miR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in rats

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...

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Main Authors: Qing Zhang, Shu‐Fang Wang
Format: Article
Language:English
Published: Wiley 2021-06-01
Series:Kaohsiung Journal of Medical Sciences
Subjects:
Online Access:https://doi.org/10.1002/kjm2.12359
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spelling doaj-f7982f8c90554d2a9113254a14b9fb2d2021-06-04T12:52:29ZengWileyKaohsiung Journal of Medical Sciences1607-551X2410-86502021-06-0137649750410.1002/kjm2.12359miR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in ratsQing Zhang0Shu‐Fang Wang1Department of Spleen‐stomach Hepatobiliary Lianyungang Hospital of Traditional Chinese Medicine Jiangsu Province ChinaDepartment of Digestive Internal Medicine Lianyungang Second People's Hospital Jiangsu Province ChinaAbstract 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.https://doi.org/10.1002/kjm2.12359dextran sodium sulfateinflammatory bowel diseaseinterleukin‐1 receptor‐associated kinase 1microRNAulcerative colitis
collection DOAJ
language English
format Article
sources DOAJ
author Qing Zhang
Shu‐Fang Wang
spellingShingle Qing Zhang
Shu‐Fang Wang
miR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in rats
Kaohsiung Journal of Medical Sciences
dextran sodium sulfate
inflammatory bowel disease
interleukin‐1 receptor‐associated kinase 1
microRNA
ulcerative colitis
author_facet Qing Zhang
Shu‐Fang Wang
author_sort Qing Zhang
title miR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in rats
title_short miR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in rats
title_full miR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in rats
title_fullStr miR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in rats
title_full_unstemmed miR‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting IRAK1 in rats
title_sort mir‐330 alleviates dextran sodium sulfate‐induced ulcerative colitis through targeting irak1 in rats
publisher Wiley
series Kaohsiung Journal of Medical Sciences
issn 1607-551X
2410-8650
publishDate 2021-06-01
description 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.
topic dextran sodium sulfate
inflammatory bowel disease
interleukin‐1 receptor‐associated kinase 1
microRNA
ulcerative colitis
url https://doi.org/10.1002/kjm2.12359
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AT shufangwang mir330alleviatesdextransodiumsulfateinducedulcerativecolitisthroughtargetingirak1inrats
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