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Inhibition of miR-16 Ameliorates Inflammatory Bowel Disease by Modulating Bcl-2 in Mouse Models.
Chen, Ye; Shan, Ting; Qu, Huiheng; Chen, Yigang; Wang, Ning; Xia, Jiazeng.
Affiliation
  • Chen Y; Department of General Surgery and Center of Translational Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, China.
  • Shan T; Department of General Surgery and Center of Translational Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, China.
  • Qu H; Department of General Surgery and Center of Translational Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, China.
  • Chen Y; Department of General Surgery and Center of Translational Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, China.
  • Wang N; Department of General Surgery and Center of Translational Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, China.
  • Xia J; Department of General Surgery and Center of Translational Medicine, The Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, China. Electronic address: xjz_wuxi@alumni.sjtu.edu.cn.
J Surg Res ; 253: 185-192, 2020 09.
Article de En | MEDLINE | ID: mdl-32361613
ABSTRACT

BACKGROUND:

In recent years, microRNA (miRNA) is considered as a potential therapy target. To study the regulatory mechanism and therapeutic effect of miRNAs on inflammatory bowel disease (IBD), we investigated microRNAs that regulate apoptosis-related protein B cell lymphoma-2 (Bcl-2). We examined the role of miR-16 in IBD and the effect of inhibiting the expression of miR-16 on disease progression. MATERIALS AND

METHODS:

Dextran sulfate sodium was used to induce ulcerative colitis in mice. RNA and protein were extracted from the rectal mucosa of mice. Real-time quantitative polymerase chain reaction and Western blotting were used to detect the expression of miR-16 and Bcl-2. The effects of miR-16 on intestinal mucosal immunity were studied by real-time quantitative polymerase chain reaction, and inflammatory factors such as interleukin-1ß, interleukin-6, and tumor necrosis factor-α were detected. The weight changes, disease activity index, length of the rectal colon, and pathological score of the mice were used to evaluate the effect of inhibiting miR-16 on disease progression. Through the establishment of overexpression and low expression cell lines of miR-16, the regulation of miR-16 on Bcl-2 was studied.

RESULTS:

MiR-16 was overexpressed in the IBD model, whereas Bcl-2 had lower expression in the mucosa. Inhibiting expression of miR-16 significantly decreased the expression of interleukin-1ß, interleukin-6, and tumor necrosis factor-α. In mice, the weight change, disease activity index, and pathological score decreased in the experimental group, in which miR-16 was inhibited. High expression of miR-16 can inhibit Bcl-2 expression.

CONCLUSIONS:

MiR-16 plays a critical role in IBD via Bcl-2 and is a promising target in IBD therapy.
Sujet(s)

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Rectocolite hémorragique / Côlon / Protéines proto-oncogènes c-bcl-2 / MicroARN / Muqueuse intestinale Type d'étude: Prognostic_studies Limites: Animals / Female / Humans Langue: En Journal: J Surg Res Année: 2020 Type de document: Article Pays d'affiliation: Chine

Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Sujet principal: Rectocolite hémorragique / Côlon / Protéines proto-oncogènes c-bcl-2 / MicroARN / Muqueuse intestinale Type d'étude: Prognostic_studies Limites: Animals / Female / Humans Langue: En Journal: J Surg Res Année: 2020 Type de document: Article Pays d'affiliation: Chine