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作 者:李金成[1,2] 姜德建[3] 吕冬[4] 谭桂山[3] 谭德明[1]
机构地区:[1]中南大学湘雅医院感染科,湖南长沙410008 [2]邵阳医专传染病学教研室 [3]中南大学药学院 [4]中南大学护理学院
出 处:《中国医师杂志》2007年第5期593-596,共4页Journal of Chinese Physician
基 金:湖南省自然科学基金资助项目(06jj3012)
摘 要:目的研究去甲基雏菊叶龙胆酮(DMB)对肝星状细胞(HSC)活化的影响及其机制。方法培养大鼠肝星状细胞株HSC-T6,分别加入1、3或10μM DMB孵育12-48 h。细胞组织化学检测α-平滑肌肌动蛋白(α-SMA)表达;酶联免疫吸附试验测定I型胶原的合成;逆转录PCR检测转化生长因子-β1(TGF-β1)和结缔组织生长因子(CTGF)mRNA水平。结果体外培养的HSC-T6表现为激活状态,表达α-SMA和合成I型胶原。处理DMB能显著降低体外培养的HSC-T6表达α-SMA细胞数目和I型胶原的合成,且呈浓度依赖性。而且,DMB能浓度依赖性降低HSC TGF-β1和CTGF mRNA水平。结论DMB能抑制HSC的活化,其作用与抑制TGF-β1-CTGF促纤维化通路有关。Objective To investigate the effects of demethylbellidifolin (DMB) on activation of hepatic stellate cells (HSC) and its underlying mechanism. Methods Rat hepatic stellate ceils line HSC-T6 were cultured and treated with different concentrations ( 1,3 or 10 μM) of DMB for 12 to 48 h. Expression of or-smooth muscle actin (α-SMA) and synthesis of I-type collagens in HSC were determined by immunohistochemistry.and ELISA assay, respectively. Messenger RNA levels of transforming growth factor-β1 (TGF-β1) and connective tissue growth factor (CTGF) were determined using RT-PCR. Results HSC-T6 cultured in vitro showed an activated status, which expressed α-SMA protein and synthesized I-type collagen. Treatment of HSC-T6 with DMB could markedly decrease α-SMA-positive cells ratio and suppress I-type collagens production in a concentration-dependent manner. Moreover, DMB concentration -dependently suppressed the mR- NA levels of both TGF-β1 and CTGF in HSC-T6. Conclusions DMB exhibits the inhibitory effects on the activation of HSC, and such effects may be related to inhibiting TGF-β1-CTGF-dependent pathway.
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