Carvacrol attenuated lipopolysaccharide-induced intestinal injury by down-regulating TLRs gene expression and regulating the gut microbiota in rabbit

Abstract This study was attended to investigate the mechanisms and effects of carvacrol (CAR) regulated lipopolysaccharide-induced (LPS) intestinal injury in rabbits. Forty 40d rabbits were allocated to a 2 (with or without CAR) × 2 (with or without LPS) factors completely random. LPS was intramuscularly injected on 28th day of the trial period, and samples were taken after injection 4h. The results showed that LPS could significantly increase IL-1β, IL-6, IL-8 and TNF-α levels in serum (P < 0.05), and increased the relative genes expression of TLR2, TLR4, MYD88, NF-κB, MAPK14, MAPK8, MAPK1, TNF-α, IL-1β, IL-6, IL-8 in the cecum (P < 0.05); The carvacarol could inhibit the increase of IL-1β, IL-6, IL-8 and TNF-α induced by LPS in serum (P < 0.05), meanwhile, inhibited the increase of genes expression of TLR2, TLR4, MYD88, NF-κB, MAPK14, MAPK8, MAPK1, TNF-α, IL-1β, IL-6, IL-8 in the cecum (P < 0.05). LPS could significantly damage the intestine such the intestinal composition was broken (P < 0.05) and the relative genes expression of ZO-1, Claudin-1 and Occludin were significantly decreased (P < 0.05), carvacarol could relived the intestinal damage induced by LPS (P < 0.05). The same phenomenon also appeared in the acetate, propionate and butyrate in cecal chyme (P < 0.05). LPS could significantly decrease the the relative abundance of Ruminococcus (P < 0.05); carvacrol could control the decrease of the relative abundance of Ruminococcus induced by LPS (P < 0.05). In conclusion, carvacrol can alleviate LPS-induced intestinal injury that reduces secretion of inflammatory cytokines by inhibiting TLRs/NF-κB/TNF-α/MAPK genes and regulating cecal microbiota in rabbits.