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未结合胆红素可改善 TNBS 诱导的结肠炎中的炎症和消化蛋白酶增加。

Unconjugated bilirubin ameliorates the inflammation and digestive protease increase in TNBS-induced colitis.

机构信息

Department of Biochemistry and Molecular Biology, Heilongjiang Provincial Science and Technology Innovation Team in Higher Education Institutes for Infection and Immunity, Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.

Department of General Surgery, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150086, P.R. China.

出版信息

Mol Med Rep. 2017 Aug;16(2):1779-1784. doi: 10.3892/mmr.2017.6825. Epub 2017 Jun 21.

DOI:10.3892/mmr.2017.6825
PMID:28656252
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5562003/
Abstract

The authors previously demonstrated that unconjugated bilirubin (UCB) may inhibit the activities of various digestive proteases, including trypsin and chymotrypsin. The digestive proteases in the lower gut are important in the pathogenesis of inflammatory bowel diseases. The effects of UCB on the inflammation and levels of digestive proteases in feces of rats with colitis have not yet been revealed. The present study investigated the effect of UCB on the inflammatory status and levels of trypsin and chymotrypsin in the feces of rats with trinitrobenzenesulfonic acid (TNBS)‑induced colitis. The data indicated that treatment with TNBS resulted in a marked reduction in weight gain, which was significantly alleviated in UCB‑treated rats. Furthermore, UCB treatment alleviated the inflammation induced by TNBS, detected via macroscopic damage and microscopic inflammation scores, and pro‑inflammatory markers including myeloperoxidase (MPO), tumor necrosis factor (TNF)‑α and interleukin (IL)‑1β. Furthermore, rats with colitis demonstrated significant increases in fecal trypsin and chymotrypsin levels, whereas UCB treatment significantly alleviated these increases. A significant positive correlation was additionally revealed among the pro‑inflammatory markers (MPO, TNF‑α and IL‑1β) and fecal digestive proteases (trypsin and chymotrypsin) in colitis. The results of the present study demonstrated that UCB ameliorated the inflammation and digestive protease increase in TNBS-induced colitis.

摘要

作者先前证明,未结合胆红素(UCB)可能抑制各种消化蛋白酶的活性,包括胰蛋白酶和糜蛋白酶。下消化道中的消化蛋白酶在炎症性肠病的发病机制中很重要。UCB 对结肠炎大鼠粪便中消化蛋白酶的炎症和水平的影响尚未揭示。本研究探讨了 UCB 对三硝基苯磺酸(TNBS)诱导的结肠炎大鼠粪便中炎症状态和胰蛋白酶、糜蛋白酶水平的影响。数据表明,TNBS 处理导致体重明显减轻,而 UCB 治疗的大鼠体重明显减轻。此外,UCB 治疗减轻了由 TNBS 引起的炎症,通过宏观损伤和微观炎症评分以及髓过氧化物酶(MPO)、肿瘤坏死因子(TNF)-α和白细胞介素(IL)-1β等促炎标志物来检测。此外,结肠炎大鼠粪便中的胰蛋白酶和糜蛋白酶水平显著升高,而 UCB 治疗显著减轻了这些升高。在结肠炎中,促炎标志物(MPO、TNF-α和 IL-1β)和粪便消化蛋白酶(胰蛋白酶和糜蛋白酶)之间还存在显著的正相关。本研究结果表明,UCB 改善了 TNBS 诱导的结肠炎中的炎症和消化蛋白酶增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/6bf5acb95fd3/MMR-16-02-1779-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/b1ae9f1b7482/MMR-16-02-1779-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/359b5b95ad69/MMR-16-02-1779-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/f764d38e0d35/MMR-16-02-1779-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/913a22fefe9f/MMR-16-02-1779-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/6bf5acb95fd3/MMR-16-02-1779-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/b1ae9f1b7482/MMR-16-02-1779-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/359b5b95ad69/MMR-16-02-1779-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/f764d38e0d35/MMR-16-02-1779-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/913a22fefe9f/MMR-16-02-1779-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0024/5562003/6bf5acb95fd3/MMR-16-02-1779-g04.jpg

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