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机构地区:[1]河北医科大学流行病学教研室,河北石家庄050017
出 处:《第四军医大学学报》2006年第18期1655-1657,共3页Journal of the Fourth Military Medical University
基 金:河北省自然科学基金项目(302489)
摘 要:目的:研究复方中药对体外培养的大鼠肝星状细胞(HSC)一氧化氮(NO)和内皮素1(ET-1)的影响,从细胞因子水平探讨复方中药抗纤维化和门脉高压的作用机理.方法:逆转录多聚酶链反应(RT-PCR)法检测中药血清对四氯化碳(CC l4)刺激的HSC中ET-1,iNOS mRNA的表达;SP法免疫细胞化学检测HSC ET-1,iNOS的表达.结果:CC l4刺激组HSC中ET-1 mRNA表达及其含量(7.09±1.71vs42.44±2.58)明显增强,与空白对照组(0.56±0.28vs12.25±1.56)比较显著升高(P<0.05),中药血清对其有显著抑制作用(P<0.05),且联合应用TGF-β1抗体对CC l4刺激HSC ET-1 mR-NA的抑制作用加强;同时CC l4刺激组HSC中iNOS mRNA和蛋白表达(0.96±0.16vs5.31±0.86)比空白对照组0.63±0.19vs4.66±1.12)轻度升高,但无显著差异.药物血清处理组iNOS mRNA和蛋白的表达均高于CC l4和空白对照组(P<0.05),且联合TGF-β1抗体作用HSC iNOS的表达高于其单独作用(P<0.05).结论:复方中药降低CC l4诱导的HSCET-1水平及增加HSC分泌NO途径而抑制HSC的收缩.AIM: To study the effect of drug serum of herbal compound on nitric oxide (NO) and endothelin -1 ( ET-1 ) in cultured hepatic, stellate cells (HSC) stimulated by carbon tetrachloride (CCl4 ) and to explore the mechanism of herbal compound against hepatic fibrosis and portal hypertension. METHODS: ET-1 and iNOS mRNA in HSC treated by drug serum of herbal compound and CCl4 were determined with reverse transcriptase-polymerase chain reaction (RT-PCR) and ET-1 and iNOS expressions were measured by immunocytochemical method. RESULTS : ET-1 mRNA and protein expressions in HSC stimulated by CCl4 markedly increased( 7.09± 1.71 vs 42.44±2.58 ) , and were notably higher than those in control group (0.56 ±0.28 vs 12.25 ± 1.56, P 〈 0.05 ) ; the expressions were inhibited by drug serum and the inhibitory effect was strengthened when combined with TGF-β antibody. Meanwhile, iNOS mRNA and protein expressions slightly went up (0. 96 ± 0. 16 vs 5.31± 0.86) when compared with control group(0.63 ±0.19 vs 4.66 ±1.12) , but the difference had no significance( P 〉 0.05 ) ; the expressions in drug serum were higher than those in CCl4 group and control group and the expression of iNOS in CCl4 + drug serum + TGF-β1 group was higher than that in other groups (P 〈 0.05). CONCLUSION: Herbal compound decreased ET-1 level and increased NO secretion in HSC stimulated by CCl4 to restrain HSC contraction.
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