Abstract：Objective The purpose of the experiment was to study mechanism of baicalin inhibiting cardiac fibroblast differentiation in diabetes rats. Methods A total of 24 male SD rats from April to June 2021 were selected as the research objects. They were divided into control group (8 cases), model group (8 cases) and treatment group (8 cases) by randomized block design. The control group was fed with common feed, the model group was injected with 45 mg/kg streptozotocin by tail vein to establish diabetes model and fed with common feed. The treatment group was injected with 45 mg/kg streptozotocin by tail vein and the baicalin solution was intraperitoneally injected at a dose of 15 μmol/L per kilogram per day after the diabetes model succeeded, fed with common feed. Blood glucose, cardiac mass index, microRNA-146a (miR-146a) and α-smooth muscle cell actin (α-SMA) were compared among three groups. Results The blood glucose and heart weight index in the treatment group were lower than that in the model group, and the differences were statistically significant (P＜0.05). The blood glucose and heart weight index in the treaatment group were higher than those in the control group, and the differences were statistically significant (P＜0.05). MiR-146a in the treatment group was higher than that in the model group, α-SMA in the treatment group was lower than that in the model group, and the differences were statistically significant (P＜0.05). MiR-146a in the treatment group was lower than that in the control group, α-SMA in the treatment group was higher than that in the control group, and the differences were statistically significcant (P＜0.05). Conclusion Baicalin inhibited cardiac fibroblast differentiation and intervened myocardial fibrosis in diabetes rats, the mechanism was related to the baicalin regulated expression of miR-146a and inhibited α-SMA protein.
Wang HJ，Cai J.The role of microRNAs in Heart Failure[J].Biochim Biophys Acta Mol Basis Dis，2017，1863（8）：2019-2030.
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