Ameliorative Effect of <i>Sipunculus nudus</i> Hydrolysate on Cisplatin-Induced Nephrotoxicity by Mitigating Oxidative Stress, Inflammation and Apoptosis

Ameliorative Effect of <i>Sipunculus nudus</i> Hydrolysate on Cisplatin-Induced Nephrotoxicity by Mitigating Oxidative Stress, Inflammation and Apoptosis

The present study investigated the protective effects and possible mechanisms of an ultrafiltration fraction of <i>Sipunculus nudus</i> hydrolysate (UFSH) on cisplatin-induced kidney damage in a mouse model. The results showed that UFSH significantly attenuated cisplatin-induced nephroto...

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Bibliographic Details
Main Authors: Susu Tao, Yi Qi, Jialong Gao, Huafang Yuan, Ruimin Wang, Xiaoqin Shen, Gang Wei, Zhilan Peng
Format: Article
Language:English
Published: MDPI AG 2025-02-01
Series:Marine Drugs
Subjects:
<i>Sipunculus nudus</i>
cisplatin
nephrotoxicity
hydrolysate
oxidative stress
inflammation
Online Access:https://www.mdpi.com/1660-3397/23/3/100
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Summary:The present study investigated the protective effects and possible mechanisms of an ultrafiltration fraction of <i>Sipunculus nudus</i> 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.
ISSN:1660-3397

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