Nobiletin ameliorates streptozotocin-cadmium-induced diabetic nephropathy via NF-κB signalling pathway in rats.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-02-01 Epub Date: 2021-08-04 DOI:10.1080/13813455.2021.1959617

Mingzhu Xu, Ruifang Wang, Hui Fan, Ziyuan Ni

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Abstract

This study sought to examine the anti-diabetic effect of nobiletin on streptozotocin (STZ)/cadmium (Cd)-induced diabetic nephrotoxic (DN) rats. The DN was induced using STZ (40 mg/kg b.w) intraperitoneally and Cd through drinking water for 12 weeks. The DN rats were treated with nobiletin of different concentrations (10, 20, and 40 mg/kg/BW). The STZ/Cd-induced DN leads to a significantly increased of the glucose levels, glycosylated haemoglobin, hepatic and kidney function markers, lipid peroxidation levels, and reduction of insulin levels, total haemoglobin, body weight, and antioxidant status markers. Our finding that nobiletin pathological impairment and diminished infiltration of neutrophil in kidney tubules and all biochemical enzymes were near normal levels in DN. More essentially, nobiletin strongly impedes the protein expression of renal nuclear NF-κB p65. Bax protein expression was significantly downregulated and elevated protein expression Bcl-2 was recorded in DN rats. These results show that nobiletin possesses antioxidant as well as anti-diabetic activities and thereby reduces chronic kidney diseases in rats.

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金雀花素能通过 NF-κB 信号通路改善链脲佐菌素-镉诱导的大鼠糖尿病肾病。

本研究旨在探讨金雀花素对链脲佐菌素（STZ）/镉（Cd）诱导的糖尿病肾毒性（DN）大鼠的抗糖尿病作用。使用 STZ（40 mg/kg b.w）腹腔诱导 DN 大鼠，并通过饮用水诱导 Cd，持续 12 周。用不同浓度（10、20 和 40 毫克/千克/体重）的金霉素治疗 DN 大鼠。STZ/Cd 诱导的 DN 会导致血糖水平、糖化血红蛋白、肝肾功能指标、脂质过氧化水平显著升高，而胰岛素水平、总血红蛋白、体重和抗氧化状态指标则会降低。我们的研究结果表明，金没药对肾小管的病理损伤和中性粒细胞浸润减少，所有生化酶都接近 DN 的正常水平。更重要的是，金没药能强烈抑制肾核 NF-κB p65 蛋白的表达。DN 大鼠的 Bax 蛋白表达明显下调，Bcl-2 蛋白表达升高。这些结果表明，金没药具有抗氧化和抗糖尿病活性，从而减少大鼠的慢性肾病。

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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.