Ulceration in the gastrointestinal (GI) mucosa is a common disorder in humans. It has been shown that cigarette smoking is closely related to the increase of peptic ulcer and also plays an inhibitory role on ulcer healing. However, the underlying mechanisms by which cigarette smoke exerts these adverse effects remain largely unknown. It is perhaps partly due to the complexity of chemical compositions in the smoke and furthermore their pathological actions are largely undefined. In this review, we have highlighted the potential adverse effects of the toxic chemical components in cigarette smoke and summarized their possible mechanisms of actions on ulcer formation and healing in the GI tract. We also discuss in detail how cigarette smoke disturbs cell proliferation, influences mucus synthesis and secretion, delays blood vessel formation, and interferes the innate immune responses during ulceration and repair in the GI mucosa.

The present study was conducted to investigate the underlying mechanisms and effective components of Polygonum hydropiper in ethanol-induced acute gastric mucosal lesions. The ethanol extract was purified on an AB-8 macroporous resin column and eluted with 60% ethanol and was then injected into the HPLC system for quantitative analysis. Sprague-Dawley rats were orally pretreated with P. hydropiper extract (PHLE; 50, 100, and 200 mg/kg) for 5 days and then absolute ethanol was administered to induce gastric mucosal damage. One hour after ethanol ingestion, the rats were euthanized and stomach samples were collected for biochemical analysis. Antioxidant enzymes and anti-inflammatory cytokines were quantified. Western blotting was used to detect the expression levels of proteins. Cell proliferation was assayed by CCK-8 assays. The proportion of total flavonoids in the final extract of P. hydropiper was 50.05%, which contained three major bioactive flavonoid constituents, including rutin, quercitrin, and quercetin. PHLE significantly increased cell viability and effectively protected human gastric epithelial cells-1 against alcohol-induced damage in vitro. PHLE pretreatment attenuated gastric mucosal injuries in a dose-dependent manner in rats, and increased the activity of superoxide dismutase, glutathione peroxidase, and glutathione, and decreased the levels of malondialdehyde in gastric tissue. Pretreatment with PHLE also reduced the generation of the proinflammatory cytokines tumor necrosis factor-a and interleukin-1b in gastric tissue by downregulating the expression of nuclear factor-kappa B. PHLE exerted protective effects against gastric injury through antioxidant and anti-inflammatory pathways. Flavonoids might be the main effective components of P. hydropiper against gastric mucosal injury.

No abstract

Background: Fengliao-Changwei-Kang(FCK), the Chinese patent drug, is a famous traditional Chinese herbal medicine formula. It has a

Background/Aim. Cell proliferation and the regulation of protein expression play an important role in gastritis, but in chronic superficial gastritis (CSG), they are rarely reported. The aim of this study was to determine the relationship between the expression of nuclear factor kappa B (NF-?B) and regulatory proteins and the rat CSG. Methods. The CSG rat model was established artificially, by chemical agents and irregular diet. The expression of epidermal growth factor receptor (EGFR) and proliferating cell nuclear antigen (PCNA) in the gastric mucosa of CSG rats was measured by immunohistochemistry, while mRNA expression levels of NF-?B p65 were detected by in situ hybridization. Results. There was more obvious infiltration of inflammatory cells in the gastric mucosa of CSG rats than in that of control rats, and the inflammation score was significantly increased. The expression levels of PCNA, EGFR, and NF-?B p65 mRNA in the gastric mucosal cells of CSG model rats increased significantly. Correlation analysis showed that the inflammation score was positively correlated with the expression levels of NF-?B p65 mRNA and EGFR, while it presented no significant correlation with the expression level of PCNA. In addition, there was a significant positive correlation between NF-?B p65 mRNA and EGFR levels. Conclusion. High expression of NF-?B and EGFR plays an important role in the occurrence and progression of CSG, and it is significantly positively correlated with the degree of inflammation in the gastric mucosa. Therefore, changes in NF-?B and EGFR expression may be used as important indicators for the assessment of CSG; changes in their expression levels are helpful to assess the degree of gastric mucosal lesions and progression of CSG.