Proliferation of gastric mucosal injury

The first part of the quercetin confrontation chronic drinking rat gastric mucosal cell proliferation role Objective: To study a major food flavonoids - quercetin confront the chronic drinking causes hyperplasia of the gastric mucosa and its mechanism. Methods: 40 male Sprague-Dawley rats (200 ~ 250g) were randomly divided into four groups: control group (tap water) as the sole source of drinking water, alcohol treatment group (6% alcohol), quercetin treatment group (per days 100mg/kg quercetin orally) and alcohol quercetin group (while drinking daily 100mg/kg quercetin orally). Western blot determination of proliferating cell nuclear antigen (PCNA) and cyclin D ₁ (the Cyclin D ₁ ) expression in to detect rat gastric mucosa cells proliferation. TBARS levels, protein carbonyl content was used as the indicator of oxidative damage of the gastric mucosa. The level of nitrate / nitrite, nitrotyrosine levels are used to detect the amount of gastric mucosal NO production. Also detected by Western blotting of iNOS and nNOS expression. Results: The control group compared to alcohol treatment seven days mucosal cell proliferation in rats increased significantly, accompanied by increased lipid peroxidation and protein oxidation level reduced nNOS activity decreased NO generation. These effects can be quercetin partially reversed. Conclusion: quercetin against chronic alcohol consumption caused the excessive proliferation of gastric mucosal cells. This effect is caused by free radicals in their elimination, addition, may be associated with enhanced nNOS activity, increasing NO production relevant. The role of the second part of the exogenous mesenchymal stem cell proliferation and its role within the gastric mucosal injury Objective: To study the in vitro culture and amplification of bone marrow mesenchymal stem cells (bone marrowmesenchymal stem cells, BMMSCs) repair of gastric mucosal injury . METHODS: Cultured bone marrow MSCs cell amplification of β-gal transgenic mice. The healthy male C57BL / 6 mice (body weight 18 to 22g), 90, were randomly divided into control and experimental groups, the experimental group was divided into the transplant and non-transplant group, n = 30. Experimental group with 0.2ml of pure ethanol feeding caused gastric damage model. 2 h after ethanol feeding transplanted mice after tail vein injection of MSCs (0.5 × 10 ^{6 / only); non-transplanted mice tail vein injection and transplantation group the same volume of PBS. Control mice 0.2ml normal saline 2 h after tail vein injection of MSCs (0.5 × 10 6 / only) cell transplantation. Ulcer index score to evaluate the extent of gastric mucosal injury. Immunohistochemical detection of positive cells of Brdu evaluate cell proliferation. the number and distribution of β-gal-positive cells evaluation of MSCs. Brdu-β-gal immune the double staining Evaluation of MSCs proliferation. Phytohemagglutinin UEA-1 and β-gal the double staining Evaluation of MSCs differentiation. Results: transplantation of MSCs in gastric mucosal injury can be found in the MSCs gathered at the site of injury, and the proliferation of gastric epithelial cells differentiate into; found only a small amount of MSCs cells scattered in the uninjured gastric mucosa of MSCs not found differentiation from gastric epithelial cells. Alcohol induced gastric mucosal injury after MSCs transplantation group damage index was not significantly lower in the transplant group. Conclusion: Intravenous injection of MSCs that can accumulate in the gastric mucosa injury site MSCs proliferation and differentiation, and accelerate the repair process of gastric mucosal injury in gastric mucosa injury.}