ABSTRACT
AIM:To investigate the ameliorative effect of salvianolic acid B on vasodilatory function in diabetic rats and the possible mechanisms.METHODS:SD rats(n=40)were fed on high-sugar and high-fat diet for 4 weeks, followed by a single intraperitoneal injection of streptozotocin(40 mg/kg).The rats with random blood glucose level over 16.7 mmol/L were considered diabetic and randomly allocated to 3 groups, namely model group, low dose(80 mg· kg-1· d-1)of salvianolic acid B group and high dose(160 mg· kg-1· d-1)of salvianolic acid B group.The rats in salvianolic acid B groups were intragastrically administered with corresponding doses of salvianolic acid B for 6 weeks. Vasodilatory function was measured as endothelium-dependent and-independent vasodilation of the aortic rings.The primary histopathological changes of aorta were observed by HE staining.Serum levels of interleukin-6(IL-6),tumor necrosis fac-tor-α(TNF-α)and C-reactive protein(CRP)were measured by ELISA.The levels of total antioxidant capacity,malondi-aldehyde(MDA)and nitric oxide(NO)in aortic tissues were evaluated by colorimetric assays.The protein levels of inter-cellular adhesion molecule-1(ICAM-1)and monocyte chemotactic protein-1(MCP-1), and the activation of nuclear fac-tor-κB(NF-κB)were determined by Western blot.RESULTS: Treatment with salvianolic acid B evidently ameliorated endothelium-dependent diastolic function and pathological changes of aorta in diabetic rats(P<0.05 or P<0.01).Sup-plementation with salvianolic acid B resulted in significant increases in NO content and total antioxidant capacity in aortic tissues,accompanied by marked decreases in the level of MDA in aorta tissues and the serum levels of IL -6, TNF-αand CRP(P<0.05 or P<0.01).Salvianolic acid B markedly down-regulated NF-κB p65 nuclear translocation and protein expression of ICAM-1 and MCP-1 in aorta tissues(P<0.05 or P<0.01).CONCLUSION:Salvianolic acid B effectively ameliorates endothelium-dependent diastolic function of aorta in diabetic rats, which might be attributed to suppression of NF-κB activation and subsequent expression of inflammatory cytokines.The beneficial effect of salvianolic acid B on vascu-lar endothelium might be derived from its antioxidant capacity.
ABSTRACT
Objective: To observe the protective effect of salvianolic acid B (Sal B) on pancreatic islet cells in diabetic rats with fluctuating blood glucose and the possible mechanisms implicated. Methods: Diabetes model in rats was established by feeding with high-sugar and high-fat diets combined with ip injection of streptozotocin (STZ). Then the rats were subjected to ip injection of insulin and/or ig administration of glucose at indicated time for 6 weeks to induce blood glucose fluctuation, with those in Sal B groups ig supplemented with Sal B 160 or 80 mg/kg. The contents of fasting blood glucose (FBG), fasting serum insulin (FINS), and glycosylated hemoglobin (GHb) and the levels of total anti-oxidant capacity (TAC), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) in both serum and pancreatic tissues were determined with commercially available kits. Pathological changes and cell apoptosis in pancreatic islets were evaluated by HE staining and TUNEL staining, respectively. Protein levels of PDX-1 in pancreatic tissues were examined by Western blotting analysis. Results: Compared with the control group, the contents of FBG, GHb, and MDA in diabetic rats were increased significantly, while the levels of FINS, TAC, and SOD activity were decreased markedly (P < 0.01). Pancreatic islets in diabetic rats became decreased in size and number, while cell apoptosis in islets increased notably (P < 0.01). Protein level of PDX-1 was significantly decreased in pancreas of diabetic rats (P < 0.01). Supplementation with Sal B resulted in a significant decrease in FBG, GHb, and MDA contents and increase in FINS, TAC, and SOD activity in diabetic rats (P < 0.05, 0.01). Sal B significantly attenuated pathological changes and reduced cell apoptosis in pancreatic islets of diabetic rats, with the expression of PDX-1 protein up-regulated evidently (P < 0.05 or 0.01). Conclusion: Sal B can significantly ameliorate pancreatic pathological changes and improve pancreatic islet function in diabetic rats with fluctuating blood glucose, which might be attributed to attenuation of oxidative stress, up-regulation of PDX-1 expression, and suppression of islet cell apoptosis.