急性肾损伤
脂质过氧化
血尿素氮
顺铂
肾
免疫印迹
药理学
肌酐
肾毒性
化学
医学
氧化应激
生物化学
内科学
化疗
基因
作者
Zeyu Song,Zhenyuan Li,Tao Pan,Teng Liu,Baifang Gong,Zhixia Wang,Kebin Liu,Huaying Fan
摘要
Abstract Objectives Acute kidney injury (AKI) caused by cisplatin (CDDP) is a complex, critical illness with no effective or specific treatment. The purpose of the study was to assess the protective effect of protopanaxadiol (PPD) on the kidneys in CDDP-induced AKI models and its possible mechanisms. Methods In vitro, the protection of PPD was assessed in HK-2. KM mice were injected with CDDP to induce AKI models in vivo. The determination of blood urea nitrogen and serum creatinine (SCr) was performed, and pathological changes were examined by histopathological examination. Immunostaining and western blot analyses were used to analyze the expression levels of proteins. Results PPD can increase the viability of HK-2 cells damaged by CDDP, improve cell morphology, and alleviate the symptoms of AKI in mice. In addition, PPD can down-regulate the protein expression of TRF and up-regulate the protein expression of Ferritin heavy chain, Glutathione peroxidase 4, and ferroptosis suppressor protein 1 reduce the iron content in cells and kidney tissues, and restore the antioxidant defense system. Conclusion PPD has an inhibitory effect on cisplatin-induced nephrotoxicity, which may be related to the inhibition of ferroptosis by regulating iron metabolism and lipid peroxidation.
科研通智能强力驱动
Strongly Powered by AbleSci AI