|
|
Mechanism research of Qianyang Decoction inhibits the proliferation of cardiac fibroblasts |
CHEN Jie RUAN Xiaofen WANG Xiaolong |
Department of Cardiovascular Medicine, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China |
|
|
Abstract Objective To discussed the mechanism of Qianyang Decoction inhibits the abnormal proliferation of cardiac fibroblasts (RCF) cells induced by angiotensin Ⅱ (Ang Ⅱ). Methods The RCF cells were divided into blank cell group, Ang Ⅱ group and Ang Ⅱ+Qianyang Decoction group. In the Ang Ⅱ group, a cell model with abnormal proliferation of cardiac fibroblasts induced by Ang Ⅱ for 24 h was selected, and the Ang Ⅱ+Qianyang Decoction group was a cell model that was induced by Ang Ⅱ and intervened with Qianyang Decoction. Western blot was used to analyze and compare the transforming growth factor-β1 (TGF-β1), Collagen Ⅰ type (Collagen Ⅰ), Collagen Ⅲ protein expression among three groups, and quantitative polymerase chain reaction was used to detect and compare the TGF-β1 and Collagen Ⅰ, Collagen Ⅲ genetic expression among three groups. Results The protein expression levels of TGF-β1, Collagen Ⅰ and Collagen Ⅲ in Ang Ⅱ group were higher than those in the blank cell group (all P < 0.01). The protein expression levels of TGF-β1 and Collagen Ⅰ, Collagen Ⅲ in Ang Ⅱ+Qianyang Decoction group were lower than those in the Ang Ⅱ group (P < 0.05 or P < 0.01). The gene expressions levels of TGF-β1, Collagen Ⅰ and Collagen Ⅲ in Ang Ⅱ group were higher than those in the blank cell group (all P < 0.01). The gene expression levels of TGF-β1, Collagen Ⅰ and Collagen Ⅲ in Ang Ⅱ+Qianyang Decoction group were lower than those in Ang Ⅱ group (P < 0.05 or P < 0.01). Conclusion Qianyang Decoction can inhibits the abnormal proliferation of RCF cells by reducing the gene and protein expression level of TGF-β1, Collagen Ⅰ and Collagen Ⅲ, hence alleviate heart muscle fibrosis.
|
|
|
|
|
[1] Yang Z,Zhang X,Guo N,et al. Substance P Inhibits the Collagen Synthesis of Rat Myocardial Fibroblasts Induced by Ang Ⅱ [J]. Med Sci Monit,2016,22:4937-4946.
[2] Huang X,Kang Y,Jiang X,et al. Tandospirone enhances the anti-myocardial fibrosis effect of valsartan in spontaneously hypertensive rats [J]. Biomed Pharmacother,2020, 126:110073.
[3] 崔琳,王幼平,谢世阳,等.血管紧张素Ⅱ对原代培养大鼠心肌成纤维细胞增殖及转分化的影响[J].中西医结合心脑血管病杂志,2017,15(21):2680-2684.
[4] 王欣,任卫东.与心肌纤维化相关的细胞因子和生长因子[J].医学综述,2019,25(9):1694-1699.
[5] Tallquist MD. Cardiac Fibroblast Diversity [J]. Annu Rev Physiol,2020,82:63-78.
[6] Bao Q,Zhang B,Suo Y,et al. Intermittent hypoxia mediated by TSP1 dependent on STAT3 induces cardiac fibroblast activation and cardiac fibrosis [J]. Elife,2020,9:49923.
[7] 丁雪峰,周京敏,朱凌倜,等.芪苈强心提取物阻断Smad3信号通路抑制血管紧张素Ⅱ诱导的心脏成纤维细胞转分化[J].中国分子心脏病学杂志,2014,14(6):1144-1148.
[8] Ames MK,Atkins CE,Pitt B. The renin-angiotensin-aldosterone system and its suppression [J]. J Vet Intern Med,2019,33(2):363-382.
[9] 高俊杰,吴琼,王肖龙,等.潜阳合剂对腹主动脉缩窄致高血压模型大鼠血压的影响[J].上海中医药杂志,2015, 49(6):74-77.
[10] Yu BT,Yu N,Wang Y,et al. Role of miR-133a in regulating TGF-β1 signaling pathway in myocardial fibrosis after acute myocardial infarction in rats [J]. Eur Rev Med Pharmacol Sci,2019,23(19):8588-8597.
[11] Vivar R,Humeres C,Anfossi R,et al. Role of FoxO3a as a negative regulator of the cardiac myofibroblast conversion induced by TGF-β1 [J]. Biochim Biophys Acta Mol Cell Res,2020:118695.
[12] Ahn MS,Eom YW,Oh JE,et al. Transient receptor potential channel TRPV4 mediates TGF-β1-induced differentiation of human ventricular fibroblasts [J]. Cardiol J,2020,27(2):162-170.
[13] 肖一佳,沈祥春,李杰平,等.心肌纤维化与TGF-β-Smad信号系统[J].中国新药杂志,2016,25(2):182-186
[14] 李同,商黔惠,刘婵,等.转化生长因子β1/Samds表达在高盐饮食致Wistar大鼠心肌纤维化中的作用及替米沙坦干预[J].中华高血压杂志,2013,21(7):648-653.
[15] 高俊杰,吴琼,陈铁军,等.潜阳合剂对腹主动脉缩窄致高血压左室肥厚的影响[J].中西医结合心脑血管病杂志,2015,13(6):746-749.
[16] Xin Z,Kejing W,Fen H,et al. MicroRNA-101 protects cardiac fibroblasts from hypoxia-induced apoptosis via inhibition of the TGF-β signaling pathway [J]. Int J Biochem Cell Biol,2015,65:155-164.
[17] 吴艳,刘婷婷,冯凯,等.微小RNA调控心肌纤维化研究进展[J].药学研究,2018,37(5):278-281.
[18] 曹帅.微小RNA与心肌纤维化关系的研究进展[J].心血管病学进展,2016,37(6):647-651.
[19] 张松林,范粉灵,魏峰,等.微小RNA-133b对心肌纤维化的影响[J].中国医学科学院学报,2019,41(5):589-594.
[20] Wu X,Zhu J,Wei Y,et al. MicroRNA-663 participates in myocardial fibrosis through interaction with TGF-β1 [J]. Exp Ther Med,2019,18(4):3172-3176.
[21] Jin X,Yu LL,Yu CX. Effect of miR-9 on myocardial fibrosis in rats via TGF-β1/Smads signaling pathway [J]. Eur Rev Med Pharmacol Sci,2019,23(16):7083-7088.
[22] 汪波,占贞贞,曾麒燕.心肌纤维化的表观遗传调控研究进展[J].中国比较医学杂志,2019,29(3):92-97.
[23] He Y,Ling S,Sun Y,et al. DNA methylation regulates α-smooth muscle actin expression during cardiac fibroblast differentiation [J]. J Cell Physiol,2019,234(5):7174-7185.
[24] Tao H,Dai C,Ding JF,et al. Epigenetic aberrations of miR-369-5p and DNMT3A control Patched1 signal pathway in cardiac fibrosis [J]. Toxicol,2018,410:182-192.
[25] Tang X,Chen XF,Wang NY,et al. SIRT2 acts as a cardioprotective deacetylase in pathological cardiac hypertrophy [J]. Circul,2017,136(21):2051-2067. |
|
|
|