To investigate the therapeutic effect of p-hydroxybenzaldehyde (HD) on experimental Crohn's disease (CD) in mice and its mechanism of action.After anesthesia,mice were intrarectally perfused with 50% ethanol solution (containing 2.5 mg of TNBS) to prepare a CD model and 10 ng/mL TNF-α-induced Caco-2 cell inflammation model;mice were observed daily for weight change and disease activity index (DAI);after administration for 7 days,mice were executed and the length of the colon was measured;colon tissue morphology was observed using H&E;MPO activity in colon tissue was measured using myeloperoxidase (MPO) kit;The protein and mRNA expression levels of pro-inflammatory factors (IL-6,IL-1β,TNF-α) in colon and Caco-2 cells were determined by ELISA kit and qPCR;In addition,the protein expression levels of p-NF-κB p65,p-AMPK and PPARγ in the colon and Caco-2 cells were detected by Western blot.The results showed that,compared with control group,mice in model group showed significant weight loss,diarrhea and blood in the stools,indicating successful modeling;Compared with model group,both HD high-dose group (40 mg/kg) and medium-dose (20 mg/kg) significantly increased the body weight,decreased the DAI score,improved the morphology of colonic tissue and decreased the MPO vitality in colonic tissue of CD mice,among which HD (40 mg/kg) had the strongest effect;HD significantly inhibited the overexpression of pro-inflammatory factors (IL-6 and TNF-α) in the intestine of CD mice and Caco-2 cells at the protein and mRNA levels.In addition,HD inhibited p-NF-κB p65 protein expression and promoted p-AMPK and PPARγ protein expression in a dose-dependent manner.HD had an ameliorative effect on enteritis and was best in the 40 mg/kg dose group and 30 μmol/L concentrate group.The mechanism may be related to the activation of PPARγ/AMPK signaling pathway and the inhibition of NF-κB signaling pathway to regulate the release of pro-inflammatory factors.

"> p-hydroxybenzaldehyde, Crohn’s disease, nuclear transcription factor-κB, AMP-dependent protein kinase, peroxisome proliferator-activated receptor γ