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肝症口服液含药血清对TGFα诱导SMMC-7721细胞增殖和ERK蛋白的影响 被引量:12

Serapharmacological study of Ganzheng oral solution on proliferation and expression of ERK in SMMC-7721 cells with transforming growth factor α
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摘要 目的观察肝症口服液含药血清对 TGFα诱导人肝癌细胞增殖和信号传导因子 ERK 影响.方法采用血清药理学方法,以病理鼠血清作对照,应用 MTT比色法观察中药鼠血清对 TGFα诱导人肝癌细胞 SMMC-7721增殖的抑制作用.用免疫组化方法检测中药血清对信号传导因子 ERK 蛋白表达影响.结果中药血清作用24h 对 SMMC-7721细胞抑制率达25%,P<0.05;作用48h 抑制率达30%,P<0.001;中药血清作用24h 对1μg·L^(-1)TGFα诱导的 SMMC-7721细胞增殖抑制率为12.3%,P>0.05;作用48h 抑制率为16%,P<0.05;中药血清作用24h 对5μg·L^(-1)TGFα诱导的 SMMC-7721细胞增殖抑制率为8.9%,P>0.05,作用48h 抑制率为17.2%,P<0.001.中药血清对 TGFα诱导的肝癌细胞 SMMC-7721增殖有明显的抑制作用,抑制效应呈时间依赖性.中药血清能抑制 ERK 蛋白在细胞核中的表达.结论肝症口服液含药血清能够抑制 TGFα诱导的人肝癌细胞增殖,阻断 TGFα在细胞内的信号传导. AIM To investigate the serapharmacological effects of Ganzheng Peroral Solution(GZPS)on proliferation and expression of ERK in human hepatocellular carcinoma SMMC- 7721 cells with transforming growth factor α(TGFα). METHODS The effects of GZPS were investigated in vitro using serum pharmacological approach compared with pathologic serum.The inhibiting effect of drug serum on SMMC-7721 cells with TGFα was observed by MTT assay. Expression of ERK was detected by immunohistochemistry. RESULTS The inhibiting rate with drug serum was 25% (P<0.05)for 24h treatment and 30%(P<0.001)for 48h treatment.The inhibiting rate with drug serum and 1μg·L^(-1) TGFα was 12.3%(P>0.05)for 24h treatment and 16% (P<0.05)for 48h treatment.The inhibiting rate with drug serum and 5μg·L^(-1) TGFα was 8.9%(P>0.05)for 24h treatment and 17.2%(P<0.001)for 48h treatment.So the drug serum could significantly inhibit the proliferation of SMMC-7721 cells with TGFα time-dependently.It also could significantly reduce the expression of ERK in nucleus. CONCLUSION The serum containing GZPS could inhibit the proliferation of SMMC-7721 cells with TGFα and the signal transduction of TGFα.
出处 《世界华人消化杂志》 CAS 2001年第9期1017-1020,共4页 World Chinese Journal of Digestology
基金 河北省自然科学基金资助 No.301394
关键词 转化生长因子Α 肝肿瘤 肿瘤细胞 细胞分裂 蛋白激酶类 信号传递 transforming growth factor alpha pharmacology liver neoplasms pathology tumor cells cultured drug effects cell division drug effects protein kinases biosynthesis signal transduction drug effects
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