RESUMO
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.
RESUMO
Objective To investigate the protective effects of fluvastatin(Flu) on rat renal fibroblasts proliferation and cytokines expression induced by cyclosperine A (CsA). Methods The fibroblasts were cultured with CsA or with CsA plus fluvastatin. The cellular proliferation was determined by MTT colorimetry. The mRNA expression of transforming growth factor β1(TGF-[β1), connetive tissue growth factor (CTGF) and c-fos was detected by BT-RCB. The protein level of flbronecfin (FN) was measured by Western blotting. Results CsA inhibited the proliferation of fibroblasts in dose- and time-dependent manner (P＜0.05). Treatment with Flu accelerated the suppression of fibroblasts resulted from CsA (P＜0.O1). CsA stimulated the expression of TGF-β1, CTGF, c-fos and FN compared with control group(P＜0.05), which could be down-regulated by Flu (P＜0.05). Conclusion Fluvastatin may relieve CsA-induced nephrotoxicity in rat fibroblasts.