Menthol ameliorates thioacetamide-induced renal fibrosis in rats by upregulating SIRT1/Nrf2 and downregulating TGF-β1/Smad3 signalling pathways.

IF 2.7 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2025-09-02 DOI:10.1080/13813455.2025.2554677

Elaheh Babaei, Masoumeh Asle-Rousta, Sanaz Mahmazi

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引用次数: 0

Abstract

Introduction: Renal fibrosis is a significant factor in the progression of chronic kidney disease. This study examined how menthol affects thioacetamide (TA)-induced biochemical, molecular, and histopathological damage that leads to renal fibrosis and dysfunction.

Methods: Male Wistar rats were treated with TA (200 mg/kg, intraperitoneally) twice a week for four consecutive weeks, along with menthol (10 mg/kg, intraperitoneally) for the same duration.

Results: Menthol effectively reduced oxidative stress and inflammation in the kidneys of rats treated with TA. It also lowered the expression of TGF-β1, SMAD3, α-SMA, and KIM-1. Furthermore, menthol prevented the decline in SIRT1 mRNA expression and protein levels while increasing the expression of Nrf2. It inhibited collagen deposition and histological damage in the kidneys and prevented the rise in serum creatinine and BUN levels.

Conclusion: Menthol provides protective effects against renal fibrosis induced by thioacetamide. Its antifibrotic effects are mediated by upregulating SIRT1/Nrf2 and downregulating TGF-β1/Smad3 pathways.

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薄荷醇通过上调SIRT1/Nrf2和下调TGF-β1/Smad3信号通路改善硫代乙酰胺诱导的大鼠肾纤维化。

肾纤维化是慢性肾脏疾病进展的重要因素。本研究探讨了薄荷醇如何影响硫代乙酰胺（TA）诱导的生化、分子和组织病理学损伤，从而导致肾纤维化和功能障碍。方法：雄性Wistar大鼠给予TA （200 mg/kg，腹腔注射），每周2次，连续4周，同时给予薄荷醇（10 mg/kg，腹腔注射）相同时间。结果：薄荷醇能有效地减轻TA大鼠肾脏氧化应激和炎症反应。降低TGF-β1、SMAD3、α-SMA、KIM-1的表达。此外，薄荷醇可以阻止SIRT1 mRNA表达和蛋白水平的下降，同时增加Nrf2的表达。它抑制胶原沉积和肾脏组织损伤，防止血清肌酐和BUN水平升高。结论：薄荷醇对硫乙酰胺致肾纤维化有保护作用。其抗纤维化作用是通过上调SIRT1/Nrf2和下调TGF-β1/Smad3通路介导的。

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.