Objective:To explore the mechanism of Yiqi Jiedu Huayu Recipe(YQJDHY)on ulcerative colitis model rats based on the negative regulation of JAK2/STAT3 pathway by SOCS.Methods:The rats with ulcerative colitis were cloned by TNBS/ethanol method,and randomly divided into normal group,model group,SASP group,YQJDHY high-dose,medium-dose and low-dose groups.Serum IL-21 and IL-22 were detected by ELISA.Real-time quantitative polymerase chain assay(RT-PCR)was used to detect IL-23,IL-6,IL-17A,cytokine signaling inhibitor 1(SOCS1),SOCS3,tyrosine protein kinase 2(JAK2),transcription activa-tor 3(STAT3),retinoic acid-associated orphan receptorγ antibody(RORγt)mRNA expressions.Results:Pathological examination of rats in model group showed obvious inflammation and ulceration,indicating successful modeling.Compared with normal group,IL-21 and IL-22 contents in model group were significantly increased(P<0.05);the down-regulation of IL-21 and IL-22 in YQJDHY groups and SASP group were statistically different(P<0.05,P<0.01).Compared with model group,IL-23,IL-6,JAK2,STAT3 and IL-17A mRNA levels in intestinal mucosa and serum of YQJDHY groups and SASP group were significantly down-regulated(P<0.01),the ex-pressions of SOCS1 and SOCS3 mRNA in intestinal mucosa were increased in YQJDHY groups(P<0.01).The levels of RORγt mRNA in serum and intestinal mucosa of YQJDHY high-dose group and SASP group were increased(P<0.01).Compared with SASP group,the mRNA levels of JAK2 and STAT3 in YQJDHY high-dose group were increased(P<0.05).Conclusion:YQJDHY can increase the levels of SOCS1 and SOCS3 in ulcerative colitis model rats,and then inhibit JAK2/STAT3 signaling pathway,down-regulate the pro-duction of inflammatory factors,and reduce immune inflammatory response.

Objective:To explore the mechanism of Yiqi Jiedu Huayu Recipe(YQJDHY)on ulcerative colitis model rats based on the negative regulation of JAK2/STAT3 pathway by SOCS.Methods:The rats with ulcerative colitis were cloned by TNBS/ethanol method,and randomly divided into normal group,model group,SASP group,YQJDHY high-dose,medium-dose and low-dose groups.Serum IL-21 and IL-22 were detected by ELISA.Real-time quantitative polymerase chain assay(RT-PCR)was used to detect IL-23,IL-6,IL-17A,cytokine signaling inhibitor 1(SOCS1),SOCS3,tyrosine protein kinase 2(JAK2),transcription activa-tor 3(STAT3),retinoic acid-associated orphan receptorγ antibody(RORγt)mRNA expressions.Results:Pathological examination of rats in model group showed obvious inflammation and ulceration,indicating successful modeling.Compared with normal group,IL-21 and IL-22 contents in model group were significantly increased(P<0.05);the down-regulation of IL-21 and IL-22 in YQJDHY groups and SASP group were statistically different(P<0.05,P<0.01).Compared with model group,IL-23,IL-6,JAK2,STAT3 and IL-17A mRNA levels in intestinal mucosa and serum of YQJDHY groups and SASP group were significantly down-regulated(P<0.01),the ex-pressions of SOCS1 and SOCS3 mRNA in intestinal mucosa were increased in YQJDHY groups(P<0.01).The levels of RORγt mRNA in serum and intestinal mucosa of YQJDHY high-dose group and SASP group were increased(P<0.01).Compared with SASP group,the mRNA levels of JAK2 and STAT3 in YQJDHY high-dose group were increased(P<0.05).Conclusion:YQJDHY can increase the levels of SOCS1 and SOCS3 in ulcerative colitis model rats,and then inhibit JAK2/STAT3 signaling pathway,down-regulate the pro-duction of inflammatory factors,and reduce immune inflammatory response.