Mechanism of Huoxue Qianyang Qutan Recipe in Inhibiting Cardiac Fibroblast Pro-liferation
Objective To investigate the impact and underlying mechanisms of Huoxue Qianyang Qutan Recipe(HQQR)on the proliferation of angiotensin Ⅱ(Ang Ⅱ)induced cardiac fibroblasts(CFs).Methods Primary CFs were i-solated and cultured from SD rats and subsequently identified.Ang Ⅱ was used to induce CFs and establish an in vitro car-diac fibrosis model.CFs were divided into a blank cell group,an Ang Ⅱ group,an Ang Ⅱ+HQQR(low dose)group,an Ang Ⅱ+HQQR(high dose)group,and an Ang Ⅱ+losartan group,treated for 48 hours.The CCK-8 method was used to detect cell proliferation levels in each group,flow cytometry was used to detect ROS levels,ELISA was used to detect hydroxyproline levels in the supernatants of each group,and Western blot was used to detect the levels of NADPH oxidase 4(NOX4),nuclear factor kappa B p65(NF-κB p65),extracellular signal-regulated kinase 1/2(ERK1/2),and p-ERK1/2.Statistical analysis was conducted on the collected data.Results HQQR significantly ameliorated Ang Ⅱ-in-duced CFs proliferation.The hydroxyproline levels in the supernatants of the Ang Ⅱ group were significantly higher than those in the blank group(P＜0.05),with ROS levels and NOX4 protein expression also significantly elevated(P＜0.05).After Ang Ⅱ stimulation of CFs,the expression of NF-κB p65 protein and the phosphorylation ratio of ERK1/2 in cells were higher than those in the blank cell group(P＜0.05).HQQR treatment effectively improved CFs proliferation and col-lagen secretion,reduced ROS levels,and significantly decreased the expression of NOX4,NF-κB p65 protein,and the phosphorylation ratio of ERK1/2,with statistically significant differences(P＜0.05).Conclusion HQQR may inhibit CFs proliferation and ameliorate myocardial fibrosis by inhibiting oxidative stress and reducing inflammatory responses.
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维普
