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胰蛋白酶抑制剂LH011可抑制葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎，减轻炎症和氧化应激。

Trypsin inhibitor LH011 inhibited DSS-induced mice colitis alleviating inflammation and oxidative stress.

作者信息

Jia Zhenmao, Wang Panxia, Xu Yuansheng, Feng Guodong, Wang Quan, He Xiangjun, Song Yan, Liu Peiqing, Chen Jianwen

机构信息

Laboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou, China.

School of Pharmaceutical Sciences, Guangzhou Medical University, Guangzhou, China.

出版信息

Front Pharmacol. 2022 Sep 27;13:986510. doi: 10.3389/fphar.2022.986510. eCollection 2022.

DOI:10.3389/fphar.2022.986510
PMID:36238566
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9551103/
Abstract

Ulcerative colitis (UC) is one type of inflammatory bowel disease, characterized by inflammation with infiltration and activation of macrophages in colonic tissue. LH011 is a trypsin inhibitor with potential anti-inflammatory effect. Here, we aim to assay the effects of LH011 on UC and further investigate the potential mechanisms and Dextran sulfate sodium (DSS, 3.5%, w/v) was used to induce UC, and lipopolysaccharide (LPS) was used to induce inflammation in RAW 264.7 cells. LH011 was administrated to mice or to RAW 264.7 cells at different concentrations. The cytokines (IL-1β, IL-6, and TNF-α) and the changes of NF-κB and Nrf2 pathways were detected. The results showed that LH011 improved DSS-induced mice colitis, including loss of weight, disease activity index (DAI), and colonic pathological damage. In addition, LH011 inhibited the expressions of IL-1β, IL-6, and TNF-α and strengthened the anti-oxidative capacity. Mechanically, LH011 downregulated the nuclear localization of NF-κB p65 and upregulated the protein expression of Nrf2. These results demonstrated that LH011 alleviated inflammation and oxidative stress during UC by inhibiting TLR4/NF-κB and activating Nrf2/Keap1/HO-1 signaling pathways.

摘要

溃疡性结肠炎（UC）是炎症性肠病的一种类型，其特征是结肠组织中巨噬细胞浸润和激活导致炎症。LH011是一种具有潜在抗炎作用的胰蛋白酶抑制剂。在此，我们旨在测定LH011对UC的影响，并进一步研究其潜在机制。使用葡聚糖硫酸钠（DSS，3.5%，w/v）诱导UC，使用脂多糖（LPS）诱导RAW 264.7细胞炎症。将不同浓度的LH011给予小鼠或RAW 264.7细胞。检测细胞因子（IL-1β、IL-6和TNF-α）以及NF-κB和Nrf2通路的变化。结果表明，LH011改善了DSS诱导的小鼠结肠炎，包括体重减轻、疾病活动指数（DAI）和结肠病理损伤。此外，LH011抑制了IL-1β、IL-6和TNF-α的表达并增强了抗氧化能力。机制上，LH011下调了NF-κB p65的核定位并上调了Nrf2的蛋白表达。这些结果表明，LH011通过抑制TLR4/NF-κB和激活Nrf2/Keap1/HO-1信号通路减轻了UC期间的炎症和氧化应激。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/96e5a5a25b96/fphar-13-986510-g008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/66d9106bda8b/fphar-13-986510-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/96e5a5a25b96/fphar-13-986510-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/3f62818a9d13/fphar-13-986510-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/0486fbb7a0f0/fphar-13-986510-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/4ae8f06028ab/fphar-13-986510-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/8387234b47a0/fphar-13-986510-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/a1f25f0610c8/fphar-13-986510-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/66d9106bda8b/fphar-13-986510-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b536/9551103/96e5a5a25b96/fphar-13-986510-g008.jpg

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