Objective To investigate the curative effect and possiblemechanism ofrifaximin treatment on monocrotaline-induced hepatic sinusoidal obstruction syndrome(HSOS)in mice.Methods Twenty-four male C57BL/6J mice were divide...Objective To investigate the curative effect and possiblemechanism ofrifaximin treatment on monocrotaline-induced hepatic sinusoidal obstruction syndrome(HSOS)in mice.Methods Twenty-four male C57BL/6J mice were divided into three groups and treatedwith solvent tcontrol,monocrotaline,and rifaximin,respectively.The histopathological changes of the liver and intestine were observed by hematoxylineosin staining.The differences were compared in liver parameters,serum liver enzymes,inflammatory factors,apoptotic factors,gut microbiota,and gut tight junction proteins among three groups of mice.The inter-group comparison was conducted using a t-test and one-way analysis of variance.Results The rifaximin-treated group had significantly improved liver histopathology.The serological levels of alanine aminotransferase and aspartate aminotransferase were(559.04±89.42)U/L and(676.90±106.25)U/L,respectively,which were significantly lower than those in the PA-HSOS model group[(846.05±148.46)U/L and(953.87±58.10)U/L,P<0.05],and were accompanied by lower levels of apoptotic cells and inflammatory factors.Additionally,the rifaximintreated mice group gut microbiota had higher diversity compared with the PA-HSOS group(P<0.05),and the Shannon index was 7.77±0.10 and 7.16±0.07,respectively,indicating apparent differences in microbiota among different groups.The abundance of Firmicutes in the rifaximin group was 39.58%±0.56%,which was significantly higher than that in the model group(24.25%±0.64%,P<0.05),while the abundance of Bacteroidetes was 54.7%±0.41%,which was significantly lower than that in the model group(70.92%±0.49%,P<0.05).Simultaneously,the expressions of gut tight junction proteins ZO-1 and Occludin showed an upward trend and validated transcription levels compared to the model group following rifaximin intervention(P<0.05).Conclusion Rifaximin can alleviate monocrotalineinduced hepatic sinusoidal obstruction syndrome in mice,and its mechanism may be via gut microbiota regulation,which in turn plays a role in improving intestinal barrier function.展开更多
文摘Objective To investigate the curative effect and possiblemechanism ofrifaximin treatment on monocrotaline-induced hepatic sinusoidal obstruction syndrome(HSOS)in mice.Methods Twenty-four male C57BL/6J mice were divided into three groups and treatedwith solvent tcontrol,monocrotaline,and rifaximin,respectively.The histopathological changes of the liver and intestine were observed by hematoxylineosin staining.The differences were compared in liver parameters,serum liver enzymes,inflammatory factors,apoptotic factors,gut microbiota,and gut tight junction proteins among three groups of mice.The inter-group comparison was conducted using a t-test and one-way analysis of variance.Results The rifaximin-treated group had significantly improved liver histopathology.The serological levels of alanine aminotransferase and aspartate aminotransferase were(559.04±89.42)U/L and(676.90±106.25)U/L,respectively,which were significantly lower than those in the PA-HSOS model group[(846.05±148.46)U/L and(953.87±58.10)U/L,P<0.05],and were accompanied by lower levels of apoptotic cells and inflammatory factors.Additionally,the rifaximintreated mice group gut microbiota had higher diversity compared with the PA-HSOS group(P<0.05),and the Shannon index was 7.77±0.10 and 7.16±0.07,respectively,indicating apparent differences in microbiota among different groups.The abundance of Firmicutes in the rifaximin group was 39.58%±0.56%,which was significantly higher than that in the model group(24.25%±0.64%,P<0.05),while the abundance of Bacteroidetes was 54.7%±0.41%,which was significantly lower than that in the model group(70.92%±0.49%,P<0.05).Simultaneously,the expressions of gut tight junction proteins ZO-1 and Occludin showed an upward trend and validated transcription levels compared to the model group following rifaximin intervention(P<0.05).Conclusion Rifaximin can alleviate monocrotalineinduced hepatic sinusoidal obstruction syndrome in mice,and its mechanism may be via gut microbiota regulation,which in turn plays a role in improving intestinal barrier function.
