Cilostazol attenuates mirabegron-induced hepatic and renal toxicity in rats: regulation of metabolic, oxidative, and inflammatory pathways.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2024-08-07 DOI:10.1080/13813455.2024.2387700

Mai M Anwar, Ibrahim M Ibrahim Laila

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引用次数: 0

Abstract

Background: Mirabegron (MIRG) is a type of β3 adrenoceptor agonist that is considered an alternative therapy for the treatment of overactive bladder (OAB) symptoms. Cilostazol (CITZ) is a selective inhibitor of phosphodiesterase (III) that has various pharmacological effects.

Objectve: The current study aimed to highlight the regulatory effects of CITZ on MIRG-induced toxicity.

Materials and methods: Male rats were divided into six groups. Blood samples were collected to determine different hepatic and kidney function levels along with serum protein electrophoresis and inflammatory factor levels. Histopathological studies and oxidative stress (OS) were also assessed. Kidney and hepatic damage were detected following the administration of MIRG, especially at high doses, due to elevated OS, inflammation, and apoptotic marker levels.

Results: Rats receiving CITZ exhibited significant improvements in both hepatic and kidney functions, with decreased inflammation and OS.

Conclusion: CITZ administration plays a beneficial role in alleviating hepatic and nephrotoxicity induced by MIRG by inhibiting OS and inflammation.

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西洛他唑减轻米拉贝琼诱导的大鼠肝肾毒性：调节代谢、氧化和炎症途径

背景：米拉贝琼（MIRG）是一种β3肾上腺素受体激动剂，被认为是治疗膀胱过度活动症（OAB）症状的替代疗法。西洛他唑（CITZ）是磷酸二酯酶（III）的选择性抑制剂，具有多种药理作用：本研究旨在强调 CITZ 对 MIRG 诱导的毒性的调节作用：雄性大鼠分为六组。收集血样以测定不同的肝肾功能水平、血清蛋白电泳和炎症因子水平。还对组织病理学研究和氧化应激（OS）进行了评估。由于OS、炎症和细胞凋亡标志物水平升高，在服用MIRG（尤其是高剂量时）后发现了肾脏和肝脏损伤：结果：接受 CITZ 治疗的大鼠肝脏和肾脏功能均有明显改善，炎症和 OS 均有所下降：结论：通过抑制OS和炎症，服用CITZ对减轻MIRG引起的肝肾毒性有益。

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.