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本文引用的文献

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Cancer Lett. 2005 Jun 8;223(2):181-90. doi: 10.1016/j.canlet.2004.09.041. Epub 2004 Nov 11.
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The COX-2 inhibitor, rofecoxib, ameliorates dextran sulphate sodium induced colitis in mice.环氧化酶-2抑制剂罗非昔布可改善葡聚糖硫酸钠诱导的小鼠结肠炎。
Inflamm Res. 2005 Apr;54(4):145-51. doi: 10.1007/s00011-004-1337-2.
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Ischemic colitis associated with rofecoxib.与罗非昔布相关的缺血性结肠炎。
Dig Liver Dis. 2005 May;37(5):372-6. doi: 10.1016/j.dld.2004.07.020.
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COX-2: a molecular target for colorectal cancer prevention.环氧化酶-2：预防结直肠癌的分子靶点。
J Clin Oncol. 2005 Apr 20;23(12):2840-55. doi: 10.1200/JCO.2005.09.051.
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Preventive and therapeutic effects of NF-kappaB inhibitor curcumin in rats colitis induced by trinitrobenzene sulfonic acid.核因子-κB抑制剂姜黄素对三硝基苯磺酸诱导的大鼠结肠炎的预防和治疗作用
World J Gastroenterol. 2005 Mar 28;11(12):1747-52. doi: 10.3748/wjg.v11.i12.1747.
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Aggravation of inflammatory bowel disease by cyclooxygenase-2 inhibitors in rats.环氧化酶-2抑制剂加重大鼠炎症性肠病
Pharmacology. 2004 Oct;72(2):77-84. doi: 10.1159/000079135.
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Inflixmab as a possible treatment for the hemorrhagic type of Crohn's disease.英夫利昔单抗作为出血型克罗恩病的一种可能治疗方法。
J Gastroenterol. 2004;39(3):284-7. doi: 10.1007/s00535-003-1290-9.
8
Curcumin suppresses lipopolysaccharide-induced cyclooxygenase-2 expression by inhibiting activator protein 1 and nuclear factor kappab bindings in BV2 microglial cells.姜黄素通过抑制BV2小胶质细胞中的激活蛋白1和核因子κB结合来抑制脂多糖诱导的环氧化酶-2表达。
J Pharmacol Sci. 2004 Mar;94(3):325-8. doi: 10.1254/jphs.94.325.
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Cyclooxygenase 2 mediates post-inflammatory colonic secretory and barrier dysfunction.环氧化酶2介导炎症后结肠分泌和屏障功能障碍。
Gut. 2003 Dec;52(12):1714-20. doi: 10.1136/gut.52.12.1714.
10
Suppression of dextran sodium sulfate-induced colitis in mice by zerumbone, a subtropical ginger sesquiterpene, and nimesulide: separately and in combination.亚热带姜倍半萜 Zerumbone 与尼美舒利单独及联合使用对葡聚糖硫酸钠诱导的小鼠结肠炎的抑制作用
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姜黄素减弱三硝基苯磺酸通过抑制环氧化酶-2的表达诱导慢性结肠炎。

Curcumin-attenuated trinitrobenzene sulphonic acid induces chronic colitis by inhibiting expression of cyclooxygenase-2.

作者信息

Jiang Hua, Deng Chang-Sheng, Zhang Ming, Xia Jian

机构信息

Department of Gastroenterology, Zhongnan Hospital of Wuhan University, Hubei Province, China.

出版信息

World J Gastroenterol. 2006 Jun 28;12(24):3848-53. doi: 10.3748/wjg.v12.i24.3848.

DOI:10.3748/wjg.v12.i24.3848
PMID:16804969
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4087932/
Abstract

AIM

To explore the possible mechanisms of curcumin in rat colitis induced by trinitrobenzene sulfonic (TNBS) acid.

METHODS

Rats with TNBS acid-induced colitis were treated with curcumin (30 mg/kg or 60 mg/kg per day ip). Changes of body weight and histological scores as well as survival rate were evaluated. Leukocyte infiltration was detected by myeloperoxidase (MPO) activity assay. The expression of cyclooxygenase-2 (COX-2) was detected by RT-PCR and Western blot. Inflammation cytokines were determined by RT-PCR. Local concentration of prostaglandin E(2) (PGE(2)) in colon mucosa was determined by ELISA.

RESULTS

Curcumin improved survival rate and histological image, decreased the macroscopic scores and MPO activity. Also curcumin reduced the expression of COX-2 and inflammation cytokines. In addition, treatment with curcumin increased the PGE(2) level.

CONCLUSION

Curcumin has therapeutic effects on TNBS acid-induced colitis, the mechanisms seem to be related to COX-2 inhibition and PGE(2) improvement.

摘要

目的

探讨姜黄素对三硝基苯磺酸（TNBS）诱导的大鼠结肠炎的可能作用机制。

方法

用TNBS诱导大鼠结肠炎，然后用姜黄素（每天腹腔注射30毫克/千克或60毫克/千克）进行治疗。评估体重变化、组织学评分以及存活率。通过髓过氧化物酶（MPO）活性测定检测白细胞浸润情况。通过逆转录聚合酶链反应（RT-PCR）和蛋白质免疫印迹法检测环氧化酶-2（COX-2）的表达。通过RT-PCR测定炎症细胞因子。用酶联免疫吸附测定法（ELISA）测定结肠黏膜中前列腺素E2（PGE2）的局部浓度。

结果

姜黄素提高了存活率，改善了组织学图像，降低了大体评分和MPO活性。姜黄素还降低了COX-2和炎症细胞因子的表达。此外，姜黄素治疗提高了PGE2水平。

结论

姜黄素对TNBS诱导的结肠炎具有治疗作用，其机制可能与抑制COX-2和提高PGE2水平有关。