Mechanism of Huangdi Anxiao (黄地安消)Capsules in Intervening T2DM Vascular Disease by EndoMT Inhibition
Objective:To investigate the effects of endothelial-to-mesenchymal transition (EndoMT) in the process of macrovascular lesions in dia-betic vascular disease and the intervention effect of Huangdi Anxiao (黄地安消) Capsules (HDAXC).Methods:The diabetic rat model was induced by high-fat and high-sugar diet combined with streptozotocin (STZ).The successfully modeled rats were divided into HDAXC groups (3,6,and 12 g/kg) and a metformin group (0.72 g/kg),and corresponding drugs were administered for 6 weeks.The general conditions of rats in each group were observed.Fasting blood glucose (FBG) was measured weekly.Pathological characteristics of thoracic aortic tissue were observed,and the expression levels of transforming growth factor β1 (TGF-β1),Smad2,Smad3 proteins and mRNA,α-smooth muscle actin (α-SMA),and vascular endothelial cadherin (VE-cadherin) proteins were detected.Results:Compared with the normal control group,the model group showed significant decrease in body weight (P<0.05 or P<0.01),significant increase in FBG (P<0.01),significant upreg-ulation of TGF-β1,Smad2,Smad3 proteins and mRNA in thoracic aortic blood vessels (P<0.01),significant upregulation of α-SMA protein expression (P<0.01),significant downregulation of VE-cadherin protein expression (P<0.01),and severe vascular endothelial pathology.Compared with the results in the model control group,after 10 weeks of treatment with HDAXC at various doses,the body weight of rats signifi-cantly increased (P<0.05 or P<0.01);the expression of TGF-β1,Smad2,Smad3 proteins and mRNA in thoracic aortic blood vessels were significantly downregulated;α-SMA protein expression was significantly downregulated (P<0.01);VE-cadherin protein expression was sig-nificantly upregulated (P<0.01);the pathological damage of thoracic aorta in rats was alleviated.Conclusion:HDAXC can inhibit the TGF-β/Smad pathway to improve macrovascular lesions caused by EndoMT,thereby reducing pathological damage in rats.
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