Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2019
Embelin can protect mice from thioacetamide-induced acute liver injury.
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Wang Huafeng, Zhang Huan, Wang Yanxia, Yang Luhong, Wang Dong
Аннотация
BACKGROUND/AIMS: Embelin is an active component isolated from Embelia ribes Burm. In this study, we explored the protective effects of embelin on acute liver injury.
METHODS: An animal model of acute liver injury was established via administration of a single injection of thioacetamide (TAA) (300 μg/g body weight) to adult mice. Embelin was administered by intragastric gavage at 50 μg/g body weight starting 2 days before TAA administration and continuing throughout the study. Survival of the mice was analyzed by the Kaplan-Meier method using the log-rank test. The acute liver injury protocol was repeated and the remaining mice were analyzed at indicated times. Hematoxylin and eosin staining and picrosirius red staining were used to examine necrosis/inflammation and liver healing, respectively. Liver function was assessed by serum alanine aminotransferase/alkaline phosphatase activity. Hepatic cleaved caspase-3 and F4/80 expression levels were examined via immunostaining. Statistical analysis was performed with GraphPad Software.
RESULTS: The survival and liver function of the mice were markedly better in the group treated with embelin prior to TAA toxication than in the TAA toxication-only group. Embelin significantly reduced TAA-induced hepatic necrosis/apoptosis. Massive inflammatory cell infiltration, which is consistent with hepatic fibrogenesis (a healing process), occurred earlier in the embelin-treated recovery group than in the spontaneous recovery group. Moreover, macrophage activities increased more rapidly with embelin treatment.
CONCLUSIONS: In summary, embelin can protect against acute liver injury. Its therapeutic value warrants further exploration.
METHODS: An animal model of acute liver injury was established via administration of a single injection of thioacetamide (TAA) (300 μg/g body weight) to adult mice. Embelin was administered by intragastric gavage at 50 μg/g body weight starting 2 days before TAA administration and continuing throughout the study. Survival of the mice was analyzed by the Kaplan-Meier method using the log-rank test. The acute liver injury protocol was repeated and the remaining mice were analyzed at indicated times. Hematoxylin and eosin staining and picrosirius red staining were used to examine necrosis/inflammation and liver healing, respectively. Liver function was assessed by serum alanine aminotransferase/alkaline phosphatase activity. Hepatic cleaved caspase-3 and F4/80 expression levels were examined via immunostaining. Statistical analysis was performed with GraphPad Software.
RESULTS: The survival and liver function of the mice were markedly better in the group treated with embelin prior to TAA toxication than in the TAA toxication-only group. Embelin significantly reduced TAA-induced hepatic necrosis/apoptosis. Massive inflammatory cell infiltration, which is consistent with hepatic fibrogenesis (a healing process), occurred earlier in the embelin-treated recovery group than in the spontaneous recovery group. Moreover, macrophage activities increased more rapidly with embelin treatment.
CONCLUSIONS: In summary, embelin can protect against acute liver injury. Its therapeutic value warrants further exploration.