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microRNA‐495 reduces visceral sensitivity in mice with diarrhea‐predominant irritable bowel syndrome through suppression of the PI3K/AKT signaling pathway via PKIB

Diarrhea‐predominant irritable bowel syndrome (IBS‐D) is one of the most common gastrointestinal disorders in the world, lacking effective therapies. The crucial roles of microRNAs (miRNAs) in IBS‐D have attracted increasing attention. The aim of this study is to investigate the effects of miR‐495 on the visceral sensitivity of the IBS‐D through the PI3K/AKT signaling pathway by targeting PKIB. Microarray data analysis was employed to screen the differentially expressed genes related to IBS‐D and regulatory miRNAs. Then, mice were perfused with acetic acid into the rectum to establish the IBS‐D model. Next, PKIB expression was measured in IBS‐D mice. Additionally, model mice were injected with a series of adenovirus vector to investigate the influence of miR‐495 on visceral sensitivity and rectal function in IBS‐D mice with the involvement of PKIB and PI3K/AKT signaling pathway. The IBS‐D mouse model was successfully established. PKIB was the target gene of miR‐495, and highly expressed in mice with IBS‐D. Silencing PKIB reduced visceral sensitivity in mice with IBS‐D, and overexpression of miR‐495 decreased visceral sensitivity in mice with IBS‐D by inhibiting PKIB. Moreover, miR‐495 upregulation inhibited PI3K/AKT signaling pathway through downregulating PKIB. To sum up, this study reveals that miR‐495 upregulation can reduce visceral sensitivity in IBS‐D via inhibition of PI3K/AKT signaling pathway by targeting PKIB. It suggests that miR‐495 presents a potential target for IBS‐D therapy.