Excessive alcohol consumption can lead to gastric ulcer and the present work was aimed to examine the protective effect of tetrahydrocoptisine (THC) in the model of ethanol-induced gastric ulcer in mice. Fasted mice treated with ethanol 75% (0.5ml/100g) were pre-treated with THC (10 or 20mg/kg, ip), cimetidine (100mg/kg, ip) or saline in different experimental sets for a period of 3days, and animals were euthanized 4h after ethanol ingestion. Gross and microscopic lesions, immunological and biochemical parameters were taken into consideration. The results showed that ethanol induced gastric damage, improving nitric oxide (NO) level, increased pro-inflammatory cytokine (TNF-α and IL-6) levels and myeloperoxidase (MPO) activity, as well as the expression of nuclear factor-κB (NF-κB) in the ethanol group. Pretreatment of THC at doses of 10 and 20mg/kg bodyweight significantly attenuated the gastric lesions as compared to the ethanol group. These results suggest that the gastroprotective activity of THC is attributed to reducing NO production and adjusting the pro-inflammatory cytokine, inhibited neutrophil accumulation and NF-κB expression.
Keywords: COX-2; ELISA; GABAA; Gastric ulcer; IL-1; IL-1β; IL-6; MPO; Myeloperoxidase; NF-κB; NO; Nitric oxide; Nuclear factor-κB; PGE2; Pro-inflammatory cytokines; THC; TLRs; TNF; TNF-α; Tetrahydrocoptisine; The enzyme-linked immunosorbent assay; aminobutyric acid; cNOS; constitutive NO synthase; cyclooxygenase-2; iNOS; inducible NO synthase; interleukin (IL)-1β; interleukin-1; interleukin-6; myeloperoxidase; nitric oxide; nuclear factor kappa B; prostaglandin E2; tetrahydrocoptisine; toll-like receptors; tumor necrosis factor; tumor necrosis factor-alpha.
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