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首页> 外文期刊>Clinical and experimental pharmacology & physiology >Tropisetron ameliorates early diabetic nephropathy in streptozotocin-induced diabetic rats
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Tropisetron ameliorates early diabetic nephropathy in streptozotocin-induced diabetic rats

机译：Tropisetron可改善链脲佐菌素诱发的糖尿病大鼠的早期糖尿病肾病

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It has been well established that oxidative stress and inflammation are involved in the pathogenesis of diabetic nephropathy. It has been shown that tropisetron exerts anti-inflammatory and immunomodulatory properties. The current study was designed to investigate protective effects of tropisetron on early diabetic nephropathy in streptozotocin-induced diabetic rats. Rats were divided into six groups: (i) untreated diabetic (streptozotocin group); (ii) untreated control; (iii) diabetic rats treated with tropisetron (3 mg/kg); (iv) normal rats treated with tropisetron (3 mg/kg); (v) diabetic rats treated with granisetron (3 mg/kg); and (vi) normal rats treated with granisetron (3 mg/kg); rats began receiving treatment at the time of diabetes induction for 2 weeks. At the termination of the experiments, bodyweight, kidney index, urinary albumin excretion, and glomerular filtration rate were measured. The levels of oxidative stress markers and tumour necrosis factor-α were also determined. Streptozotocin-treated animals showed significant loss of bodyweight and renal enlargement and dysfunction. Diabetic rats also exhibited an increase in malondialdehyde along with a significant decrease in glutathione, superoxide dismutase activity, and catalase activity. Furthermore, the diabetic animals demonstrated a significant rise in renal cortical, urinary tumour necrosis factor-α, and urinary albumin excretion. Both granisetron and tropisetron decreased blood glucose in diabetic animals, but this decrease was not significant for granisetron. Treatment with tropisetron, but not granisetron, prevented increases in oxidative stress and tumour necrosis factor-α, decreased urinary cytokine excretion and albuminuria, and improved renal morphological damage. In conclusion, the present study suggests that tropisetron may be a protective agent in early diabetic nephropathy, and its action is mediated, at least in part, by anti-oxidative and anti-inflammatory mechanisms that appear to be independent of the 5-HT3 receptor.
机译：众所周知，氧化应激和炎症与糖尿病性肾病的发病机理有关。已经显示托吡司琼具有抗炎和免疫调节特性。当前的研究旨在研究托吡酯对链脲佐菌素诱发的糖尿病大鼠早期糖尿病肾病的保护作用。将大鼠分为六组：（i）未经治疗的糖尿病（链脲佐菌素组）; （ii）未经处理的对照; （iii）用托吡司琼（3 mg / kg）治疗的糖尿病大鼠; （iv）接受tropisetron（3 mg / kg）治疗的正常大鼠; （v）用格拉司琼（3 mg / kg）治疗的糖尿病大鼠; （vi）接受格拉司琼（3 mg / kg）治疗的正常大鼠;大鼠在诱导糖尿病时开始接受治疗2周。在实验结束时，测量体重，肾脏指数，尿白蛋白排泄和肾小球滤过率。还测定了氧化应激标志物和肿瘤坏死因子-α的水平。链脲佐菌素治疗的动物体重明显减轻，肾脏增大，功能障碍。糖尿病大鼠还表现出丙二醛增加，同时谷胱甘肽，超氧化物歧化酶活性和过氧化氢酶活性显着下降。此外，糖尿病动物表现出肾皮质，尿液肿瘤坏死因子-α和尿白蛋白排泄的显着增加。 Granisetron和tropisetron均可降低糖尿病动物的血糖，但对于Granisetron而言，降幅并不明显。用托吡司琼而不是格拉司琼治疗可以防止氧化应激和肿瘤坏死因子-α的增加，减少尿细胞因子排泄和蛋白尿，并改善肾脏的形态学损害。总之，本研究表明，托吡司琼可能是早期糖尿病肾病的一种保护剂，其作用至少部分地由似乎独立于5-HT3受体的抗氧化和抗炎机制介导。 。

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