were polygonal or fusiform, and with typical paving stone-like growth characteristics. At the same time, the cells showed positive staining for factor Ⅷ-related antigen and CD31 and angiogenic ability. Conclusion Cardiac microvascular endothelial cells cultured by this method possess high purity. The method is simple and convenient, and it can be used for basic and clinical research of cardiovascular diseases.
    Dynamic observation of Tfh and Tfr cells in CIA mice
    2018, 38(4):  538-540. 
    Asbtract ( 120 )   PDF (418KB) ( 295 )  
    Related Articles | Metrics
    Advances in CRISPR/Cas9 gene-editing system
    Cheng CHENG Peng-cheng SHU Xiao-zhong PENG
    2018, 38(4):  543-547. 
    Asbtract ( 165 )   PDF (456KB) ( 583 )  
    Related Articles | Metrics
    CRISPR/Cas9 gene-editing system has been broadly used in various fields of bioscience and medicine in recent years. It can be guided by RNA to specific DNA site thus achieving targeted gene editing. Off-target effect and editing efficiency remain two crucial issues facing the system. Currently, a number of researches have been focused on the optimization of the system by reducing off-target effects and increasing editing efficiency, which will help enhance its safety and expand its application.
    Apoptosis and efferocytosis in atherosclerosis plaques
    2018, 38(4):  548-552. 
    Asbtract ( 167 )   PDF (418KB) ( 372 )  
    Related Articles | Metrics
    Apoptosis is an important feature of atherosclerotic plaques, and it has beneficial and detrimental effects depending on the cell type and plaque stage. Because apoptotic cells in advanced plaques launch proatherogenic inflammatory responses, efferocytosis is available to withstand atherosclerosis progression. Several efferocytosis systems, composed of different phagocytic receptors, apoptotic ligands, and bridging molecules, can be distinguished. Impaired efferocytosis pathway causes an overdue clearance of apoptotic cells and promotes secondary necrosis and the formation of necrotic core which leads to the instability and even rupture of plaques.
    Mitochondrial fusion-fission and heart failure
    2018, 38(4):  553-556. 
    Asbtract ( 265 )   PDF (317KB) ( 474 )  
    Related Articles | Metrics
    Mitochondrial fusion、fission and dynamic transformation between the two are commonly known as mitochondrial dynamics. Mitochondrial fusion-fission is related to a variety of biological functions of mitochondria, including regulation of energy metabolism, production of reactive oxygen species, m aintenance of Ca2+ homeostasis and influence of cellular death.It is reported that cardiac development、energy metabolism and ion homeostasis are closely related to the balance of mitochondrial fusion-fission.Mitochondrial fusion-fission disorders could cause myocardial cell dysfunction、damage and even the death of myocardial cells, which result in heart failure ultimately. Developing drugs aiming to reconstruct the balance of mitochondrial fusion-fission may provide new ideas and strategies for the treatment of chronic heart failure.
    Research progress of monogenetic disorders of the lipid metabolism
    2018, 38(4):  557-562. 
    Asbtract ( 156 )   PDF (1586KB) ( 581 )  
    Related Articles | Metrics
    Monogenetic disorders of the lipid metabolism are closely related to atherosclerotic cardiovascular diseases. Different mutations contribute to different pathogenesis and clinical presentations. Mutations in endogenous lipid metabolic pathway increase the levels of serum low density lipoprotein cholesterol or total cholesterol; mutations in exogenous lipid metabolism cause hypertriglyceridemia and mixed dyslipidemia; mutations in the reverse cholesterol transport lead to high density lipoprotein abnormalities.
    Cell biological properties of microglia and its role in neurons regulation
    2018, 38(4):  563-567. 
    Asbtract ( 200 )   PDF (435KB) ( 707 )  
    Related Articles | Metrics
    Microglia are resident immune cells within the brain parenchyma. In physiological conditions, microglia are highly dynamic, expressing multiple immune receptors and neurotransmitter receptors, tightly monitoring the microenvironment of central nervous system (CNS). Major recent developments have revealed these immune cells actively modulate the functions of neurons, potentially affecting neuronal activity and synaptic pruning, contributing to synaptic plasticity, and preventing neurotoxicity. The functional changes of microglia play an important role in the development, maturation and degeneration of the brain.
    Progress in the mechanism study on colitis associated cancer
    2018, 38(4):  568-572. 
    Asbtract ( 152 )   PDF (438KB) ( 645 )  
    Related Articles | Metrics
    The ulcerative colitis is closely related to the development of colitis associated cancer. The main mechanisms related to the occurrence, development and malignant transformation of CAC includes NF-κB pathway, signal transducers and activator of transcription (STAT) and related protein pathways, intestinal microflora imbalance, the immune microenvironment and Toll-like receptor (TLR) -related pathway and so on.
    Research progress in long non-coding RNAs involved in invasion and metastasis of breast cancer
    2018, 38(4):  573-577. 
    Asbtract ( 172 )   PDF (349KB) ( 418 )  
    Related Articles | Metrics
    Long non-coding RNAs(lncRNAs) which are defined as RNAs of more than 200 nucleotides in length don’t encode protein. LncRNAs are closely related to the development of breast cancer.Plenty of lncRNAs are dysregulated in breast cancer,and they can regulate the invasion and metastasis of breast cancer through various mechanisms such as transcription and post-transcriptional regulation which is greatly important to guide the treatment and prognosis of breast cancer.
    Role of programmed cell death receptor 1 signaling pathway in cancer immunotherapy
    Weipeng Xiong
    2018, 38(4):  578-582. 
    Asbtract ( 268 )   PDF (664KB) ( 443 )  
    Related Articles | Metrics
    Research in immunotherapy has achieved important progress in tumor treatments. Programmed cell death receptor 1 (PD-1) is mainly expressed on the T lymphocyte surface and serves as an important immune regulator. The interactions of PD-1 and its ligand, PD-L1, involve in tumor-induced immunosuppression. Some of the approved antibody drugs targeting PD-1/PD-L1 signaling showed significant clinical benefits.
    Preliminary exploration on the teaching methods in endoscopic endonasal lacrimal surgery training for ophthalmologists
    2018, 38(4):  583-585. 
    Asbtract ( 165 )   PDF (353KB) ( 425 )  
    Related Articles | Metrics
    The extensive application of transnasal endoscopy for the treatment of rhino-orbital related diseases s ophthalmologists to master the skill in lacrimal surgery. Unlike other ocular surgeries, endoscopic endonasal procedures requires a thorough understanding of the anatomical structures inside the nose as well as the skilled use of endoscopes, which makes the training more specialized and difficult. The step-by-step mode combined with other learning methods is designed to enhance surgical skills and shorten the learning curve during residency and fellowship training. It is anticipated to promote the minimally invasive and precise targeting therapy for lacrimal diseases.
    Application of standardized patients in the teaching of preoperative evaluations in anesthesia residents
    2018, 38(4):  586-588. 
    Asbtract ( 118 )   PDF (288KB) ( 350 )  
    Related Articles | Metrics
    Standardized patients (SPs) are trained to portray a specific patient in a consistent, standardized fashion. SPs are widely used in many medical schools, and its efficacy for education and evaluation in the medical community has been well established. Preoperative evaluation by anesthesiologist is a critical aspect of patient safety. But there are several defects in the current anesthesia education of preoperative evaluation and management. The residents are not provided with enough skills that are needed in the clinical practice, which could be complemented by SPs simulation. As a supplement of traditional teaching methods, SPs could improve the efficiency in the teaching of preoperative evaluation and enhance the competence of anesthesia residents.