Open AccessmiR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in rats
Author(s) -
Zhang Qing,
Wang ShuFang
Publication year - 2021
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12359
Subject(s) - ulcerative colitis , proinflammatory cytokine , colitis , myeloperoxidase , inflammation , pathogenesis , medicine , inflammatory bowel disease , immunology , downregulation and upregulation , pharmacology , cancer research , disease , chemistry , biochemistry , gene
Abstract Ulcerative colitis (UC) is a chronic multifactorial inflammatory bowel disease that severely impairs patients' life quality. microRNAs (miRNAs) have been reported to exhibit potential therapeutic effects in the management of UC. With the aim to investigate the regulatory effects of miR‐330 on UC‐related colon tissue damage and inflammation, a rat model of experimental colitis was established by oral administration of dextran sodium sulfate (DSS). DSS‐treated rats showed mucosal damage, colonic inflammation, and elevated myeloperoxidase activity compared with the healthy controls. Dual‐luciferase reporter assay confirmed the binding of interleukin‐1 receptor‐associated kinase 1 (IRAK1) and miR‐330. Subsequently, rats were intracolonically injected with miR‐330 argomir with/without administration of IRAK1 during DSS treatment. The miR‐330 overexpression reduced DSS‐induced colonic injury and the production of proinflammatory cytokines. The level of IRAK1 was negatively regulated by the expression of miR‐330. IRAK1 overexpression abolished the protective effect of miR‐330 on DSS‐induced colonic inflammation and mucosal injury in rats. In conclusion, we clarify the role of miR‐330 in pathogenesis of UC, suggesting miR‐330 alleviated DSS‐induced colitis by downregulating IRAK1, shedding lights on miR‐330 as a therapeutic candidate for UC treatment.