Mechanisms Of "Changbingfang" Stimulated By Acupoint Catgut Embedding In Treating Rats With Experimental Colitis

Objective:To investigate the mechanisms of acupoint catgut embedding on the rats with experimental colitis.Methods:Twenty-four SD rats were randomly divided into a normal control group(NC), a model group (MO), a Mesalazine groups (ME) and an acupoint catgut embedding group (CI) with 6 rats in each group. The rats in Mesalazine group were given mesalazine through intragastriclly administration everyday and the rats in acupoint catgut embedding group were given catgut point-embedding therapy. The symptoms of changes in histopathology were detected 15 days after the treatment. Colonic histopathologic changes were observed by immunohistochemical staining and the expression of IL-17, Foxp3,β2AR, NF-KBp65 was observed by Immunohistochemistry. The protein expression ofβ2AR, NF-KBp65 was analyzed by western blot method and the expression of STAT6mRNA was detected by RT-PCR.Results:Compared with the control group, there was elevated expression of IL-17, NF-KBp65, STAT6mRNA (P<0.01),and decreased expression of Foxp3,P2AR (P< 0.01) in experimental UC rats.After experimental UC rats treated with mesalazine, the level of IL-17, NF-κBp65, STAT6mRNAwas significantly decreased (P<0.01) accompanied by significant up-regulation of Foxp3,βAR expression (P<0.01) in Mesalazine group.Compared with the model group, the level of IL-17, NF-κBp65, STAT6mRNA was also decreased(P<0.01) accompanied by significant up-regulation of Foxp3,β2AR (P<0.01) in acupoint catgut embedding group. Conclusion:The expression ofβ2AR, Foxp3 is decreased,and the expression of IL-17, NF-KBp65, and STAT6mRNA is increased, which is a possible pathogenesis of experimental UC rats.NF-κB/STAT6 double signal transduction pathways play an important role for pathogenic process of experimental UC in rats.Acupoint catgut embedding therapy can inhibit the expression of IL-17,NF-κBp65,STAT6mRNA to play anti-inflammatory role.