Protective effect of camellia oil against ethanol-induced acute injury of gastrointestinal mucosa in mice

• Main Authors: Pang-Shuo Tu, 杜邦碩
• Other Authors: 顏國欽
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/76349175360739580297

碩士 === 國立中興大學 === 食品暨應用生物科技學系所 === 104 === The incidence of alcohol-ulcer is increasing in the recent years because of modern lifestyle changes and stress to cause the drinking culture prevailed. Excessive alcohol consumption leads to gastric mucosal damage, and severe cases cause bleeding, ulceration or perforation forming. Camellia oil (Camellia oleifera Abel.) is commonly used in Taiwan and has been shown with health effects for gastrointestinal tract in folk medicine. Our previous study has been demonstrated that camellia oil exerts the potential antioxidant activity to prevent the gastrointestinal mucosal damage caused by ketoprofen. However, the preventive effect of camellia oil on ethanol-induced ulcer remains unclear. The aim of this study was to evaluate the preventive effect of camellia oil on ethanol-induced acute gastric injury in vitro and in vivo. In in vitro study, our results showed that ethanol (3% to 7%) was cytotoxic to RGM-1 cells to cause cell shrinkage. RGM-1 cells pretreated with camellia oil (50 and 75 μg/mL) reduced the decrease of ethanol-induced cell viability. Camellia oil reduced apoptotic cells induced by ethanol. In addition, camellia oil possibly down-regulated pro-apoptotic proteins such as cytochrome c, Bax and caspase-3 and up-regulated the anti-apoptotic proteins such as Bcl-2 and heat shock protein (HSP) 90, 70, 60 and 32 expressions. Results from wound-healing assay showed that pretreatment with camellia oil (50 and 75 μg/mL) enhanced the ability of migration in ethanol-induced RGM-1 cells. In animal experiments, pre-feeding mice with camellia oil (1 and 2 mL/kg b.w.) effectively improved ethanol (5 mL/kg b.w.)-induced gastric injury and oxidative damage, enhanced superoxide dismutase (SOD), catalase (CAT), glutathion peroxidase (GPx), and other antioxidant enzymes activity, and suppressed malondialdehyde (MDA) and nitrite oxide (NO) content. The results from histological evaluation revealed that camellia oil inhibited the inflammatory cytokines such as TNF-α, IL-6, COX-2 and iNOS expression in ethanol-induced gastric tissue. Furthermore, camellia oil ameliorated the decrease of gastric tissue defensive factors (such as HSP90, HSP70, HSP60, HSP32 and PGE2) and exhibited a reduction of the pro-apoptotic proteins, including cytochrome c, Bax and caspase-3 expression, and an induction of the anti-apoptotic protein Bcl-2, leading to improvement of the ethanol-induced gastric lesions in a dose-dependent effect. The camellia oil showed the better preventive effects when compared with olive oil at the dose of 2 mL/kg b.w. administration in mice, and Lansoprazole-treated group had a similar ability. In summary, camellia oil has the potential to ameliorate the oxidative damage of gastric damage in vitro and in vivo through suppressing apoptosis and inflammatory effects and enhancing the HSP expressions and PGE2, resulting in protection of the ethonal-induced gastric injury.