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水解产物通过减轻氧化应激、炎症和细胞凋亡对顺铂诱导的肾毒性的改善作用。

Ameliorative Effect of Hydrolysate on Cisplatin-Induced Nephrotoxicity by Mitigating Oxidative Stress, Inflammation and Apoptosis.

作者信息

Tao Susu, Qi Yi, Gao Jialong, Yuan Huafang, Wang Ruimin, Shen Xiaoqin, Wei Gang, Peng Zhilan

机构信息

School of Ocean and Tropical Medicine, Guangdong Medical University, Zhanjiang 524023, China.

College of Food Science & Technology, Guangdong Provincial Key Laboratory of Aquatic Products Processing and Safety, Zhanjiang 524088, China.

出版信息

Mar Drugs. 2025 Feb 24;23(3):100. doi: 10.3390/md23030100.

DOI:10.3390/md23030100
PMID:40137286
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11943811/
Abstract

The present study investigated the protective effects and possible mechanisms of an ultrafiltration fraction of hydrolysate (UFSH) on cisplatin-induced kidney damage in a mouse model. The results showed that UFSH significantly attenuated cisplatin-induced nephrotoxicity by inhibiting increases in blood urea nitrogen (BUN) and serum creatinine (SCr). Additionally, UFSH treatment significantly alleviated cisplatin-induced renal histopathological changes, such as significant dilation of renal tubules, cast formation, and tubular cell necrosis, as well as tubulointerstitial fibrosis. Moreover, UFSH decreased cisplatin-induced oxidative stress by increasing the activities of antioxidant enzymes SOD and GSH-Px, while reducing the malondialdehyde (MDA) level in the kidney. Furthermore, UFSH significantly inhibited cisplatin-induced increases in inflammatory cytokines, including Interleukin 1-beta (IL-1β), Interleukin-6 (IL-6), and Tumor necrosis factor-alpha (TNF-α). Western blotting revealed that UFSH inhibited the phosphorylation of the inflammation-associated MAPK/NF-κB signaling pathway, lowered the expression of the apoptosis-related protein Bax, and reversed the reduction in the anti-apoptotic Bcl-2 protein. This investigation demonstrated that UFSH can ameliorate cisplatin-induced nephrotoxicity by mitigating oxidative stress, inflammation, and apoptosis.

摘要

本研究在小鼠模型中探究了水解产物超滤组分(UFSH)对顺铂诱导的肾损伤的保护作用及可能机制。结果显示,UFSH通过抑制血尿素氮(BUN)和血清肌酐(SCr)升高,显著减轻了顺铂诱导的肾毒性。此外,UFSH治疗显著减轻了顺铂诱导的肾脏组织病理学变化,如肾小管显著扩张、管型形成、肾小管细胞坏死以及肾小管间质纤维化。而且,UFSH通过提高抗氧化酶超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性,同时降低肾脏中丙二醛(MDA)水平,减少了顺铂诱导的氧化应激。此外,UFSH显著抑制了顺铂诱导的炎性细胞因子升高,包括白细胞介素1-β(IL-1β)、白细胞介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)。蛋白质免疫印迹法显示,UFSH抑制了炎症相关的丝裂原活化蛋白激酶/核因子-κB(MAPK/NF-κB)信号通路的磷酸化,降低了凋亡相关蛋白Bax的表达,并逆转了抗凋亡蛋白Bcl-2的减少。本研究表明,UFSH可通过减轻氧化应激、炎症和凋亡来改善顺铂诱导的肾毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/3e87fb38d473/marinedrugs-23-00100-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/bf8f55cb13b4/marinedrugs-23-00100-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/8cd641ab1582/marinedrugs-23-00100-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/1ecc5b6e48ea/marinedrugs-23-00100-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/60aba713b088/marinedrugs-23-00100-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/7c909ead62af/marinedrugs-23-00100-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/7b5569f89a46/marinedrugs-23-00100-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/66ff263565f7/marinedrugs-23-00100-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/82716ecfcab2/marinedrugs-23-00100-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/fea72d446a9c/marinedrugs-23-00100-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/29c590fc7808/marinedrugs-23-00100-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/3e87fb38d473/marinedrugs-23-00100-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/bf8f55cb13b4/marinedrugs-23-00100-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/8cd641ab1582/marinedrugs-23-00100-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/1ecc5b6e48ea/marinedrugs-23-00100-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/60aba713b088/marinedrugs-23-00100-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/7c909ead62af/marinedrugs-23-00100-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/7b5569f89a46/marinedrugs-23-00100-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/66ff263565f7/marinedrugs-23-00100-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/82716ecfcab2/marinedrugs-23-00100-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/fea72d446a9c/marinedrugs-23-00100-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/29c590fc7808/marinedrugs-23-00100-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3290/11943811/3e87fb38d473/marinedrugs-23-00100-g011.jpg

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