Background: Diabetic Nephropathy remains a major cause of morbidity and mortality in patients suffering from renal dysfunction. This study accessed the nephroprotective role of Adropinin against streptozotocin (STZ) induced diabetic nephropathy in rats and scrutinizes the possible mechanism of action.
Methods: STZ (45 mg/kg) dose was used for inducing diabetic nephropathy (DN) and rats were divided into different groups and received the dose-dependent treatment of Adropinin. Blood glucose level, body weight, tissue weight, antioxidant, renal, hepatic parameters, and cytokines were determined. At the end of the experimental study, renal histopathology was performed.
Results: Adropinin significantly (P< 0.001) boosted plasma insulin levels and reduced the blood glucose level. Adropinin considerably increased body weight and reduced kidney weight and kidney hypertrophy. Adropinin significantly (P< 0.001) reduced urine outflow, microalbumin, total protein, blood urea nitrogen (BUN), uric acid and increased the creatinine, creatinine clearance. Adropinin significantly (P< 0.001) reduced the indole sulfate level in the serum, kidney and reduced in the urine. Adropinin significantly (P< 0.001) reduced the total cholesterol, triglyceride, low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL) and increased the level of high-density lipoprotein (HDL). Adropinin significantly (P< 0.001) increased the level of antioxidant enzymes such as glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and reduced the level of malonaldehyde (MDA), 8-hydroxy-2ʹ -deoxyguanosine (8-OHdG). Adropinin significantly (P< 0.001) reduced the level of interleukin-1β (IL-1β), interleukin-6 (IL-6), transforming growth factor beta (TGF-β) and increased the level of interleukin-10 (IL-10), respectively. Adropinin treatment showed improvement in renal histopathology.
Conclusion: We can say that Adropinin showed the nephroprotective effect against the STZ-induced diabetic nephropathy rats via inflammatory and antioxidant pathway.



中文翻译：

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Adropinin 对链脲佐菌素诱导的大鼠糖尿病肾病的肾保护作用：炎症机制和 YAP/TAZ 因子


背景：糖尿病肾病仍然是肾功能不全患者发病和死亡的主要原因。本研究探讨了 Adropinin 对链脲佐菌素 (STZ) 诱导的大鼠糖尿病肾病的肾保护作用，并探讨了可能的作用机制。

方法：采用STZ（45 mg/kg）剂量诱导糖尿病肾病（DN），将大鼠分为不同组，接受Adropinin剂量依赖性治疗。测定血糖水平、体重、组织重量、抗氧化剂、肾脏、肝脏参数和细胞因子。实验研究结束时，进行肾脏组织病理学检查。

结果： Adropinin 显着（P<0.001）提高血浆胰岛素水平并降低血糖水平。 Adropinin 显着增加体重并减少肾脏重量和肾脏肥大。 Adropinin 显着（P<0.001）减少尿流量、微量白蛋白、总蛋白、血尿素氮（BUN）、尿酸，并增加肌酐、肌酐清除率。 Adropinin 显着（P<0.001）降低血清、肾脏中吲哚硫酸盐的水平，并降低尿液中吲哚硫酸盐的水平。 Adropinin 显着（P<0.001）降低总胆固醇、甘油三酯、低密度脂蛋白（LDL）、极低密度脂蛋白（VLDL）并增加高密度脂蛋白（HDL）水平。 Adropinin 显着 (P< 0.001) 增加抗氧化酶如谷胱甘肽 (GSH)、超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT) 的水平，并降低丙二醛 (MDA)、8-羟基-2ʹ-脱氧鸟苷 (8- OHdG）。 Adropinin 显着 (P< 0.001) 降低白细胞介素 1β (IL-1β)、白细胞介素 6 (IL-6)、转化生长因子 β (TGF-β) 水平，并增加白细胞介素 10 (IL-10) 水平）， 分别。 Adropinin 治疗显示肾脏组织病理学有所改善。

结论： Adropinin通过炎症和抗氧化途径对STZ诱导的糖尿病肾病大鼠发挥肾保护作用。