Swertiamarin mitigates nephropathy in high-fat diet/streptozotocin-induced diabetic rats by inhibiting the formation of advanced glycation end products.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-04-01 Epub Date: 2021-10-16 DOI:10.1080/13813455.2021.1987478

Kirti Parwani, Farhin Patel, Pranav Bhagwat, Haritha Dilip, Dhara Patel, Vijay Thiruvenkatam, Palash Mandal

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Abstract

Context: The molecular mechanism by which Swertiamarin (SM) prevents advanced glycation end products (AGEs) induced diabetic nephropathy (DN) has never been explored.

Objective: To evaluate the effect of SM in preventing the progression of DN in high fat diet-streptozotocin-induced diabetic rats.

Materials and methods: After 1 week of acclimatisation, the rats were divided randomly into five groups as follows: (1) Control group, which received normal chow diet; (2) High-fat diet (HFD) group which was fed diet comprising of 58.7% fat, 27.5% carbohydrate and 14.4% protein); (3) Aminoguanidine (AG) group which received HFD + 100 mg/k.b.w.AG (intraperitoneal); (4) Metformin (Met) group which received HFD + 70 mg/k.b.w. the oral dose of Met and (5) SM group which was supplemented orally with 50 mg/k.b.w.SM along with HFD. After 12 weeks all HFD fed animals were given a single 35 mg/k.b.w. dose of streptozotocin with continuous HFD feeding for additional 18 weeks. Later, various biochemical assays, urine analyses, histopathological analysis of kidneys, levels of AGEs, expression of various makers, and in-silico analysis were performed.

Results: The diabetic group demonstrated oxidative stress, increased levels of AGEs, decreased renal function, fibrosis in the renal tissue, higher expression of the receptor for advanced glycation end products (RAGE), which were ameliorated in the SM treated group. In-silico analysis suggests that SM can prevent the binding of AGEs with RAGE.

Conclusions: SM ameliorated DN by inhibiting the oxidative stress induced by AGEs.HighlightsSM reduces the levels of hyperglycaemia-induced advanced glycation end products in serum and renal tissue.SM prevents renal fibrosis by inhibiting the EMT in the kidney tissue.The in-silico analysis proves that SM can inhibit the binding of various AGEs with RAGE, thereby inhibiting the AGE-RAGE axis.

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獐牙菜苷通过抑制高级糖化终产物的形成，减轻高脂饮食/链脲佐菌素诱导的糖尿病大鼠的肾病。

背景：Swertiamarin (SM) 预防高级糖化终产物（AGEs）诱导的糖尿病肾病（DN）的分子机制尚未探明：目的：评估獐牙菜素在预防高脂饮食-链脲佐菌素诱导的糖尿病大鼠DN进展方面的作用：经过 1 周的适应性训练后，将大鼠随机分为以下 5 组：(1) 对照组，摄入正常饲料；(2) 高脂饮食（HFD）组，摄入含 58.7% 脂肪、27.5% 碳水化合物和 14.4% 蛋白质的食物；(3) 氨基胍（AG）组，摄入 HFD + 100 mg/k.b.w.AG（经腹腔注射）。b.w.AG（腹腔注射）；(4) 二甲双胍（Met）组：HFD + 70 mg/k.b.w. 的口服二甲双胍剂量；(5) SM 组：在喂食 HFD 的同时口服 50 mg/k.b.w.SM 补充剂。12 周后，所有以高密度脂蛋白喂养的动物都要接受单次 35 mg/k.b.w. 剂量的链脲佐菌素治疗，并持续喂养高密度脂蛋白 18 周。随后，对动物进行了各种生化检测、尿液分析、肾脏组织病理学分析、AGEs水平、各种造物主的表达以及分子内分析：结果：糖尿病组表现出氧化应激、AGEs水平升高、肾功能下降、肾组织纤维化、高级糖化终产物受体（RAGE）表达升高，而这些症状在SM治疗组中得到了改善。室内分析表明，SM能阻止AGEs与RAGE结合：SM通过抑制AGEs诱导的氧化应激改善了DN，亮点SM降低了血清和肾组织中由高血糖诱导的高级糖化终产物的水平，SM通过抑制肾组织的EMT防止了肾纤维化。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.

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