丹酚酸B抗心肌纤维化的机制研究
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篇名: 丹酚酸B抗心肌纤维化的机制研究
TITLE:
摘要: 目的:研究丹酚酸B(Sal B)对血管紧张素Ⅱ(Ang Ⅱ)诱导的心肌成纤维细胞增殖、Ⅲ型胶原分泌及基质金属蛋白酶9(MMP-9)、Smad2/3、Smad7蛋白表达的影响,探讨其抗心肌纤维化的作用机制。方法:将细胞分为空白对照组(培养液)、AngⅡ模型组和Sal B低、中、高浓度组(12.5、25、50 μmol/L),用空白或含药培养液培养细胞1 h后,除空白对照组外的其余各组均加入1     μmol/L的AngⅡ诱导细胞增殖,共同作用24 h。分别采用MTT法和苏木精-伊红染色法考察Sal B对细胞增殖的影响;采用Western blot法检测Sal B对细胞Ⅲ型胶原、MMP-9 、Smad2/3、Smad7蛋白表达的影响。结果:与空白对照组比较,AngⅡ模型组细胞明显增殖,Ⅲ型胶原、MMP-9、Smad2/3蛋白表达明显增强,Smad7蛋白表达明显减弱,差异均有统计学意义(P<0.05);与AngⅡ模型组比较,Sal B各浓度组细胞的增殖均受到抑制,Ⅲ型胶原、MMP-9、Smad2/3蛋白表达均减弱,Smad7蛋白表达均增强,除Sal B低、中浓度组细胞Ⅲ型胶原与Sal B高浓度组细胞Smad2/3蛋白表达变化不显著外,其余各指标差异均有统计学意义(P<0.05)。结论:Sal B抗心肌纤维化的作用可能与抑制心肌成纤维细胞的增殖,下调Ⅲ型胶原、MMP-9、Smad2/3蛋白表达和上调Smad7蛋白表达有关。
ABSTRACT: OBJECTIVE: To study the effects of salvianolic acid B (Sal B) on angiotensin Ⅱ (Ang Ⅱ)-induced cardiac fibroblast proliferation, secretion of type Ⅲ collagen, protein expressions of matrix metalloproteinase 9 (MMP-9), Smad2/3, Smad7, and explore its mechanism of anti-myocardial fibrosis. METHODS: Cells were divided into blank control group (culture medium) Ang Ⅱ model group, Sal B low-dose, medium-dose, high-dose groups (12.5, 25, 50 μmol/L). After cultured 1 h by blank or drug-containing culture, except for blank control group, cells in other groups were added 1 μmol/L Ang Ⅱ to induce proliferation. for 24 h. MTT method and hematoxylin-eosin staining method were adopted investigate the effect of Sal B on proliferation. Western blot method was adopted to detect the effects of Sal B on protein expressions of type Ⅲ collagen, MMP-9, Smad2/3, Smad7. RESULTS: Compared with blank control group, cells in Ang Ⅱ model group were significantly proliferated, protein expressions of type Ⅲ collagen, MMP-9, Smad2/3 were obviously enhanced, protein expression of Smad7 was obviously weakened, with statistical significances (P<0.05). Compared with Ang Ⅱ model group, the cell proliferation in Sal B groups were inhibited, protein expressions of type Ⅲ collagen, MMP-9, Smad2/3 were weakened, while protein expression of Smad7 was enhanced. Except the protein expression of type Ⅲ collagen in Sal B low-dose and medium-dose groups, the protein expression of Smad2/3 in Sal B high-dose group did not change significantly, other indexes had statistical significances (P<0.05). CONCLUSIONS: The anti-myocardial fibrosis effect of Sal B may be associated with inhibiting the proliferation of cardiac fibroblasts, down-regulating protein expressions of type Ⅲ collagen, MMP-9, Smad2/3 and up-regulating protein expression of Smad7.
期刊: 2017年第28卷第28期
作者: 罗红,王春花,赵玲璐,杨宇,陈世平,徐旖旎,杨红宇,沈祥春
AUTHORS: LUO Hong,WANG Chunhua,ZHAO Linglu,YANG Yu,CHEN Shiping,XU Yini,YANG Hongyu,SHEN Xiangchun
关键字: 丹酚酸B;心肌成纤维细胞;Ⅲ型胶原;基质金属蛋白酶9;转化生长因子β1信号通路
KEYWORDS: Salvianolic acid B; Cardiac fibroblasts; Type Ⅲ collagen; Matrix metalloproteinase 9; Transforming growth factor β1 signaling pathway
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