Article · Volume 59, Issue 1 · pp. 359–369
Conessine Attenuates Diabetic Nephropathy in Rats through Inhibition of Hyperglycemia-Induced Oxidative Stress, Inflammation and Apoptosis
Lin Li1, Qian Wang1, Yungiang Wang2, Chenchen Li1, Yan Gao1, Li Zhang1
- 1Department of Nephrology, Affiliated Hospital of Hebei University, (Key Laboratory of Skeletal Metabolic Physiology for Chronic Kidney Disease in Hebei Province), Baoding, CHINA.
- 2Kidney Ward Dialysis Center, Army Hospital of the 82nd Group Army, Baoding, CHINA.
Abstract
Background One type of chronic kidney disease is diabetic nephropathy. One of the main causes of end-stage renal disease and chronic kidney disease is diabetic nephropathy. The objective of this study was to assess the effects of treating diabetic nephropathy with conessine extract on male wistar rats with diabetes that had been triggered by streptozotocin. Materials and Methods Twenty-four rats were split up into four groups. The regular diet was fed to the negative control animals in the first group. After receiving a single intravenous injection of streptozotocin to cause diabetes, the remaining 18 rats were split equally into three groups: the diabetic control group was placed in group 2, the third group received oral treatment with 20 mg/ kg of conessine, and the fourth group received oral treatment with 5 mg/kg of gliclazide. Results In comparison to the negative control, the rats in the second group had higher glucose and lipid peroxide levels and lower SOD, CAT, GR, GPx, and GSH activity. Diabetes also led to an increase in immunoglobulins, interleukin-6, and carboxymethyl lysine. Potassium and sodium levels were lowered, while kidney function metrics were also raised. renal tissues also displayed significant histological alterations. Conclusion Conessine treatments, administered to the diabetic rats in the third improved all altered biochemical and pathological tests that were getting closer to the negative control.
Keywords: Conessine; Diabetic nephropathy; Streptozotocin; Antioxidants
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