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希拉季特对5-氟尿嘧啶(5-FU)诱导的大鼠肾毒性的分子和细胞效应研究。

Investigation of the molecular and cellular effects of Shilajit on 5-fluorouracil (5-FU)-induced nephrotoxicity in rats.

作者信息

Ezer Mehmet, Öztürkler Melek, Yıldız-Dalgınlı Kezban, Atakişi Emine, Beşeren-Havadar Hatice, Atakişi Onur

机构信息

Kafkas University Medical School, Department of Urology, Kars, Türkiye.

Kafkas University Department of Chemistry, Faculty Science and Letter, Kars, Türkiye.

出版信息

Iran J Basic Med Sci. 2025;28(5):565-574. doi: 10.22038/ijbms.2025.80989.17525.

Abstract

OBJECTIVES

This study aimed to evaluate the protective effects of shilajit on 5-fluorouracil (5-FU)-induced nephrotoxicity in a rat model.

MATERIALS AND METHODS

Twenty male Sprague Dawley rats were divided into four groups: Control, 5-FU, shilajit, and 5-FU + shilajit. 5-FU was administered intraperitoneally at 200 mg/kg, while shilajit was given orally at 200 mg/kg. Kidney tissues were analyzed for oxidative stress markers, protein expression (SIRT2, SIRT3, β-catenin, E-cadherin, and caspase-3), and histopathological changes.

RESULTS

5-FU significantly increased oxidative stress parameters and kidney damage markers. Shilajit co-administration with 5-FU reduced oxidative stress and increased anti-oxidant status and SIRT2, SIRT3, and cell adhesion protein expression. Histopathological evaluation showed reduced renal damage in the shilajit + 5-FU group compared to the 5-FU group.

CONCLUSION

Shilajit exhibited significant protective effects against 5-FU-induced nephrotoxicity, improving oxidative parameters, protein expression, and kidney histopathology. Further studies are needed to elucidate its molecular mechanism and therapeutic potential.

摘要

目的

本研究旨在评估希拉季特对5-氟尿嘧啶(5-FU)诱导的大鼠肾毒性的保护作用。

材料与方法

将20只雄性Sprague Dawley大鼠分为四组:对照组、5-FU组、希拉季特组和5-FU+希拉季特组。5-FU以200mg/kg的剂量腹腔注射,而希拉季特以200mg/kg的剂量口服。分析肾组织的氧化应激标志物、蛋白表达(SIRT2、SIRT3、β-连环蛋白、E-钙黏蛋白和半胱天冬酶-3)以及组织病理学变化。

结果

5-FU显著增加氧化应激参数和肾损伤标志物。希拉季特与5-FU联合使用可降低氧化应激,提高抗氧化状态,并增加SIRT2、SIRT3和细胞黏附蛋白的表达。组织病理学评估显示,与5-FU组相比,希拉季特+5-FU组的肾损伤减轻。

结论

希拉季特对5-FU诱导的肾毒性具有显著的保护作用,可改善氧化参数、蛋白表达和肾脏组织病理学。需要进一步研究以阐明其分子机制和治疗潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb89/12258796/3d44dfef5601/IJBMS-28-565-g001.jpg

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