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首页> 外文期刊>RSC Advances >Tropisetron modulates peripheral and central serotonin/insulin levels via insulin and nuclear factor kappa B/receptor for advanced glycation end products signalling to regulate type-2 diabetes in rats
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Tropisetron modulates peripheral and central serotonin/insulin levels via insulin and nuclear factor kappa B/receptor for advanced glycation end products signalling to regulate type-2 diabetes in rats

机译：Tropisetron通过胰岛素和核因子kappa B /受体调节外周和中枢血清素/胰岛素水平，从而为晚期糖基化终产物提供信号，从而调节大鼠的2型糖尿病

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Despite its known central effect, 5% of serotonin is found centrally, while around 95% is found peripherally. Serotonin is stored and co-released with insulin upon pancreatic islets stimulation by glucose. This fact raises the curiosity regarding its possible role in diabetes. Hence, in this study, we assessed the possible modulatory effects of tropisetron, a 5-HT3 receptor antagonist, on type 2 diabetes mellitus models in rats. The rats were allocated into two groups: normal and diabetic. The latter group was treated with metformin (500 mg kg ~(?1) , p.o.), tropisetron (1 and 2 mg kg ~(?1) , i.p.), and a combination of metformin and tropisetron (1 mg kg ~(?1) ). The different treatment regimens corrected glucose and lipid homeostasis manifested by the decrease in serum levels of glucose, fructosamine, homeostasis model of insulin resistance, triglycerides, total cholesterol, free fatty acid, as well as receptor for advanced glycation end products. Additionally, the treatments elevated levels of insulin, serotonin, and homeostasis model of β-cell function. On the molecular level, treatments corrected the altered insulin signaling cascade (phosphorylated insulin receptor substrate 1, phosphorylated protein kinase B, and glucose transporter 4), and inhibited β-catenin and phosphorylated nuclear factor kappa B p65 in the assessed soleus skeletal muscle. A similar pattern was duplicated in the hippocampus. This study provided evidence for the role of tropisetron on type 2 diabetes mellitus via modulating the insulin signaling cascade (insulin, phosphorylated insulin receptor substrate 1, phosphorylated protein kinase B, and glucose transporter 4), improving lipid/glucose profile, decreasing inflammatory markers (receptor for advanced glycation end products, and phosphorylated nuclear factor kappa B p65), as well as increasing 5-HT and reducing β-catenin.
机译：尽管已知其中心作用，但在中央发现了5％的血清素，而在外周发现了约95％的血清素。血清胰岛素在葡萄糖刺激胰岛后与胰岛素共同储存和释放。这一事实引起了人们对其在糖尿病中可能作用的好奇。因此，在这项研究中，我们评估了5-HT3受体拮抗剂tropisetron对大鼠2型糖尿病模型的可能调节作用。将大鼠分为两组：正常组和糖尿病组。后者用二甲双胍（500 mg kg〜（？1），口服），托吡司琼（1和2 mg kg〜（？1），ip）以及二甲双胍和tropisetron（1 mg kg〜（？ 1））。不同的治疗方案纠正了葡萄糖和脂质体内稳态，表现为血清葡萄糖，果糖胺，胰岛素抵抗体内稳态模型，甘油三酸酯，总胆固醇，游离脂肪酸以及晚期糖基化终末产物受体的水平降低。另外，治疗增加了胰岛素，血清素和β细胞功能稳态模型的水平。在分子水平上，治疗纠正了评估的比目鱼骨骼肌中改变的胰岛素信号传导级联（磷酸化的胰岛素受体底物1，磷酸化的蛋白激酶B和葡萄糖转运蛋白4），并抑制了β-catenin和磷酸化的核因子κBp65。在海马中复制了相似的模式。这项研究通过调节胰岛素信号传导级联（胰岛素，磷酸化的胰岛素受体底物1，磷酸化的蛋白激酶B和葡萄糖转运蛋白4），改善脂质/葡萄糖谱，降低炎症标志物，提供了托吡司琼在2型糖尿病中的作用的证据。晚期糖基化终产物的受体，磷酸化的核因子κB p65），以及增加5-HT和减少β-catenin。

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