Objective To understand the effect of astaxanthin on intestinal injury of septic mice,and explore the mechanism.Methods Septic mice model was constructed by cecum ligation and puncture(CLP).Sixty-two male Balb/c mice were randomly divided into 4 groups by random number method:Sham surgery+solvent control group(Sham+Vehi group,n=11),Sham surgery+astaxanthin group(Sham+Asta group,n=11),sepsis model+sol-vent control group(CLP+Vehi group,n=20),and sepsis model+astaxanthin group(CLP+Asta group,n=20).In astaxanthin-containing groups,astaxanthin was dissolved in edible olive oil(40 mg/mL),and 100 mg/(kg·d)was gavaged for 7 days before surgery.In solvent-containing groups,the solvent was treated with an equal amount of olive oil by gavage(2.5 mL/kg).Five mice from the Sham groups and 12 mice from the CLP groups were ran-domly selected to observe their 7-day survival after surgery.The remaining mice were given fluorescent isothiocya-nate dextran(FD-40)gavage at 18 hours after surgery.Changes in mice intestinal tissue morphology,intestinal functional injury indicators,intestinal tissue oxidative stress indicators,inflammatory factors expression,and ex-pression of key protein of peroxisome proliferator-activated receptor γ(PPARγ)/nuclear factor kappa B(NF-κB)were detected 24 hours after surgery.Results There were no statistical differences in mice survival rate,intestinal injury indicators,intestinal inflammatory factor levels,oxidative stress indicators,and intestinal tissue injury scores between Sham+Vehi and Sham+Asta groups(all P＞0.05).Compared with the Sham+Vehi group,the survival rate of mice in the CLP+Vehi group decreased significantly;serum diamine oxidase(DAO)activities,levels of in-testinal fatty acid binding protein(I-FABP),D-lactate,and FD-40 increased significantly;levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),interleukin-6(IL-6)and malondialdehyde(MDA)in intestinal tissue in-creased significantly;superoxide dismutase(SOD)activity decreased;intestinal morphological injury score was higher;the expression of PPARγ in intestinal tissue increased,and the ratios of both p-IκBα/IκBα and p-p65/p65 in-creased(all P＜0.05).Compared with the CLP+Vehi group,the survival rate of mice in the CLP+Asta group im-proved;serum DAO activities,levels of I-FABP,D-lactate and FD-40 all decreased significantly;levels of TNF-α,IL-1β,IL-6 and MDA in intestinal tissue decreased significantly;SOD activity increased;intestinal morphological injury score decreased;PPARγ expression in intestinal tissue increased,and the ratios of both p-IκBα/IκBα and p-p65/p65 decreased(all P＜0.05).Conclusion Astaxanthin decreases intestinal injury in CLP-induced septic mice,and its mechanism may be related to the regulation of PPARγ/NF-κB signaling pathway,as well as the inhibi-tion of inflammatory response and oxidative stress.