Yini Ye

Effect of polysaccharides from Angelica sinensis on gastric ulcer healing.

Our previous study showed that a crude extract from Angelica sinensis (ASCE), which mainly consisted of polysaccharides, significantly promoted migration and proliferation of normal gastric epithelial cells. These results strongly suggest that ASCE has a direct wound healing effect on gastric mucosa. However, there is no report concerning the effect of ASCE on gastric ulcer healing in animal models. In this study, we found that ASCE promoted ulcer healing. The area of the ulcer was reduced. This was accompanied with a significant increase in mucus synthesis when compared with the control. Angiogenesis was inhibited by the treatment of ASCE. Cell proliferation, ODC and EGFR protein expression was not affected in this process. Thus, the mechanism of how ASCE accelerates ulcer healing in addition to its effect on mucus synthesis remains to be investigated.

Protective role of cyclooxygenase inhibitors in the adverse action of passive cigarette smoking on the initiation of experimental colitis in rats

Clinical and experimental findings had indicated that cigarette smoke exposure, and cyclooxygenase-2, are strongly associated with inflammatory bowel disease. The present study aimed to evaluate the role of cyclooxygenase-2 in the pathogenesis of experimental inflammatory bowel disease as well as in the adverse action of cigarette-smoke exposure. Rats were pretreated with different cyclooxygenase-2 inhibitors (indomethacin, nimesulide, or SC-236 (4-[5-(4-chlorophenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benzenesulfonamide)) along with cigarette-smoke exposure before 2,4,6-trinitrobenzenesulfonic acid-enema. Results indicated that pretreatment with cyclooxygenase-2 inhibitors not only protected against 2,4,6-trinitrobenzenesulfonic acid-induced inflammatory bowel disease, but also attenuated the potentiating effect of cigarette-smoke exposure on colonic damage. Furthermore, the colonic cyclooxygenase-2 protein and mRNA expression was markedly induced by 2,4,6-trinitrobenzenesulfonic acid-enema, and it was potentiated further by cigarette-smoke exposure, while the cyclooxygenase-1 expression was not changed. The present study suggests that the highly induced cyclooxygenase-2 expression not only plays a pathogenic role in 2,4,6-trinitrobenzenesulfonic acid-induced inflammatory bowel disease, but also contributes to the adverse action of cigarette-smoke exposure on this disorder.

Interaction of Cigarette Smoking with Cyclooxygenase-2 on Ulcerative Colitis-Associated Neoplasia in Mice

The interactions of cigarette smoking with COX-2 on colitis and colitis-associated adenoma formation were studied. Mice were induced with colitis and exposed to cigarette smoke (CS) and/or SC236 (a COX-2 inhibitor). Results indicated that CS did not alter acute colonic inflammation. Addition of SC236 abolished the induction of proliferation and oxidative damage by colitis. Chronic SC236 treatment abolished the promoting effect of CS on colonic adenoma formation, via suppression of COX-2- and VEGF-mediated proliferation and angiogenesis, and reversed bcl-2-mediated inhibition of apoptosis by CS. To conclude, COX-2 inhibitor could be an implication on cancer prevention in smokers with chronic colitis.