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Background <p>Cisplatin (CIS), a broadly used chemotherapy, is linked with hepatotoxicity caused by oxidative injury and inflammation. The current study explores the hepato-protective effects of diallyl disulfide (DDS), a natural organosulfur compound, against CIS-induced hepatotoxicity.</p> Method <p>In this investigation, rats were allocated to control, DDS (10&#xa0;mg/kg), CIS (7&#xa0;mg/kg), and DDS + CIS groups.</p> Results <p>DDS reduces liver damage caused by CIS, as shown by lowering serum ALT and AST. Histopathological evaluations revealed significant liver tissue architecture preservation in DDS-treated groups. DDS treatment ameliorates hepatic oxidative stress induced by CIS and significantly restores GSH levels and SOD activity, while it notably reduces MDA levels. Also, cytokines (TNF-α and IL-6) were markedly suppressed by DDS. Significantly, DDS inhibited NLRP3 inflammasome activation, p38 MAPK, and ERK1/2 phosphorylation, as well as VCAM-1 expression, reducing associated effects of inflammation.</p> Conclusions <p>These findings highlight that DDS alleviates CIS-induced liver toxicity by mitigating oxidative injury and inflammation, suggesting it is a promising intervention for chemotherapy-associated liver injury.</p>

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Diallyl disulfide prevents cisplatin-induced hepatotoxicity by regulating p38 MAPK, ERK1/2, NLRP3, and VCAM-1 signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月2日

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  • Nehad A. Shaer

摘要

Background

Cisplatin (CIS), a broadly used chemotherapy, is linked with hepatotoxicity caused by oxidative injury and inflammation. The current study explores the hepato-protective effects of diallyl disulfide (DDS), a natural organosulfur compound, against CIS-induced hepatotoxicity.

Method

In this investigation, rats were allocated to control, DDS (10 mg/kg), CIS (7 mg/kg), and DDS + CIS groups.

Results

DDS reduces liver damage caused by CIS, as shown by lowering serum ALT and AST. Histopathological evaluations revealed significant liver tissue architecture preservation in DDS-treated groups. DDS treatment ameliorates hepatic oxidative stress induced by CIS and significantly restores GSH levels and SOD activity, while it notably reduces MDA levels. Also, cytokines (TNF-α and IL-6) were markedly suppressed by DDS. Significantly, DDS inhibited NLRP3 inflammasome activation, p38 MAPK, and ERK1/2 phosphorylation, as well as VCAM-1 expression, reducing associated effects of inflammation.

Conclusions

These findings highlight that DDS alleviates CIS-induced liver toxicity by mitigating oxidative injury and inflammation, suggesting it is a promising intervention for chemotherapy-associated liver injury.