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Title: [Protective effects and mechanism of glycosides/phenol component of Moutan Cortex on renal injury of diabetic nephropathy rats]. Author: Chen J, Zhang MH, Zhang L, Zhao D, Feng L, Jia XB. Journal: Zhongguo Zhong Yao Za Zhi; 2016 Jun; 41(11):1990-1998. PubMed ID: 28901091. Abstract: To evaluate the protective effects of glycosides/phenol component of Moutan Cortex (MC) on renal injury of diabetic nephropathy (DN) rats based on renal function parameters and histopathological examinations(HE staining and transmission electron microscope),and explore its possible mechanism by establishing DN rat models induced by high-sugar high-fat diet combined with streptozotocin (STZ). The results showed that compared with the model group, the MC glycosides/phenol component high and low dose groups(0.808, 0.404 g•kg⁻¹•d⁻¹) could significantly improve serum creatinine, blood urea nitrogen, urine protein and other abnormal renal function parameters. HE staining and transmission electron microscope results showed thickening of glomerular basement membrane, proliferation of mesangial cells and damages of podocyte structure in major rats of model group. However, the intervention of glycosides/phenol component of MC could effectively protect the glomerular injury. To explore its possible mechanism, the expressions of TGF-β1, fibronectin (FN) and collagen Ⅳ in renal tissues of rats in each group were detected by Western blot and immunohistochemical assay, and the phosphorylation levels of downstream effect factors (Smad2/3, p38MARK) of TGF-β1 were detected. The results showed that glycosides/phenol component of MC could effectively antagonize the activity of TGF-β1, lower the expressions of fibronectin (FN) and collagen Ⅳ inextracellular matrix (ECM), and resist against the thickening of glomerular basement membrane. More importantly, its protective effect on renal injury in DN rats may be associated with interfering the conduction of Smad, MARK pathways and resisting against the TGF-β1-induced ECM accumulation.[Abstract] [Full Text] [Related] [New Search]