Effect of baicalin on renal fibrosis in rats with diabetic nephropathy by TGF-β1 / 医学研究生学报

ABSTRACT

ObjectiveDiabetic nephropathy (DN) is a pathological process involving the kidney that develops from Diabetes Mellitus (DM). The onset is hidden and difficult to reverse. Baicalin is an important flavonoid compound in Scutellaria Baicalensis. It has the functions of clearing heat and detoxifying, anti-inflammatory and anti-oxidant. In recent years, the role of baicalin in lowering blood glucose and lipids and improving metabolic syndrome has received widespread attention. Therefore, we observed the protective effect of baicalin on the kidneys of DN rats and explored its possible regulatory mechanism.MethodsForty-five male SD rats were randomly divided into a normal control group, a DN model group, and a baicalin-treated group, with 15 rats in each group. The normal group was routinely bred, and the DN model was established in the model group and the baicalin treatment group, and the corresponding preparations were given gavage treatment. After a fixed time point, rat body weight, fasting blood glucose (FBG), blood urea nitrogen (BUN), and serum creatinine (Scr) levels were measured, and the histopathological changes of the kidneys in each group were observed. TGF-β1 and α- SMA protein expression was measured by Western blot.ResultsCompared with the DN group, the FBG, BUN, Scr and 24h urine output of the baicalin treatment group were significantly decreased, and the body weight did not change significantly. Histopathological observation showed that compared with DN group, the pathological damage, glycogen deposition and fibrosis of the rats in the baicalin treatment group were significantly improved. Compared with the DN group, the results of Western blot showed that the expression of TGF-β1 and α-SMA protein in the baicalin treatment group were significantly decreased (P<0.05).ConclusionBaicalin can delay the progression of DN and improve renal fibrosis, and its mechanism may be closely related to the inhibition of α-SMA expression by baicalin by low regulation of TGF-β1.