Effects of Tongluo recipe on p38 mitogen-activated protein kinase-fibronectin pathway in the kidney of diabetic rats / 第二军医大学学报

ABSTRACT

Objective To study the effects of Tongluo recipe on p38 mitogen-activated protrin kinase (p38 MAPK)- fibronectin(FN) signal pathway in the kidney of streptozotocin-induced diabetic rats, so as to explore the possible mechanism by which Toogluo recipe protects the kidney. Methods Male Sprague-Dawley(SD) rats were randomly divided into 3 groups(n = 7): control group (CON group), model group(DM group)and Toogluo recipe group(DM+TLR group). Rats in the DM group and DM+TLR groups were administered with streptozotocin (65 mg/kg) by intraperitoneal injection to induce diabetic model. Rats in DM + TLR group were also given 1g/(kg·d) of Toogluo recipe orally after successfully establishment of diabetic model, and rats in DM and CON groups were only given equivalent volume of ddH2O. The interference lasted for 12 weeks. Biochemical indices were obtained by automatic analyzer. Coomassie brilliant blue assay was used to measure the 24-hour urine protein. Kidney cortex was subjected to PAS staining. Western blotting analysis was used to detect the protein expression of total p38 MAPK (t-p38 MAPK), phosphorylated p38 MAPK (p-p38 MAPK), total cAMP response element-binding protein (t-CREB), phosphorylated CREB (p-CREB) and FN. Results Compared with CON group, the average left kidney mass/body mass (LKM/BM), blood glucose(BG), blood urea nitrogen(BUN), serum creatinine(Scr), 24-hour urine proteins(24 h UP) and urine protein/creatinine (UP/Ucr) were significantly increased in the DM group (P< 0.05); the average BM was significantly decreased(P<0.05); and the expression of p-p38 MAPK, p-CREB, FN was increased by 2.37, 2.21, and 2.03 folds, respectively (P< 0.05). Compared with DM group, the average LKM/BM, Scr, 24 h UP and UP/Ucr were significantly decreased (P<0.05) in DM+TLR group, and the expression of p-p38 MAPK, p-CREB, FN was significantly decreased(P< 0.05). Conclusion Tongluo recipe can protect the kidney in diabetic nephropathy rats, probably through inhibition of the p38 MAPK-FN pathway.