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Aim To investigate the effects of Periplane-ta americana extract Ento-A on the immune function in immunosuppressed mice . Methods Immunosup-pressed mouse model was induced by intraperitoneal injection of cyclophosphamide in KM mice .To evalu-ate the effects of Ento-A on the immune function in im-munosuppressed mice , neutral red method and MTT assay were used respectively to detect the effects of En-to-A on the phagocytosis of peritoneal macrophages and T cell proliferation rate in mice; with sheep red blood cell as immunogen , the effects of Ento-A on the pro-duction of serum hemolysin were evaluated;peripheral blood was tested and immune organ index calculated . Results Compared with model control group , the high, medium and low doses of Ento-A could improve the expression of serum hemolysin in immunosup-pressed mice ( P<0.01 ) , and increase the spleen in-dex(P<0.01) and thymus index (P>0.05), signifi-cantly increased the content of WBC ( P<0.01 ) , PLT ( P<0.01 ) , HGB ( P<0.01 ) , while the contents of RBC was on the rise , with no significant difference ( P>0.05 ) in peripheral blood , significantly enhanced phagocytic function and T lymphocyte proliferative abil-ity in a dose-dependent manner ( P<0.01 ) .Conclu-sion Ento-A can enhance the immune function of im-munosuppressed mice .
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AIM:To identify the expression of fermitin family homolog 2 (FERMT2) in hepatocellular carci-noma ( HCC) tissues and the effect of FERMT 2 on the cell growth and related protein expression .METHODS:Real-time PCR and immunohistochemistry were used to detect FERMT 2 expression in the HCC tissues .The technique of CRISPR/Cas9 was applied to construct stable FERMT2 knockout MHCC97H cell line.WST-1 assay and flow cytometry were used to measure the cell viability , cell-cycle distribution and cell apoptosis .Western blot was used to determine the expression of related proteins in the MHCC97H cells.RESULTS:In HCC tissues, the expression level of FERMT2 was higher than that in adjacent liver tissues (P<0.05).High expression of FERMT2 was significantly correlated with postoperative recurrence of tumor.Knockout of FERMT2 gene evidently inhibited MHCC97H cell viability and accelerated cell apoptosis .Mean-while, the expression levels of proliferating cell nuclear antigen , cyclins, cyclin-dependent kinases 2 and anti-apoptotic fac-tors were significantly downregulated in MHCC97H cells with FERMT2 knockout (P<0.05).CONCLUSION:FERMT2 may function as a promoter of hepatocarcinogenesis and progression via regulating the cell viability , cell-cycle distribution and cell apoptosis , which is related with the expression of cell cycle regulators and anti-apoptotic factors .
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Objective To investigate the relationship between CYP2J2*7 mutation(G-76T) and coronary heart disease (CHD) in Chinese Hanpopulation and to study the effects of CYP2J2 geneover-expressionon the proliferation and migrationof aortic smooth muscle cells of ApoE-/- mice. Methods CYP2J2*7 genotype was detectedin 500 patients with CHD and 478 controlsubjects by the Polymerase Chain Reaction-Restriction Frag-ment Length Polymorphism (PCR-RFLP). Culturedaortic smooth muscle cells of ApoE-/- mice were divided into control group, sham transfectiongroup and CYP2J2 over-expression group. Cell proliferation and migration were investigated after CYP2J2 over-expressionby MTS and Transwell assay. Results The frequency of CYP2J2*7 in CHD group was significantly higher than that incontrol group (10.00% vs. 6.49%, P = 0.046). Same is the case in female cases(P = 0.026). Compared with these of aortic smooth muscle cells incontrol group and sham trans-fectiongroup, the cell proliferation in 24, 48, 72 h, and the cell migration in 48 h after CYP2J2 over-expression in CYP2J2 group were significantly suppressed. Conclusions CYP2J2*7 mutation might increase the risk of CHD in Chinese Han population. CYP2J2 over-expression can suppress the proliferation and migration of aortic smooth muscle cells and CYP2J2 might have the effect of anti-atherosclerosis.
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Abstrac:Aim To study the effect of hydroxysafflor yellow A ( HYSA ) on the proliferation of vascular smooth muscle cells ( VSMCs) and the related molecu-lar mechanism. Methods The inhibitory effects of hydroxysafflor yellow A on VSMC proliferation was de-tected using cell culture, MTT assay, Western blot and immunohistochemical staining. Results The results showed that HYSA inhibited cell proliferation induced by PDGF in a dose-dependent (5,10,20,40 μmol· L-1 ) manner, reduced proliferating cell nuclear anti-gen ( PCNA ) expression and blocked PDGFR-MEK-ERK1/2 signaling pathway activated by PDGF in VSMCs. Conclusion HYSA inhibits VSMCs prolifer-ation via reducing the expression of PCNA and blocking signal transduction of MEK-ERK1/2 in VSMCs.
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AIM: To investigate the effect of inhibiting myosin light chain kinase ( MLCK) on endothelin-1 (ET-1) induced proliferation and apoptosis of rat pulmonary artery smooth muscle cells (PASMCs).METHODS: Rat PASMCs were cultured and stimulated with ET-1.The cells were randomly divided into control group , ET-1 group and ET-1+MLCK inhibitor group (ET-1+M).Western blotting, MTT assay, [3H]-TdR incorporation and flow cytometry were employed to test the expression of myosin light chain (MLC) and MLCK, cell proliferation, cell cycle and apoptotic rate of PASMCs ,respectively .The phosphorylation of MLC was determined by glycerol-PAGE coupled with Western blotting .RE-SULTS:Compared with control group , the protein expression of MLCK and MLC phosphorylation significantly enhanced af -ter ET-1 stimulation.ET-1 markedly induced the proliferation and decreased the percentage of apoptotic rate in the PASMCs.However, pretreatment with ML-7, a MLCK inhibitor, significantly reversed the above effects induced by ET-1. CONCLUSION:MLCK inhibitor effectively inhibits the ET-1-induced proliferation and the cell cycle progression .
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Objective To investigate the effects of constant magnetic field (CMF) on proliferation, apopto-sis and nitric oxide (NO) secretion of rat bone marrow-derived endothelial progenitor cells (EPCs) intervened by C-reactive protein (CRP). Methods EPCs were isolated from rat bone marrow by density gradient centrifugation and cultured on fibronectin-coated dishes. The cells were divided into five groups, i. e., control group, CRP (12 μg/ml) group, CRP plus CMF (0.1, 0. 5, 1.0 mT) groups. Samples were collected 24 hours after incubation. Cell proliferation was measured by MTT chromatometry. Apoptosis rate was detected by flow-cytometry. NO content of culture medium was measured by nitrate reductase method. Results As compared with control group, cell prolifer-ation in CRP group reduced significantly (0. 265±0. 008 vs 0. 316±0. 011, P < 0.05), NO secretion also de-creased significantly [(22.7±4.5) μmol/L vs (37.6±3.8) μmol/L, P < 0.05], cell apoptosis rate elevated sig-nificantly [(10.8±0. 8) % vs (4.2±0.5)% ,P < 0.05]. Cell proliferation in CRP plus 0. 5 mT or 1.0 mT CMF group (0. 295±0. 009,0. 302±0. 010) were much more than those in CRP group (P<0.05), NO secretion contents [(28.3±4.9) μmol/L, (29.2±5.6) μmol/L]were also much more than those in CRP group (P < 0.05) , apopto-sis rate [(7.4±0.5)% ,(6.9±0.6)%]was significantly lower than that in CRP group (P <0.05). Conclusion CMF at intensity of 0.5 mT and 1.0 mT can antagonize the effects of CR, promote proliferation of EPCs and secretion of NO and inhibit apoptosis rate of EPCs.