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目的:通过观察丹参酮ⅡA(TSN)对AngⅡ诱导的心肌成纤维细胞(CFs)增殖及Ⅰ型胶原合成的影响,探讨其抗心肌纤维化的作用机制。方法:差速贴壁法提取原代CFs,采用四氮唑盐(MTT)比色法测定细胞数目,ELISA法检测Ⅰ型胶原合成,RT-PCR法半定量检测Ⅰ胶原mRNA表达。结果:①AngⅡ组OD值高于空白对照组,两者比较有显著性差异(P<0.01);AngⅡ+TSN组OD值低于AngⅡ组,两者比较有显著性差异(P<0.01)。②AngⅡ组有促进心肌成纤维细胞分泌Ⅰ型胶原的作用,与空白对照组比较,有显著性差异(P<0.01);AngⅡ+TSN组Ⅰ型胶原含量低于AngⅡ组,两者比较,有显著性差异(P<0.01)。③AngⅡ组Ⅰ型胶原mRNA表达高于空白对照组,两者比较有显著性差异(P<0.05);AngⅡ+TSN组Ⅰ型胶原mRNA表达低于AngⅡ组,两者比较有显著性差异(P<0.05)。结论:AngⅡ可直接诱导CFs的增殖,促进其分泌Ⅰ型胶原,并能显著增加Ⅰ型胶原mRNA的表达;TSN对AngⅡ诱导的CFs增殖及Ⅰ型胶原分泌增加,及Ⅰ型胶原mRNA表达增强均有抑制作用。提示:TSN抗心肌纤维化作用的产生可能与丹参酮ⅡA抑制心脏局部的RAS系统有关。
OBJECTIVE: To observe the effect of tanshinone II A (TSN) on the proliferation of Ang II-induced cardiac fibroblasts (CFs) and the synthesis of type I collagen, and to explore the mechanism of anti-myocardial fibrosis. METHODS: Primary CFs were extracted by differential adherent method. The number of cells was determined by MTT colorimetric method. Collagen type I synthesis was detected by ELISA. Semi-quantitative detection of I collagen mRNA expression by RT-PCR. Results: 1The OD value of AngII group was higher than that of blank control group, there was a significant difference between them (P<0.01). The OD value of AngII+TSN group was lower than that of AngII group. There was a significant difference between the two groups (P<0.01). 2AngII group promoted the secretion of type I collagen from cardiac fibroblasts, and there was significant difference compared with the blank control group (P<0.01). The content of type I collagen in AngII+TSN group was lower than that of AngII group. There was significant difference between the two groups. Sexual difference (P<0.01). The expression of type I collagen mRNA in the 3AngII group was higher than that in the blank control group (P<0.05). The expression of type I collagen mRNA in the AngII+TSN group was lower than that in the AngII group. There was a significant difference between the two groups (P< 0.05). Conclusion: Ang II can directly induce the proliferation of CFs, promote the secretion of type I collagen, and increase the expression of type I collagen mRNA. The increase of Ang II-induced CFs proliferation, type I collagen secretion and the enhancement of type I collagen mRNA expression by AngII. There is inhibition. Tip: The production of anti-myocardial fibrosis by TSN may be related to the inhibition of local RAS system by tanshinone IIA.