摘要This study aimed to determine the regulatory mechanism of dietary zinc lactate(ZL)supplementation on intestinal oxidative stress damage in a paraquat(PQ)-induced piglet model.Twenty-eight piglets(mean body weight 9.51±0.23 kg)weaned at 28 d of age were randomly divided into control,ZL,PQ,and ZL+PQgroups(n=7 in each group).The ZL-supplemented diet had little effect on growth performance under normal physiological conditions.However,under PQ challenge,ZL supplementation significantly improved average daily gain(P＜0.05)and reduced the frequency of diarrhea.ZL improved intestinal morphology and ultra-structure by significantly increasing the expression level of the jejunal tight junction protein,zonula occludens-1(ZO-1)(P＜0.05),and intestinal zinc transport and absorption in PQ-induced piglets,which reduced intestinal permeability.ZL supplementation also enhanced the expression of antioxidant and anti-inflammatory factor-related genes and decreased inflammatory cytokine expression and secretion in PQ-induced piglets.Furthermore,ZL treatment significantly inhibited the activation of constitutive androstane receptor(CAR)signaling(P＜0.01)in PQ-induced piglets and altered the structure of the gut microbiota,especially by significantly increasing the abundance of beneficial gut microbes,including UCG_002,Rumi-nococcus,Rikenellaceae_RC9gut_group,Christensenellaceae_R_7_group,Treponema,unclassified_Christense-nellaceae,and unclassified_Erysipelotrichaceae(P＜0.05).These data reveal that pre-administration of ZL to piglets can suppress intestinal oxidative stress by improving antioxidant and anti-inflammatory capacity and regulating the crosstalk between CAR signaling and gut microbiota.