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Exploration of the protective mechanisms of Icariin against cisplatin-induced renal cell damage in canines

文献类型： 外文期刊

作者： Liu, Jiayi 1 ; Xie, Liuwei 1 ; Zhai, He 1 ; Wang, Dongwei 1 ; Li, Xiao 2 ; Wang, Yao 1 ; Song, Mingqiang 1 ; Xu, Chao 2 ;

作者机构： 1.Criminal Invest Police Univ China, Coll Police Dog Technol, Shenyang, Peoples R China

2.Chinese Acad Agr Sci, Inst Special Wild Econ Anim & Plants, Changchun, Peoples R China

关键词： Icariin; cisplatin; MDCK cells; apoptosis of cells; protection effect

期刊名称：FRONTIERS IN VETERINARY SCIENCE （ 影响因子：3.2； 五年影响因子：3.5 ）

ISSN：

年卷期： 2024 年 11 卷

页码：

收录情况： SCI

摘要： This study delves into the protective mechanisms of Icariin (ICA) against cisplatin-induced damage in Madin-Darby canine kidney (MDCK) cells. Comprising two distinct phases, the investigation initially employed a single-factor randomized design to ascertain the minimal cisplatin concentration eliciting MDCK cell damage, spanning concentrations from 0 to 16 mmol/L. Concurrently, various concentrations of ICA (ranging from 5 to 50 mmol/L) were combined with 1 mmol/L cisplatin to determine the most efficacious treatment concentration. Subsequent investigations utilized four treatment groups: control, 1 mmol/L cisplatin, 1 mmol/L cisplatin + 20 mmol/L ICA, and 1 mmol/L cisplatin + 25 mmol/L ICA, aimed at elucidating ICA's protective mechanisms. Findings from the initial phase underscored a significant reduction in MDCK cell viability with 1 mmol/L cisplatin in comparison to the control (P < 0.01). Notably, the inclusion of 20 and 25 mmol/L ICA substantively ameliorated MDCK cell viability under 1 mmol/L cisplatin (P < 0.01). Moreover, cisplatin administration induced an elevation in inflammatory factors, malondialdehyde (MDA), reactive oxygen species (ROS), and Bax protein levels, while concurrently suppressing superoxide dismutase (SOD), catalase (CAT), and Bcl-2 expression (P < 0.01). Conversely, supplementation of 20 and 25 mmol/L ICA demonstrated a marked increase in mitochondrial membrane potential and levels of SOD, CAT, and Bcl-2 (P < 0.01). These interventions effectively attenuated inflammatory responses and suppressed Bax protein expression (P < 0.05), consequently mitigating cisplatin-induced apoptosis in MDCK cells (P < 0.01). In summary, these findings elucidate the role of ICA in impeding apoptosis in cisplatin-induced MDCK cells by regulating inflammatory responses, oxidative stress, and autophagic protein expression.

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