双氢青蒿素对血管紧张素Ⅱ诱导的心肌成纤维细胞增殖和活性的影响

Effects of Dihydroartemisinin on the proliferation and activity of cardiac fibroblasts induced by angiotensinⅡ

目的探讨双氢青蒿素(DHA)对血管紧张素Ⅱ(AngⅡ)诱导的心肌成纤维细胞增殖和分泌活性的影响。方法以乳鼠的心肌组织中的成纤维细胞为研究对象。实验设置为:对照组、AngⅡ组、DHA组和DHA+AngⅡ组,采用噻唑兰法检测每组细胞的增殖情况;用ELISA分析细胞孵育液中所含的Ⅰ型胶原蛋白(ColⅠ)以及纤黏连蛋白(FN)的水平;免疫印迹法分析胞质内的α-平滑肌肌动蛋白(α-SMA)和转化生长因子β1(TGF-β1)的含量。结果DHA组的细胞数、细胞悬浮液中ColⅠ和FN含量、细胞中α-SMA和TGF-β1蛋白含量与对照组相比均没有显著差异(P>0.05)。与对照组相比,AngⅡ组细胞(0.1272±0.0026)显著增殖(P<0.05);细胞悬浮液中ColⅠ(0.8397±0.0371)和FN(0.7555±0.0820)含量均增加(P<0.05);胞质内α-SMA(0.229±0.029)和TGF-β1(0.193±0.023)的量增多(P<0.05)。与AngⅡ组相比,DHA+AngⅡ组的细胞数量(0.1201±0.0021)显著下降;细胞悬浮液中ColⅠ(0.6213±0.0216)和FN(0.5581±0.0463)含量均减少(P<0.05);细胞中α-SMA(0.097±0.014)和TGF-β1(0.048±0.007)蛋白含量下降(P<0.05)。结论AngⅡ能促进心肌成纤维细胞增殖并增强其分泌活性,而双氢青蒿素能拮抗AngⅡ的这种功效。

Objective To explore the effect of dihydroartemisinin(DHA)on the proliferation and secretory activity of cardiac fibroblasts induced by angiotensinⅡ(AngⅡ).Methods Fibroblasts in myocardial tissue of suckling rats were studied.The cells were arranged into control group,AngⅡgroup,DHA group and DHA+AngⅡgroup.The proliferation of cells in each group was detected by thiazolam method;ELISA was used to detect the content of type I collagen(Col I)and fibronectin(FN)in cells suspension in each group;Immunoblotting was used to analyze the protein content ofα-smooth muscle actin(α-SMA)and transforming growth factorβ1(TGF-β1)in cells of each group;The number of cells,the contents of ColⅠand FN in cell suspension,α-SMA and TGF-β1of cell have not significant difference between the control group and the DHA group(all P>0.05).Results Matched with the control group,the cells in AngⅡgroup proliferated(0.1272±0.0026)obviously(P<0.05);the contents of ColⅠ(0.8397±0.0371)and FN(0.7555±0.0820)in cell suspension increased(P<0.05);α-SMA(0.229±0.029)and TGF-β1(0.193±0.023)protein content raised(P<0.05).Matched with the AngⅡgroup,the number of cells(0.1201±0.0021)in DHA+AngⅡgroup decreased obviously(P<0.05);the contents of ColⅠ(0.6213±0.0216)and FN(0.5581±0.0463)in cell suspension decreased(P<0.05);in cellsα-SMA(0.097±0.014)and TGF-β1(0.048±0.007)protein content reduced(P<0.05).Conclusion AngⅡcan promote the proliferation and enhance the secretory activity of myocardial fibroblasts,and dihydroartemisinin can antagonize the effect of AngⅡ.