Study on mechanism of Zhenwu decoction in inhibiting the progression of chronic heart failure mediated by lncRNA NEAT1/miR-31-5p/IGFBP7 molecular axis
Objective:To investigate the mechanism of Zhenwu decoction in inhibiting the progression of chronic heart failure(CHF)through lncRNA NEAT1/miR-31-5p/IGFBP7 molecular axis.Methods:Male SD rats were di-vided into control group,model group,positive control group and Zhenwu decoction low-dose,medium-dose and high-dose groups with 10 rats in each group.In addition to the control group,the CHF model was established by intrabito-neal injection of adriamycin in the other groups.The positive control group was given metoprolol intragastric admin-istration,and the Zhenwu decoction low-dose,medium-dose and high-dose groups were given Zhenwu decoction intra-gastric administration(crude drug content 6,12,18 g/kg).Left ventricular ejection fraction(LVEF),left ventricular fractional shortening(LVFS),serum brain natriuretic peptide(BNP)level,heart weight ratio,myocardial pathological changes,the levels of tumor necrosis factor-α(TNF-α),interleukin-iβ(IL-1β),malondialdehyde(MDA),superoxide dismutase(SOD)and the expression of lncRNA NEAT1,miR-31-5p and IGFBP7 in myocardial tissue were detec-ted.Rat myocardial H9c2 cells were cultured,and dual luciferase reporter gene assay was used to detect lncRNA NEAT1 targeting miR-31-5p and miR-31-5p targeting IGFBP7.Results:Compared with model group,LVEF and LVFS in Zhenwu decoction low,medium and high dose groups increased,and serum BNP level decreased(P＜0.05).Compared with model group,the levels of TNF-α,IL-1β and MDA decreased,while the level of SOD increased in Zhenwu decoction low,medium and high dose groups(P＜0.05).Compared with model group,the expressions of ln-cRNA NEAT1 and IGFBP7 decreased and the expression of miR-31-5p increased in Zhenwu decoction low-dose,me-dium-dose and high-dose groups(P＜0.05).In H9c2 cardiomyocytes,lncRNA NEAT1 targeted miR-31-5p and miR-31-5p targeted IGFBP7.Conclusion:Zhenwu decoction may improve cardiac function and reduce inflammation and oxidative stress in CHF rats through lncRNA NEAT1/miR-31-5p/IGFBP7 molecular axis.
万方数据
维普
