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芝麻酚对白化大鼠乙酸诱导的炎症性肠病中髓过氧化物酶和结肠形态的影响研究。

Investigation of sesamol on myeloperoxidase and colon morphology in acetic acid-induced inflammatory bowel disorder in albino rats.

作者信息

Kondamudi Phani Krishna, Kovelamudi Hemalatha, Mathew Geetha, Nayak Pawan G, Rao Mallikarjuna C, Shenoy Rekha R

机构信息

Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, Karnataka 576104, India.

出版信息

ScientificWorldJournal. 2014 Jan 30;2014:802701. doi: 10.1155/2014/802701. eCollection 2014.

DOI:10.1155/2014/802701
PMID:24616646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3926374/
Abstract

BACKGROUND

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of gastrointestinal tract of immune, genetic, and environmental origin. In the present study, we examined the effects of sesamol (SES), which is the active constituent of sesame oil in the acetic acid (AA) induced model for IBD in rats.

METHODS

The groups were divided into normal control, AA control, SES, and sulfasalazine (SS). On day 7, the rats were killed, colon was removed, and the macroscopic, biochemical, and histopathological evaluations were performed.

RESULTS

The levels of MPO, TBARS, and tissue nitrite increased significantly (P < 0.05) in the AA group whereas they reduced significantly in the SES and SS treated groups. Serum nitrite levels were found to be insignificant between the different groups.

CONCLUSIONS

The mucosal protective effects of sesamol in IBD are due to its potential to reduce the myeloperoxidase and nitrite content.

摘要

背景

炎症性肠病（IBD）是一种起源于免疫、遗传和环境因素的胃肠道慢性炎症性疾病。在本研究中，我们研究了芝麻油的活性成分芝麻酚（SES）在醋酸（AA）诱导的大鼠IBD模型中的作用。

方法

将大鼠分为正常对照组、AA对照组、SES组和柳氮磺胺吡啶（SS）组。在第7天，处死大鼠，取出结肠，进行宏观、生化和组织病理学评估。

结果

AA组中髓过氧化物酶（MPO）、硫代巴比妥酸反应物（TBARS）和组织亚硝酸盐水平显著升高（P < 0.05），而在SES和SS治疗组中显著降低。不同组之间血清亚硝酸盐水平无显著差异。

结论

芝麻酚在IBD中的黏膜保护作用归因于其降低髓过氧化物酶和亚硝酸盐含量的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/d09883595f18/TSWJ2014-802701.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/69a547dc87ee/TSWJ2014-802701.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/b767dffd1537/TSWJ2014-802701.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/5b6af3210bcf/TSWJ2014-802701.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/ed2372b9a444/TSWJ2014-802701.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/b731dcbbe566/TSWJ2014-802701.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/035504e36cd1/TSWJ2014-802701.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/d09883595f18/TSWJ2014-802701.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/69a547dc87ee/TSWJ2014-802701.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/b767dffd1537/TSWJ2014-802701.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/5b6af3210bcf/TSWJ2014-802701.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/ed2372b9a444/TSWJ2014-802701.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/b731dcbbe566/TSWJ2014-802701.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/035504e36cd1/TSWJ2014-802701.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8448/3926374/d09883595f18/TSWJ2014-802701.007.jpg

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