The effects of anti-inflammatory on activation of nuclear factor-kappaB and expression of cell adhesion molecules in patients with ulcerative colitis.
- Author:
Youqin CHEN
1
;
Huatian GAN
;
Qin OUYANG
;
Dan XU
;
Yun PAN
;
Zhoucun A
Author Information
1. Department of Life Sciences, Dali College, Dali 671000, China.
- Publication Type:Journal Article
- MeSH:
Adult;
Anti-Inflammatory Agents;
therapeutic use;
Colitis, Ulcerative;
drug therapy;
metabolism;
Female;
Humans;
Intercellular Adhesion Molecule-1;
biosynthesis;
genetics;
Intestinal Mucosa;
metabolism;
Male;
NF-kappa B;
metabolism;
Prednisone;
therapeutic use;
RNA, Messenger;
biosynthesis;
genetics;
Sulfasalazine;
therapeutic use;
Vascular Cell Adhesion Molecule-1;
biosynthesis;
genetics
- From:
Journal of Biomedical Engineering
2004;21(5):732-736
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study is to assess the effects of anti-inflammatory on activation of nuclear factor-kappaB and mRNA and protein expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in intestinal mucosal biopsy specimens from patients with ulcerative colitis (UC). A total of 27 cases with UC were investigated. 15 cases received sulfasalazine (SASP) treatment or SASP and glucocorticoid treatment, 12 cases did not receive any medication related with UC. Normal mucosa from 9 colon cancer cases served as control. Ten pieces of intestinal mucosal biopsy specimens were obtained from each patient. The mRNA expression of ICAM-1 and VCAM-1 were determined by reversal transcription-polymerase chain reaction (RT-PCR). The protein levels of ICAM-1 and VCAM-1 were measured by enzyme linked immunosorbent assay (ELISA). NF-kappaB DNA binding activity was evaluated by electrophoretic mobility shift assay (EMSA). The results showed that NF-kappaB DNA binding activity, mRNA and protein expression of ICAM-1 and VCAM-1 were increased significantly in patients with UC, compared with normal control (P<0.05). Glucocorticoids and SASP markedly inhibited NF-kappaB activation and significantly decreased mRNA and protein expression of ICAM-1 and VCAM-1 (P<0.05). Adhesion molecules (ICAM-1 and VCAM-1) gene activation had significant positive correlation with the NF-kappaB DNA binding activity (r=0.8652 P<0.05, r=0.7902, P<0.05, respectively). We concluded that NF-kappaB is a major and essential factor in regulating the expression of adhesion molecules, it plays an important role in the pathogenesis of UC. SASP and glucocorticoids ameliorate UC via inhibition of NF-kappaB activation and reduction of adhesion molecules expression.
