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作 者:殷静[1] 程真顺[1] 谭维军[1] 张莉[1] 谭秋月[1]
机构地区:[1]武汉大学中南医院呼吸科,湖北武汉430071
出 处:《武汉大学学报(医学版)》2013年第5期657-661,共5页Medical Journal of Wuhan University
摘 要:目的:研究丹参酮ⅡA磺酸钠注射液(STS)对大鼠肺成纤维细胞转化生长因子β1(TGF-β1)Smad信号通路的影响,探讨STS抑制肺成纤维细胞(LFB)增殖、转化的可能机制。方法:体外分离培养大鼠肺成纤维细胞,实验分为3组:①空白对照组;②TGF-β1刺激组;③联合处理组:STS+TGF-β1刺激组,培养48h,待细胞生长同步化后,用MTT法检测丹参酮ⅡA对肺成纤维细胞增殖的影响,用RT-PCR法分析丹参酮ⅡA磺酸钠和TGF-β1作用后肺成纤维细胞Smad3、Smad7 mRNA表达水平的变化,以及对Ⅰ型胶原mRNA的影响。结果:丹参酮ⅡA磺酸钠在80-640mg/L浓度范围对5μg/L TGF-β1刺激的肺成纤维细胞增殖均具有明显的抑制作用,并呈剂量依赖性(P<0.05);丹参酮ⅡA磺酸钠在浓度160mg/L时能明显下调TGF-β1刺激的肺成纤维细胞内Smad3 mRNA、Smad3/Smad7 mRNA及Ⅰ型胶原mRNA的表达(P<0.05),并能上调Smad7 mRNA表达(P<0.05)。结论:丹参酮ⅡA磺酸钠能抑制LFB的增殖、转化及胶原的合成,机制可能是丹参酮ⅡA磺酸钠下调了大鼠TGF-β1 Smad信号通道的Smad3/Smad7水平,从而抑制LFB的增殖、转化。Objective: To study the effects of sulfotanshinone sodium (STS) on transforming growth factor beta 1 (TGF-~,) signaling pathway in lung fibroblasts of rats, and attempt to investigate its mechanism in prevention the proliferation and the transformation of lung fibroblasts. Methods: Rat lung fibroblasts were cultured in vitro and divided into three groups, blank control group, TGF-β1 stimulated group, and combined treatment group which was stimulated with STS and TGF-β1. After treatment for 48 hours, the mRNAs level of Smad3, Smad7, and collagen were assayed by reverse transcriptase polymerase chain reaction (RT-PCR). Results: STS ranged 80-640 mg/L had obvious inhibitory effect on lung fibroblasts stimulated by 5 μg/L TGF-β1 in a dose-dependent manner (P〈0.05), and 160 mg/L STS could down-regulate the mRNA levels of Smad3, Smad3/Smad7, and collagen type 0.05), and could up-regulate the expression restrain the proliferation and transformation I of TGF-β1 stimulated lung fibroblasts (all P 〈 of Smad7 mRNA (P〈0.05). Conclusion: STS can of lung fibroblasts, and synthesis of collagen. Themechanisms may be that STS can block TGF-β1 Smad signaling pathway and decrease the level of Smad3/SmadT.
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