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.
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.
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。
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