Oncology Department, Faculty of Medicine, Van Yüzüncü Yıl University, Van, Turkey.
Eur Rev Med Pharmacol Sci. 2024 Feb;28(4):1327-1339. doi: 10.26355/eurrev_202402_35454.
The occurrence of nephrotoxicity and hepatotoxicity as a result of cisplatin administration is a major concern in clinical practice. This study examined the potential protective effects of administering mesenchymal stem cells (MSCs) on the renal and hepatic damage caused by cisplatin. Moreover, the study investigated the potential protective effects of administering Adipose-Derived Mesenchymal Stem Cells (ADMSC) to counteract the harmful effects of cisplatin-induced kidney and liver damage.
Male Sprague-Dawley rats were divided into three groups: normal control, cisplatin + saline, and cisplatin + ADMSC. Cisplatin was administered to induce toxicity, and ADMSC was administered intravenously as a potential therapeutic intervention. Biochemical parameters and histopathological changes were assessed in the kidney and liver tissues. Statistical analyses were performed using a one-way ANOVA.
Cisplatin increased malondialdehyde (MDA), tumor necrosis factor alfa (TNF-alfa), IL-6, alanine transaminase (ALT), creatinine, Galectin-3, Tissue growth factor beta 1 (TGF-beta 1), compared to the normal control group. Cisplatin-MSC reduced these levels. Histopathology showed that cisplatin caused kidney tubular epithelial necrosis, luminal necrotic debris, tubular dilatation, interstitial inflammation, liver sinusoidal and central vein dilatation, congestion, necrosis, and cytoplasmic vacuolization. ADMSC administration significantly reduced histopathological changes.
These findings highlight the potential therapeutic benefits of mesenchymal stem cell (MSC) administration in mitigating cisplatin-induced nephrotoxicity and hepatotoxicity. MSC treatment demonstrated protective effects by reducing oxidative stress, inflammatory markers, and histopathological alterations. Further investigations are warranted to elucidate the precise mechanisms underlying these protective effects and evaluate their clinical implications for managing cisplatin-induced organ damage.
顺铂给药导致的肾毒性和肝毒性是临床实践中的主要关注点。本研究探讨了给予间充质干细胞（MSCs）对顺铂引起的肾和肝损伤的潜在保护作用。此外，研究还探讨了给予脂肪来源间充质干细胞（ADMSC）以抵消顺铂诱导的肾和肝损伤的有害影响的潜在保护作用。
雄性 Sprague-Dawley 大鼠分为三组：正常对照组、顺铂+生理盐水组和顺铂+ADMSC 组。给予顺铂诱导毒性，静脉给予 ADMSC 作为潜在的治疗干预。评估肾和肝组织中的生化参数和组织病理学变化。使用单因素方差分析进行统计分析。
与正常对照组相比，顺铂增加了丙二醛（MDA）、肿瘤坏死因子α（TNF-α）、IL-6、丙氨酸转氨酶（ALT）、肌酐、半乳糖凝集素-3、组织生长因子β1（TGF-β1）。顺铂-MSC 降低了这些水平。组织病理学显示，顺铂引起肾小管上皮细胞坏死、管腔坏死碎片、管状扩张、间质炎症、肝窦和中央静脉扩张、充血、坏死和细胞质空泡化。ADMSC 给药显著减少了组织病理学变化。
这些发现强调了给予间充质干细胞（MSC）在减轻顺铂诱导的肾毒性和肝毒性方面的潜在治疗益处。MSC 治疗通过降低氧化应激、炎症标志物和组织病理学改变显示出保护作用。需要进一步研究阐明这些保护作用的精确机制，并评估其在管理顺铂诱导的器官损伤方面的临床意义。
