The Expressions Of Hsa_circ₀023397 And MiR-106b In The Intestinal Mucosal Tissues Of Active Crohn's Disease

Background and Objective: In our previous study,the circ RNA microarray was used to screen circ RNAs that were differentially expressed in Crohn's disease?CD?and healthy controls.On this basis,further biological information analysis revealed that hsa_circ₀023397 has multiple mi R-106 b binding sites.The main purpose of this study is to expand the sample size to further verify the expression of hsa_circ₀023397 and mi R-106 b in CD and its potential association with autophagy.It is aimed to provide new ideas for the molecular diagnosis and targeted therapy of CD.Methods: Based on the circ RNA chip detection,hsa_circ₀023397 and mi R-106 b expresssion levels were analysed in 40 active CD patients and 40 health controls by the real-time quantitative reverse transcription-polymerase chain reaction?q RT-PCR?.The expression of autophagy related protein ATG16L1 and LC3-II/LC3-I were assessed by Western Blot.Results: The expression of mi R-106 b and hsa_circ₀023397 in pathological mucosa specimens of 40 patients with active CD and 40 healthy controls were detected by q RT-PCR.The expression of mi R-106 b in active CD was higher than that in healthy controls?P <0.01?,hsa_circ₀023397 expression was lower than the healthy control group?P <0.01?.In addition,statistical analysis suggested that the area under the ROC curve of diagnostic activity CD of hsa_circ₀023397 was 0.844?P <0.01?,with sensitivity and specificity of 0.80 and 0.85.The results of Western Blot showed that the LC3-II / LC3-I ratio of intestinal mucosa in active CD patients was significantly lower than that in healthy controls?P <0.05?.In active CD patients,ATG16L1 protein in intestinal mucosa was significantly lower than healthy controls?P <0.05?.Conclusion:There may be a new mechanism that remains to be further studied for the overexpression of mi R-106 b due to the down-regulation of hsa_circ₀023397,leading to the down-regulation of ATG16L1 expression and reduction of the autophagy in the intestinal mucosal tissues of patients with active CD.