Effects of Ethanol on the Gastric Mucosa

Ginseng, the Root of Panax ginseng C.A. Meyer, Protects Ethanol-Induced Gastric Damages in Rat through the Induction of Cytoprotective Heat-Shock Protein 27

“…Animal models serve as an essential tool for analyzing molecular mechanisms involved in alcohol-induced gastric diseases. Intragastric application of ethanol in animals causes acute gastric mucosal injuries characterized by linear hemorrhages, mucosal erythema and edema, scattered petechiae and erosive changes [2][3]. Furthermore, ethanol-induced gastric damages have been shown to be associated with signaling molecules that are involved in the process of inflammation, apoptosis as well as oxidative stress.…”

“…Excessive ethanol ingestion leads to gastric lesions characterized by mucosa edema, subepithelial hemorrhages, cellular exfoliation and inflammatory cell infiltration. Consequently, ethanol abuse impairs the integrity of the gastric mucosa barrier and histology [2][3]. Pharmacotherapy against ethanol-induced gastric damages has primarily been focused on the enhancement of mucosal defense mechanisms, thereby accelerating healing and preventing relapses [4][5][6][7].…”

Gastroprotective Effect of an Ethanolic Extract from Neoglaziovia variegata (Arruda) Mez (Bromeliaceae) in Rats and Mice

“…Thus, this irritant agent causes the formation of gastric ulcer. The presence of HCl enhances and accelerates this process (Laine and Weinstein, 1988;Guslandi, 1987;Szabo, 1987). The results of the investigations of ethanol-induced and ethanol/HCl-induced ulcers revealed a signifi cant Nv-EtOH-induced gastroprotective effect at higher doses.…”

Studies on gastroprotective activity of ethyl acetate leave fraction obtained from Canthium coromandelicum (Burm.f.) Alston in albino rats

“…Therefore, inhibition of prostaglandin synthesis by NSAIDs weakens the gastric mucosal system, leading to the formation of various lesions in the region of gastric epithelium [38] . Similarly, Ethanol and HCl were necrotizing substances and its excessive use results in sever gastritis, characterized by edema of mucous membrane, hemorrhages of sub epithelial tissues, cell exfoliation and infiltration of inflammatory cells [5] . In addition, ethanol also causes generation of free radicals, increase lipid peroxidation, decreasing production of gastric mucus and inhibition of PGs [39] .…”

“…In most of the countries people were habituated with alcoholic beverages. Scientifically alcohol is a necrotizing agent and its excessive use results sever gastritis with adhering symptoms like mucous membrane edema, sub epithelial hemorrhages, cell exfoliation and inflammatory cells infiltration [5] . Several classes of pharmacological agents were reported to be effective in the treatment and prevention of the acid peptic ulcer disorders.…”