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绿茶提取物联合水果可通过调节 microRNA-21 表达和 NF-κB 活性改善 DSS 诱导的结肠炎。

Green Tea Extract Containing Fruit Ameliorates DSS-Induced Colitis via Modulating MicroRNA-21 Expression and NF-κB Activity.

机构信息

Department of Nutritional Science and Food Management, Ewha Womans University, Seoul 03760, Korea.

Graduate Program in System Health Science and Engineering, Ewha Womans University, Seoul 03760, Korea.

出版信息

Nutrients. 2022 Jun 28;14(13):2684. doi: 10.3390/nu14132684.

DOI:10.3390/nu14132684
PMID:35807865
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9268562/
Abstract

The aim of the present study was to examine the effect of green tea extract containing fruit (GTP) on dextran-sulfate-sodium (DSS)-induced colitis, the regulatory mechanisms of microRNA (miR)-21, and the nuclear factor-κB (NF-κB) pathway. Different doses of GTP (50, 100, and 200 mg/kg) were administered orally once daily for 14 days, followed by GTP with 3% DSS for 7 days. Compared with the DSS-treated control, GTP administration alleviated clinical symptoms, including the disease activity index (DAI), colon shortening, and the degree of histological damage. Moreover, GTP suppressed miR-21 expression and NF-κB activity in colon tissue of DSS-induced colitis mice. The mRNA levels of inflammatory mediators, such as tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), were downregulated by GTP. Colonic nitric oxide (NO) and prostaglandin E2 (PGE2) production, and myeloperoxidase (MPO) activity were also lowered by GTP. Taken together, our results revealed that GTP inhibits DSS-induced colonic inflammation by suppressing miR-21 expression and NF-κB activity, suggesting that it may be used as a potential functional material for improving colitis.

摘要

本研究旨在探讨含[水果名]的绿茶提取物(GTP)对葡聚糖硫酸钠(DSS)诱导的结肠炎的影响,以及 microRNA(miR)-21 和核因子-κB(NF-κB)通路的调节机制。不同剂量的 GTP(50、100 和 200mg/kg)每天口服一次,连续 14 天,然后用 3% DSS 处理 7 天。与 DSS 处理的对照组相比,GTP 给药可缓解临床症状,包括疾病活动指数(DAI)、结肠缩短和组织学损伤程度。此外,GTP 抑制了 DSS 诱导的结肠炎小鼠结肠组织中 miR-21 表达和 NF-κB 活性。促炎介质如肿瘤坏死因子-α(TNF-α)、白细胞介素 6(IL-6)、白细胞介素-1β(IL-1β)、诱导型一氧化氮合酶(iNOS)和环氧化酶-2(COX-2)的 mRNA 水平也被 GTP 下调。GTP 还降低了结肠中一氧化氮(NO)和前列腺素 E2(PGE2)的产生以及髓过氧化物酶(MPO)的活性。总之,我们的结果表明,GTP 通过抑制 miR-21 表达和 NF-κB 活性来抑制 DSS 诱导的结肠炎症,表明它可能被用作改善结肠炎的潜在功能性物质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174c/9268562/9e635137b0ef/nutrients-14-02684-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/174c/9268562/e9b3d9014886/nutrients-14-02684-g002.jpg
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