The Regulation Mechanism Of Shaoyao Decoction On The Immune Barrier Of UC Rats

Objective:(1)To clarify that PI3K-Akt-m TOR steady-state regulation of intestinal mucosal immune barrier is an important mechanism for the development of ulcerative colitis.Preliminary clarification that the m TOR pathway is the key point of PI3K-Akt-m TOR homeostasis regulation.(2)It is clarified that Shaoyao Decoction can protect and repair the immune barrier damage of ulcerative colitis by regulating the steady state change of PI3K-Akt-m TOR.It provides a new scientific basis for the treatment of ulcerative colitis by Shaoyao Tang,provides a new target for the treatment of ulcerative colitis,and enriches the theoretical and experimental basis of traditional Chinese medicine in preventing and treating ulcerative colitis.Methods:TNBS / ethanol-induced UC rats were established,and the mesalazine drug group was used as the therapeutic effect evaluation.The therapeutic effects of Shaoyao Tang and rapamycin were observed.According to the pathology of rat colon tissue,serum IL-6,IL-17 The results were used to judge the inflammation.Western Blotting method was used to detect STAT3 protein,compared with rapamycin,to see if Shaoyao Decoction participated in PI3K-Akt-m TOR pathway.Results:After drug intervention in UC model rats,compared with the model group,the mesalazine group,Shaoyao Decoction group,rapamycin group,Shaoyao Decoction +rapamycin group can significantly reduce the serum IL-6 and IL-17 of rats Content(P<0.05);the treatment group can significantly reduce the expression of STAT3 protein except the mesalazine group(P<0.05),of which there is no statistical difference between the Shaoyao Decoction group and the rapamycin group(P>0.05);Compared with the model group,each drug group can reduce the inflammatory response and repair the intestinal mucosal immune barrier in UC rats,and improve the disease activity index(DAI score)and histopathology score of rats.Conclusion:Shaoyao Decoction may play a therapeutic role by reducing the expression of STAT3 protein and slowing down the production of inflammatory factors through the steady-state regulation of PI3K-Akt-m TOR,thereby protecting and repairing the immune barrier damage of ulcerative colitis.