Changes And Mechanisims Of Inflammation Related Factors In Colon Tissue From Rat Model Of Ulcerative Colitis With Abnormal Sapra Syndrome

Objective: Following the humoral theory of Uyghur traditional medicine, to construct a rat model of ulcerative colitis(UC) with abnormal Sapra syndrome, detected the difference of IL-1α、IL-1β、iNOS、eNOS hnRNA and mRNA expression in colon tissues from normal group and UC with abnormal Sapra syndrome model group, and discussed regulatory mechanism of transcription factor NF-κB. Methods: Based on the establishment of abnormal Sapra syndrome rat model, using TNBS/ethanol to induce UC with abnormal Sapra syndrome model, rats were randomly divided into two groups: normal group and UC with abnormal Sapra syndrome model group. Applied the method of quantitative RT-PCR to detect the difference of IL-1α、IL-1β、iNOS、eNOS hnRNA and mRNA expression in colon tissues from two groups and analysis the differential expression, While using the method of chromatin immunoprecipitation-quantitative PCR(ChIP-qPCR) to detect the affinity of NF-κB with IL-1α、IL-1β、iNOS、eNOS regulatory sequence and elucidate the molecular mechanisms of differentially expressed. Results:(1) Rats’ signs, symptoms and colonic mucosa damage in UC with abnormal Sapra syndrome model group all showed that UC with abnormal Sapra syndrome model was successfully established.(2) Compared with the normal group, The expression of IL-1α、IL-1β、iNOS hnRNA were upregulated in the UC with abnormal Sapra syndrome model group and showed the statistical significance between the two groups(P<0.05), but expression of eNOS hnRNA no statistical significance between the two groups(P > 0.05); the expression of IL-1α、IL-1β、iNOS、eNOS mRNA were upregulated in the UC with abnormal Sapra syndrome model group and showed the statistical significance between the two groups(P<0.05);(3) ChIP-qPCR results showed that in the colon tissue of rats from UC with abnormal Sapra syndrome model group, the NF-κB binding to the regulatory sequences of candidate gene IL-1α、IL-1β、iNOS, which enhance transcriptional activity, but for eNOS that regulatory effect is no obvious. Conclusion:(1) Appears immune dysfunction in the colon tissue of rats from UC with abnormal Sapra syndrome model group.(2) In the UC with abnormal Sapra syndrome model group, NF-κB binding to the regulatory sequences of candidate gene IL-1α、IL-1β、iNOS, which enhance transcriptional activity, thereby upregulated hnRNA expression of candidate genes.(3) In the colon tissue of rats from UC with abnormal Sapra syndrome group, changes of inflammation related factors not only regulated by NF-κB, but also associated with post-transcriptional regulation of another transcription factor.