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This research investigates the protective effects of diallyl disulfide against liver damage caused by cisplatin chemotherapy.

June 4, 2026Journal of Umm Al-Qura University for Medical Sciences0 citationsOpen Access

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

NSNehad A. Shaer

Key Points

This research investigates the protective effects of diallyl disulfide against liver damage caused by cisplatin chemotherapy.
Rats were divided into control, DDS (10 mg/kg), CIS (7 mg/kg), and DDS + CIS groups.
Liver damage was assessed through serum ALT and AST levels, histopathology, and oxidative stress markers.
Cytokine levels, inflammasome activation, and signaling pathway phosphorylation were measured.
DDS reduced liver damage, evidenced by lower serum ALT and AST levels.
Histopathological analysis showed significant preservation of liver tissue architecture in DDS-treated groups.
DDS treatment decreased hepatic oxidative stress, restoring GSH levels and SOD activity while lowering MDA; it also suppressed TNF-α and IL-6 levels.

Abstract

Abstract 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.

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