Journal of ethnopharmacology · 2026
Rosavin mitigates hepatic fibrosis via KLF14-mediated suppression of P2X7 receptor-dependent inflammatory signaling cascades.
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Wang Wan-Ling, Xu Zi-Yi, Wang Ze-Hao, Guo Xin, Liu Xue-Kun, Song Jian
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Rhodiola crenulata (Hook. f. & Thomson) H. Ohba is a medicinal plant known for its prominent hepatoprotective and immunomodulatory properties. Rosavin (RSV), a phenylpropanoid glycoside isolated from its roots, exhibits regulatory effects on hepatic inflammation.
AIM OF THE STUDY: This study elucidates the hepatoprotective activity of RSV and its underlying mechanism in hepatic fibrosis.
MATERIALS AND METHODS: C57BL/6 mice were pretreated with thioacetamide (TAA) prior to RSV administration. RNA sequencing analyzed related signaling pathways. Hepatocyte inflammatory injury models were established by treating LX-2 with TGF-β, and HepG2 with TNF-α. Murine peritoneal macrophages (MPMs) were stimulated in vitro with LPS/ATP. To evaluate the functional role of Kruppel-like factor 14 (KLF14), siKLF14 was transfected into LX-2, HepG2, and MPMs. Dual-luciferase reporter assays verified the interaction between KLF14 and the P2X7r promoter.
RESULTS: RNA sequencing identified the NOD-like receptor/neutrophil extracellular traps (NETs) signaling pathway is essential for RSV-mediated hepatoprotection against TAA-induced liver injury in mice. RSV upregulated KLF14 expression while downregulating the P2X7r-NLRP3 pathway and its target genes. Silencing of KLF14 by siRNA markedly upregulated P2X7r expression at both mRNA and protein levels in mouse liver, thereby aggravating hepatic inflammatory responses. Deficiency of KLF14 in LX-2, HepG2, and MPMs impaired the inhibitory effect of RSV on the P2X7r-NLRP3 pathway. KLF14 might bind to the P2X7r promoter. Additionally, RSV reduced pyroptosis in MPMs, attenuating the inflammatory.
CONCLUSIONS: RSV attenuated the inflammatory response via the KLF14-P2X7r/NLRP3 pathway and inhibited fibrogenesis, suggesting RSV as a potential therapeutic agent for hepatic fibrosis.
AIM OF THE STUDY: This study elucidates the hepatoprotective activity of RSV and its underlying mechanism in hepatic fibrosis.
MATERIALS AND METHODS: C57BL/6 mice were pretreated with thioacetamide (TAA) prior to RSV administration. RNA sequencing analyzed related signaling pathways. Hepatocyte inflammatory injury models were established by treating LX-2 with TGF-β, and HepG2 with TNF-α. Murine peritoneal macrophages (MPMs) were stimulated in vitro with LPS/ATP. To evaluate the functional role of Kruppel-like factor 14 (KLF14), siKLF14 was transfected into LX-2, HepG2, and MPMs. Dual-luciferase reporter assays verified the interaction between KLF14 and the P2X7r promoter.
RESULTS: RNA sequencing identified the NOD-like receptor/neutrophil extracellular traps (NETs) signaling pathway is essential for RSV-mediated hepatoprotection against TAA-induced liver injury in mice. RSV upregulated KLF14 expression while downregulating the P2X7r-NLRP3 pathway and its target genes. Silencing of KLF14 by siRNA markedly upregulated P2X7r expression at both mRNA and protein levels in mouse liver, thereby aggravating hepatic inflammatory responses. Deficiency of KLF14 in LX-2, HepG2, and MPMs impaired the inhibitory effect of RSV on the P2X7r-NLRP3 pathway. KLF14 might bind to the P2X7r promoter. Additionally, RSV reduced pyroptosis in MPMs, attenuating the inflammatory.
CONCLUSIONS: RSV attenuated the inflammatory response via the KLF14-P2X7r/NLRP3 pathway and inhibited fibrogenesis, suggesting RSV as a potential therapeutic agent for hepatic fibrosis.