Frontiers in pharmacology · 2026
Dicaffeoylquinic acid alleviates alcoholic liver disease by targeting PLA2G4B and inhibiting the MAPK signaling pathway.
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Wang Linlin, Wang Hailong, Miao Yu, Hasimu Hamulati, Ji Tengfei, Huang Hua, Du Guanhua, Aisa Haji Akber, Xin Xuelei
Аннотация
INTRODUCTION: Alcoholic liver disease (ALD) is a serious global health burden with limited effective therapies. 4,5-Dicaffeoylquinic acid (DCA-C), a monomer from Artemisia scoparia, exhibits multiple bioactivities, but its protective effects and exact mechanisms against ALD remain unclear.
METHODS: Ethanol-induced ALD mouse models were treated with DCA-C at 10, 30, and 100 mg/kg. Liver injury, lipid accumulation, and inflammation were evaluated. Transcriptomic sequencing and molecular docking were used to identify key targets. PLA2G4B overexpression models in vitro and in vivo were constructed to validate the mechanism.
RESULTS: DCA-C dose-dependently alleviated alcoholic liver injury, with the 100 mg/kg dose being most effective, as shown by reduced serum ALT/AST, decreased hepatic triglycerides, and suppressed pro-inflammatory cytokines. PLA2G4B was identified as a core target of DCA-C. DCA-C directly bound PLA2G4B, downregulated its expression, and reduced arachidonic acid (AA) release, thereby inhibiting MAPK signaling (ERK, p38, JNK phosphorylation). PLA2G4B overexpression abolished the protective effects of DCA-C in vitro and in vivo.
DISCUSSION: DCA-C protects against ALD via targeting PLA2G4B and inhibiting the AA-MAPK pathway. DCA-C is a promising candidate for ALD treatment and warrants further development.
METHODS: Ethanol-induced ALD mouse models were treated with DCA-C at 10, 30, and 100 mg/kg. Liver injury, lipid accumulation, and inflammation were evaluated. Transcriptomic sequencing and molecular docking were used to identify key targets. PLA2G4B overexpression models in vitro and in vivo were constructed to validate the mechanism.
RESULTS: DCA-C dose-dependently alleviated alcoholic liver injury, with the 100 mg/kg dose being most effective, as shown by reduced serum ALT/AST, decreased hepatic triglycerides, and suppressed pro-inflammatory cytokines. PLA2G4B was identified as a core target of DCA-C. DCA-C directly bound PLA2G4B, downregulated its expression, and reduced arachidonic acid (AA) release, thereby inhibiting MAPK signaling (ERK, p38, JNK phosphorylation). PLA2G4B overexpression abolished the protective effects of DCA-C in vitro and in vivo.
DISCUSSION: DCA-C protects against ALD via targeting PLA2G4B and inhibiting the AA-MAPK pathway. DCA-C is a promising candidate for ALD treatment and warrants further development.