Objective: To investigate the effects of Qingchang Huashi decoction (QHD) on the expressions of peroxidase body growth activated receptor-γ(PPAR-γ) and nuclear factor-κB(NF-κB) p65 in colonic mucosa of rats with ulcerative colitis

and study the mechanism of Qingchang Huashi decoction in rats with ulcerative colitis. Method: Eighty male Wistar rats were divided randomly into eight groups:normal group (ig NS 2 mL·d-1)

model group (ig NS 2 mL·d-1)

QHD low-dose group

QHD medium-dose group

QHD high-dose group (ig QHD 8

16

32 g·kg-1)

SASP group (ig SASP 0.67 g·kg-1)

SASP+BADGE group (ig SASP 0.67 g·kg-1+ip BADGE 20 mg·kg-1)

and QHD medium-dose+BADGE group (ig QHD 16 g·kg-1+ip BADGE 20 mg·kg-1)

with 10 rats in each group. TNBS was used in all of the groups except for normal group to establish the ulcerative colitis model in rats. SASP and BADGE that is the inhibitor of PPAR-γ were used as positive control drug. The general conditions and the colonic pathology morphology were observed. Western blot and Real-time PCR were performed to detect the protein and mRNA expressions of PPAR-γ and NF-κB p65.The expressions of mucoprotein2(MUC2) and trefoil factor3(TFF3) in colonic mucosa extract were detected by the method of ELISA. Result: Obvious inflammation and ulceration were observed in model group

which suggested that the model was successful. The protein and mRNA expressions of PPAR-γ in the model group were significantly lower than the normal group (P<0.01). Compared with the normal group

expressions of PPAR-γ in QHD and SASP increased slightly (P<0.05)

however

these effects were reduced when QHD and SASP were combined with BADGE (P<0.05). At the same time

the protein and mRNA expressions of NF-κB p65 increased significantly in model group (P<0.01). QHD could decline the expression of NF-κB (P<0.05)

while QHD combined with BADGE could not inhibit its expression any more (P<0.05). Moreover

SASP and QHD were able to increase the expressions of MUC2 and TFF3 in colonic mucosa

but these effects were weakened when combined with BADGE. Conclusion: Qingchang Huashi decoction can improve general conditions and colonic inflammation of TNBS-induced model rats. Its mechanisms may be that Qingchang Huashi decoction can activate PPAR-γ signaling pathway by inhibiting inflammation and expression of NF-κB p65

improving secretion of MUC2 and TFF3 at mucous membrane

and restoring the intestine barrier.