| Objective: To analyze the expression levels of TPL2 in serum and colon tissue.In addition,the correlation between TPL2 and the degree of inflammatory lesions in patients with ulcerative colitis was explored,and to preliminarily explore the regulation of TPL2 on inflammation-related genes Its role and regulatory mechanism lay a theoretical foundation for the pathogenesis of ulcerative colitis and provide potential therapeutic targets for the diagnosis and treatment of ulcerative colitis in clinical treatment.Methods: The specimen tissue,serum samples,basic information of patients with ulcerative colitis and healthy patients were collected from January 2020 to December2021.The disease severity of UC patients was scored using the modified Mayo scoring system,which was divided into mild,moderate and severe.First,the lesion degree and inflammation degree of the specimens in each group were evaluated by HE staining,and then the control group and 10 patients with mild and severe UC were selected.Western blot and q RT-PCR were used to detect the expression of TPL2 and inflammation-related genes i NOS and Cox-2 in each group.The expression in the samples was evaluated by q RT-PCR to evaluate the expression levels of IL-6,IL-10,and IL-18.Then,the Caco-2 cell line was treated with IL-1β in vitro,and the expressions of TPL2 and inflammation-related genes i NOS and Cox-2 were detected by Western blot and q RT-PCR.The regulation of TPL2 in inflammation was further clarified using knockdown the expression of TPL2 by si RNA.Finally,the expressions of p-JNK,JNK,p-ERK and ERK were detected by Western blot to clarify the regulatory effect of TPL2 on JNK and ERK pathways.Results: 26 healthy patients and 63 UC patients(24 mild,18 moderate,21 severe UC patients)were included.Statistical analysis indicated that there was no significant difference in gender,age and disease duration among the groups.Further Extent classification analysis showed that the lesions of mild UC patients were mainly E2 type,the lesions of moderate UC patients were mainly E3 type,and the severe UC patients were mainly E3 type.The histological damage score and inflammation score also showed that the tissue damage score and inflammation score of patients with mild and severe UC showed a gradient increase and had a statistical difference compared with the control group.Subsequently,Western blot detection and q RT-PCR showed that there was no significant difference in the expression of TPL2 between patients with mild UC and healthy people,while the expression of TPL2 was significantly increased in severe UC patients.Additionally,c-reactive protein and erythrocyte sedimentation rate test indicated that the CRP in the mild and severe UC lesion groups increased significantly compared with the normal group.Furthermore,there was no significancy in the expression of i NOS and COX2 comparing with the health group.However,there was significantly up-regulated in the severe lesion group with statistical difference.In vitro experiments showed that the expression of TPL2,i NOS and COX2 increased with increasing concentrations of IL-1β.Finally,by knocking down TPL2,the expression of i NOS and COX2 can be inhibited.At the same time,by knocking down the expression of TPL2,we found that p-ERK/ERK and p-JNK/JNK were reduced to a certain extent(compared with the effect of IL-1β alone).Conclusion: Compared with the healthy control group,the expression of TPL2 in the mucosal tissue of UC patients was significantly increased,and it was highly correlated with the degree of UC lesions.In vitro experiments further proved that the expression of TPL2 increased with the increase of the degree of inflammation,and had a regulatory effect on inflammation-related genes(i NOS and COX2).TPL2 may regulate the inflammatory response of UC through ERK and JNK pathways. |