Conclusions
Melatonin improves renal function, relieves oxidative stress, and protects the renal tissue via the Wnt/β-catenin signaling pathway and the TGF-β1-Smad2/3 signaling pathway in STZ-induced DN rats.
Methods
100 SPF male Sprague-Dawley rats were divided into four groups: low dose melatonin group, medium dose melatonin group and high dose melatonin group. Rats were 35 mg/kg STZ once to establish a DN model, and control rats were given the corresponding dose of normal saline. A renal function test was used to measure urine protein (UP), blood urea nitrogen (BUN) and serum creatinine (Scr). Pathological changes of renal tissues were obtained by HE staining and Masson staining. Oxidative stress-related indicators were measured in a STZ-induced DN rat. Western blot was used to measure target proteins in renal tissues.
Objective
This research aimed to explore the protective effect of melatonin on diabetic nephropathy (DN) rats induced by streptozotocin (STZ) and its related signaling pathways.
Results
The levels of UP, BUN and Scr in the model group were significantly higher than control group (P<0.05). After administration of melatonin, each administration group was significantly decreased compared to the model group. Pathological changes of renal tissues in the high dose group were the closest to the control group. After administration of melatonin, activities of SOD, CAT and GSH-Px were significantly increased in the medium dose group and the high dose group (P<0.05), while the activity of MDA was significantly decreased (P<0.05). The expression of Wnt4 and β-catenin in the model group were higher than the control group (P<0.01). When melatonin was given, the expression of Wnt4 and β-catenin in the medium dose group and the high dose group were significantly lower than the model group. Levels of TGF-β1, p-Samd2 and p-Samd3 in the control group were lower than the model group (P<0.05), and were decreased in the medium dose group and the high dose group. Conclusions: Melatonin improves renal function, relieves oxidative stress, and protects the renal tissue via the Wnt/β-catenin signaling pathway and the TGF-β1-Smad2/3 signaling pathway in STZ-induced DN rats.