In conclusion, our study indicates that EA can decrease the expression of hypothalamic CRF and CRF-R1, relieve mental disorders, meanwhile reduce the expression of CRF-R1 in the gastrointestinal mucosa, decrease IMMC, increase ZO-1 expression, and adjust TJs to repair the intestinal mucosal barrier, suggesting a potentially dual therapeutic role for EA in alleviating the gastrointestinal and psychological symptoms of IBS, meaning that EA may regulate disorders of gut-brain interaction in IBS rats. This evidence concerns the gene TJP1 and irritable bowel syndrome.