Berberine ameliorates intestinal injury in sepsis by regulating Nrf2/HO-1 pathway
AIM To explore the effects of berberine on intestinal injury in sepsis rats and its mechanism.METHODS Forty male healthy SD rats were randomly divided into sham group,model group,berberine low,medium,and high dose(25,50,100 mg·kg-1)groups,with 8 rats in each group,and the corresponding dose was given by gavage for 7 d.Sepsis model was prepared by cecum ligation and perforation(CLP).After 24 h of modeling,the rats were anesthetized and the ileum specimens were collected.The pathological changes of the ileum were observed and scored under light microscope.The contents of serum heme oxygenase-1(HO-1),diamine oxidase(DAO),intestinal fatty acid binding protein(iFABP),tumor necrosis factor-α(TNF-α),interleukin(IL)-6 and IL-1β were detected by ELISA.The content of malondialdehyde(MDA)and the activity of superoxide dismutase(SOD)in ileum were detected by colorimetric analysis.The protein levels of HO-1,nuclear factor E2-related factor 2(Nrf2)and IL-1β in ileum were detected by Western blot.RESULTS Compared with the sham group,ileum histopathological score was significantly increased in the model group(P＜0.01),and contents of HO-1,IL-1β,IL-6,TNF-α,DAO,iFABP in serum,and MDA in intestinal tissue were increased,while SOD activity was decreased,and the expressions of Nrf2,HO-1 and IL-1β protein in the model group were significantly increased(P＜0.01).Compared with the model group,the ileum histopathologic score of the berberine high dose group was significantly decreased(P＜0.01),the contents of IL-1β,IL-6,TNF-α,DAO,iFABP in serum and MDA in intestinal tissue were also decreased(P＜0.05),while the HO-1 content in serum and SOD activity in intestinal tissue were increased(P＜0.01),and the protein expressions of Nrf2 and HO-1 in the berberine high dose group were significantly increased,but the IL-1β protein expression was decreased(P＜0.05).CONCLUSION Berberine can effectively improve intestinal damage caused by sepsis,and its mechanism may be related to the up-regulation of Nrf2/HO-1 expression.
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