Resveratrol abrogates adhesion molecules and protects against TNBS-induced ulcerative colitis in rats

被引:48
作者
Abdallah, Dalaal M. [2 ]
Ismael, Naglaa R. [1 ]
机构
[1] Fayoum Univ, Dept Zool, Fac Sci, Al Fayyum 63514, Egypt
[2] Cairo Univ, Dept Pharmacol & Toxicol, Fac Pharm, Cairo 11562, Egypt
关键词
colitis; resveratrol; sulphasalazine; myeloperoxidase; oxidative stress; INFLAMMATORY-BOWEL-DISEASE; KAPPA-B ACTIVATION; TRINITROBENZENE SULFONIC-ACID; NITRIC-OXIDE; SUPPRESSES COLITIS; OXIDATIVE DAMAGE; EXPRESSION; INHIBITION; STRESS; MODEL;
D O I
10.1139/Y11-080
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Resveratrol, a polyphenol compound with anti-inflammatory properties, has been previously evaluated for its beneficial effects in several ulcerative colitis models. However, the current study elucidates the effect of resveratrol on adhesion molecules, as well as its antioxidant efficacy in a trinitrobenzene sulfonic acid (TNBS)-induced ulcerative-colitis model. Colitis was induced by rectal instillation of TNBS, followed by daily per os administration of either sulphasalazine (300 mg/kg) or resveratrol (2 and 10 mg/kg) for 7 days. Administration of resveratrol decreased the ulcerative area and colon mass index; these effects were further supported by the reduction in colon inflammation grades, as well as histolopathological changes, and reflected by the stalling of body mass loss. The anti-inflammatory effects of resveratrol were indicated by lowered myeloperoxidase activity, and by suppressing ICAM-1 and VCAM-1 levels in the colon and serum. In addition, it restored a reduced colonic nitric oxide level and reinstated its redox balance, as evidenced by the suppression of lipid peroxides and prevention of glutathione depletion. The anti-ulcerative effect of the higher dose of resveratrol was comparable with those of sulphasalazine. The study confirms the anti-ulcerative effect of resveratrol in TNBS-induced experimental colitis via reduction of neutrophil infiltration, inhibition of adhesive molecules, and restoration of the nitric oxide level, as well as the redox status.
引用
收藏
页码:811 / 818
页数:8
相关论文
共 48 条
[41]   Resveratrol (Trans-3,5,4′-trihydroxystilbene) Induces Silent Mating Type Information Regulation-1 and Down-Regulates Nuclear Transcription Factor-κB Activation to Abrogate Dextran Sulfate Sodium-Induced Colitis [J].
Singh, Udai P. ;
Singh, Narendra P. ;
Singh, Balwan ;
Hofseth, Lorne J. ;
Price, Robert L. ;
Nagarkatti, Mitzi ;
Nagarkatti, Prakash S. .
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, 2010, 332 (03) :829-839
[42]   DETERMINATION OF MALONALDEHYDE PRECURSOR IN TISSUES BY THIOBARBITURIC ACID TEST [J].
UCHIYAMA, M ;
MIHARA, M .
ANALYTICAL BIOCHEMISTRY, 1978, 86 (01) :271-278
[43]   Protective role of heme oxygenase-1 on trinitrobenzene sulfonic acid-induced colitis in rats [J].
Wang, WP ;
Guo, X ;
Koo, MWL ;
Wong, BCY ;
Lam, SK ;
Ye, YN ;
Cho, CH .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2001, 281 (02) :G586-G594
[44]   Resveratrol suppresses IL-6-induced ICAM-1 gene expression in endothelial cells: Effects on the inhibition of STAT3 phosphorylation [J].
Wung, BS ;
Hsu, MC ;
Wu, CC ;
Hsieh, CW .
LIFE SCIENCES, 2005, 78 (04) :389-397
[45]   Anti-oxidant Effects of Resveratrol on Mice with DSS-induced Ulcerative Colitis [J].
Yao, Jun ;
Wang, Jian-Yao ;
Liu, Lei ;
Li, Ying-Xue ;
Xun, An-Ying ;
Zeng, Wei-Sen ;
Jia, Chun-Hong ;
Wei, Xiao-Xia ;
Feng, Ju-Ling ;
Zhao, Li ;
Wang, Li-Sheng .
ARCHIVES OF MEDICAL RESEARCH, 2010, 41 (04) :288-294
[46]   Effect of Z-103 on TNB-induced colitis in rats [J].
Yoshikawa, T ;
Yamaguchi, T ;
Yoshida, N ;
Yamamoto, H ;
Kitazumi, S ;
Takahashi, S ;
Naito, Y ;
Kondo, M .
DIGESTION, 1997, 58 (05) :464-468
[47]   Resveratrol and Piceatannol Inhibit iNOS Expression and NF-κB Activation in Dextran Sulfate Sodium-Induced Mouse Colitis [J].
Youn, Jin ;
Lee, Jeong-Sang ;
Na, Hye-Kyung ;
Kundu, Joydeb Kumar ;
Surh, Young-Joon .
NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL, 2009, 61 (06) :847-854
[48]   Resveratrol prevents endothelial dysfunction and aortic superoxide production after trauma hemorrhage through estrogen receptor-dependent hemeoxygenase-1 pathway [J].
Yu, Huang-Ping ;
Hwang, Tsong-Long ;
Hwang, Tsann-Long ;
Yen, Chia-Hung ;
Lau, Ying-Tung .
CRITICAL CARE MEDICINE, 2010, 38 (04) :1147-1154