Immunopharmacology and immunotoxicology · 2025
Moscatilin protects concanavalin A-induced autoimmune liver disease in mice.
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Zhang Ying, Wang Jiafeng, Liu Furui, Liu Qiao, He Jinqiao
Аннотация
BACKGROUND: Moscatilin has been shown to effectively suppress inflammation in macrophages in mice treated with concanavalin A (ConA). However, further investigation is needed to fully elucidate the specific underlying mechanisms.
METHODS: A murine model of autoimmune liver disease was induced by administering ConA. Inflammatory markers were quantified using enzyme-linked immunosorbent assay (ELISA), while M1 and M2 macrophage biomarkers were analyzed by western blotting. Apoptosis was assessed via TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, and immunohistochemical staining was used to identify macrophage surface biomarkers.
RESULTS: Moscatilin significantly reduced ConA-induced liver injury, as evidenced by decreased levels of alanine aminotransferase (ALT) and aspartate transaminase (AST), leading to improved survival in mice. Subsequent experiments confirmed that moscatilin inhibited cell apoptosis by downregulating cleaved caspase-3 and Bax. Additionally, it exhibited anti-inflammatory effects by modulating levels of interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α), while promoting the expression of interleukin 10 (IL-10). Moreover, moscatilin influenced M1/M2 macrophage polarization by downregulating CD86 and inducible nitric oxide synthase (iNOS), and upregulating arginase 1 (Arg1) and CD206. Our findings suggest that moscatilin alleviates ConA-induced liver injury by inhibiting apoptosis and promoting M1/M2 macrophage polarization.
CONCLUSIONS: These results provide valuable insights into the potential therapeutic applications of moscatilin in autoimmune liver diseases.
METHODS: A murine model of autoimmune liver disease was induced by administering ConA. Inflammatory markers were quantified using enzyme-linked immunosorbent assay (ELISA), while M1 and M2 macrophage biomarkers were analyzed by western blotting. Apoptosis was assessed via TdT-mediated dUTP Nick-End Labeling (TUNEL) staining, and immunohistochemical staining was used to identify macrophage surface biomarkers.
RESULTS: Moscatilin significantly reduced ConA-induced liver injury, as evidenced by decreased levels of alanine aminotransferase (ALT) and aspartate transaminase (AST), leading to improved survival in mice. Subsequent experiments confirmed that moscatilin inhibited cell apoptosis by downregulating cleaved caspase-3 and Bax. Additionally, it exhibited anti-inflammatory effects by modulating levels of interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α), while promoting the expression of interleukin 10 (IL-10). Moreover, moscatilin influenced M1/M2 macrophage polarization by downregulating CD86 and inducible nitric oxide synthase (iNOS), and upregulating arginase 1 (Arg1) and CD206. Our findings suggest that moscatilin alleviates ConA-induced liver injury by inhibiting apoptosis and promoting M1/M2 macrophage polarization.
CONCLUSIONS: These results provide valuable insights into the potential therapeutic applications of moscatilin in autoimmune liver diseases.