| 引用本文:郑鹏1，王俊帅1，占大钱1，王敏1，夏海发2，刘旭东1，明晓青1，周代星1，冯俊1.丹参酮ⅡA通过NLRP3/Caspase-1信号通路对心肌成纤维细胞的保护作用[J].世界中医药,2021,(06):. |
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| 丹参酮ⅡA通过NLRP3/Caspase-1信号通路对心肌成纤维细胞的保护作用 |
| Protective Effect of Tanshinone ⅡA on Cardiac Fibroblasts through the NLRP3/Caspase-1 Signaling Pathway |
| 投稿时间：2020-07-17 |
| DOI：10.3969/j.issn.1673-7202.2021.06.011 |
| 中文关键词: 丹参酮ⅡA 脓毒症 心肌成纤维细胞 NLRP3/Caspase-1信号通路 |
| English Keywords:Tanshinone ⅡA Sepsis Cardiac fibroblast NLRP3/Caspase-1 signaling pathway |
| 基金项目:国家自然科学基金项目(81701887)——Protectin DX调节中性粒细胞活化在脓毒症致急性肺损伤中的作用及其机制研究;湖北省自然科学基金项目(2020CFB577) |
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| 中文摘要: |
| 目的:探讨丹参酮ⅡA对心肌成纤维细胞损伤的保护作用及可能机制。方法:分离和培养大鼠心肌成纤维细胞(Cardiac Fibroblast,CFs)。以脂多糖(LPS)刺激CFs建立脓毒症心肌损伤体外模型,以不同浓度丹参酮ⅡA预处理CFs 30 min后,给予LPS刺激,设对照组,LPS模型组,LPS+不同浓度TSA(2 μmol/L、10 μmol/L、50 μmol/L)组;采用蛋白质免疫印迹试验法(Western blotting)检测CFs的NLRP3和Caspase-1蛋白表达水平,酶联免疫吸附试验(ELISA)检测细胞上清中IL-1β和IL-18的含量。结果:LPS刺激24 h后,CFs的NLRP3蛋白的表达水平最高。LPS模型组NLRP3和Caspase-1蛋白的表达较对照组明显升高(P<0.01)。与LPS模型组比较,丹参酮ⅡA(10 μmol/L、50 μmol/L)处理组NLRP3和Caspase-1蛋白的表达均明显降低(P<0.05);丹参酮ⅡA处理组的IL-1β和IL-18水平均明显低于LPS模型组(P<0.05)。结论:丹参酮ⅡA能抑制LPS诱导的心肌成纤维细胞内NLRP3/Caspase-1炎症反应信号通路分子的表达,这可能是其保护心肌细胞的分子机制之一。 |
| English Summary: |
| To explore the protecting role and mechanism of tanshinone ⅡA in lipopolysaccharide (LPS)-induced cardiac fibroblast injure.Methods:Rat cardiac fibroblasts (Cardiac Fibroblast，CFs) were Isolated and cultured.Lipopolysaccharide (LPS) was used to stimulate CFs to establish an in vitro model of septic myocardial injury.After CFs were pretreated with different concentrations of Tanshinone ⅡA for 30 min，they were given LPS stimulation.A control group，an LPS model group and LPS+different TSA (2 μmol/L，10 μmol/L，50 μmol/L) were set up.Western blotting was used to detect the NLRP3 and Caspase-1 protein expression levels of CFs，and the enzyme-linked immunosorbent assay (ELISA) was used to detect the content of 1β and IL-18.Results:After 24 h of LPS stimulation，the expression level of NLRP3 protein in CFs was the highest.The expression of NLRP3 and Caspase-1 protein in the LPS model group was significantly higher than that in the control group (P<0.01).Compared with the LPS model group，the expressions of NLRP3 and Caspase-1 protein in the Tanshinone ⅡA (10 μmol/L，50 μmol/L) treatment group were significantly reduced (P<0.05); the level of IL-1β and IL-18 in the Tanshinone ⅡA treatment group was significantly lower than that of the LPS model group (P<0.05).Conclusion:Tanshinone ⅡA may be a potent agent to protect against myocardial dysfunction in sepsis by regulating NLRP3/Caspase-1 signaling pathway. |
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