| Objective: To investigate the mechanisms that quercetin, a major flavonoid in the human diet, plays an important role in antiproliferative effects on hyperproliferation in gastric mucosa treated by chronic ethanol intake.Methods: Forty male Sprague-Dawley rats (200-250 g) were randomly divided into four groups: control group (tap water ad libitum), ethanol treated group (6 % (v/v) ethanol as only water intake), quercetin treated group (intragastric gavage 100 mg/kg of quercetin per day), and ethanol plus quercetin co-treated group (provided quercetin in rats during their 6% ethanol drinking). Expression levels of PCNA and cyclin D1 were detected by Western blot to assay cell proliferation in rat gastric mucosa. To demonstrate the influence of quercetin on the production of ROS/RNS extracellular, changes in tissue thiobarbituric acid reactive substance levels (TBARS), protein carbonyl content and the NOx (nitrite and nitrate) and nitrotyrosine (NT) levels were determined. The activity of iNOS andnNOS were also detected by Western blot.Results: Compared to control animals, cell proliferation in the gastricmucosa of animals subjected to ethanol treatment for 7 days wassignificant increased, accompanied by an increase in ROS generation anddecrease in NO generation and nNOS activity. This function wasabolished by the co- administration of quercetin.Conlusion: Antioxidant action of quercetin resides, in part, in its ability tostimulate nNOS and enhance production of NO that would interact withendogenously produced reactive oxygen to inhibit hyperproliferation inchronic ethanol consumption gastric mucosa. Objective: To explore the implication of cultured mesenchymal stem cells (MSCs) in the treatment of damaged gastric mucosa.Methods: MSCs from transgenic mice expressingβ-gal were cultured and expanded ex vivo. Ninety male wild-type C57BL/6 mice (18-22 g) were randomly divided into three groups: one control group and two gastric injury groups. Gastric injury was induced by gavage with 0.2ml pure ethanol, control mice received saline. One group of mice with mucosa injury and control animals were received MSCs (0.5×10~6) by intravenous injection, while another anamals were received saline as the same way as MSCs injection. The degree of gastric injury was evaluated by calculating the ulcer index (UI). Cells derived from MSCs were identified by immunohistochemistry using anti-β-gal antibody. The proliferation of MSCs was identified by double staining using anti-β-gal and anti-Brdu antibodies, while the differentiation of MSCs was identified by anti-β-gal antibody and UEA-1 lectin, a marker of gastric epithelial cells double staining.Results:β-gal-positive, expanded MSCs could be found homing in both normal and damage gastric mucosa. Also, significant amounts and localization of MSCs correlated to the severity of mucosa. In MSCs-transplanted mice, rapid regeneration of gastric mucosa was accompanied by rapid proliferation of MSCs, in which the UI was significantly decreased than those of saline-transplanted mice. Base on UEA-1 andβ-gal double staining, there was few number of MSCs differentiating into gastric epithelial cells in 72 h after transplantation. No UEA-1 positive staining could be found inβ-gal positive cells of control mice.Conlusion: These data suggest that transplantation of MSCs in a damaged gastric mucosa model accelerate gastric wound healing as the homing and proliferation of exdogenous MSCs, in part, in its ability to transdifferentiate into the epithelium. The MSCs transplantation may be a feasible approach to managing patients with gastric damage, such as gastric ulcer; however, the mechanism by which MSC cells induce enhanced tissue repair is not yet known and needs further investigation. |
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