Wang Zhongzhi, Hasegawa Junichi, Wang Xinhui, Matsuda Akiko, Tokuda Takahiro, Miura Norimasa, Watanabe Tatsuo
Division of Pharmacotherapeutics, Department of Pathophysiological and Therapeutic Science, School of Medicine, Tottori University Faculty of Medicine, Yonago 683-8503, Japan.
Yonago Acta Med. 2011 Mar;54(1):11-9. Epub 2011 Mar 1.
We investigated the mechanism underlying the protective effects of ginger against gastric damage induced by aspirin in rats. Gastric mucosal lesions were produced by orally administering 200 mg/kg aspirin suspended in 1% carboxymethylcellulose solution to pyloric-ligated male Wistar rats. Ginger powder (200 mg/kg) markedly reduced the aspirin-induced gastric hemorrhagic ulcer area. The total acidity of gastric juice was not significantly influenced by aspirin or ginger. Ginger powder did not affect the aspirin-induced reduction in mucosal prostaglandin E2 (PGE2) content; however, it did ameliorate the aspirin-induced increases in mucosal activity of the inducible form of NO synthase (iNOS) and plasma tumor necrosis factor (TNF)-α and interleukin (IL)-1β levels. In the next experiment, high and low doses of 6-gingerol and 6-shogaol were used instead of ginger powder in the same experimental model to examine their roles in the anti-ulcer mechanism of ginger. Both 6-gingerol and 6-shogaol reduced aspirin induced ulcer formation, mucosal iNOS and plasma TNF-α and IL-1β levels. In conclusion, ginger powder prevents the aspirin induced gastric ulcer formation by reducing mucosal iNOS activity and the plasma levels of inflammatory cytokines but does not affect gastric juice or acid production or mucosal PGE2 content. This protective effect of ginger powder against gastric ulcers may be attributable to both gingerol and shogaol.
我们研究了生姜对大鼠阿司匹林诱导的胃损伤保护作用的潜在机制。通过向幽门结扎的雄性Wistar大鼠口服200mg/kg悬浮于1%羧甲基纤维素溶液中的阿司匹林来产生胃黏膜损伤。生姜粉(200mg/kg)显著减少了阿司匹林诱导的胃出血性溃疡面积。胃液的总酸度未受到阿司匹林或生姜的显著影响。生姜粉未影响阿司匹林诱导的黏膜前列腺素E2(PGE2)含量的降低;然而,它确实改善了阿司匹林诱导的诱导型一氧化氮合酶(iNOS)黏膜活性增加以及血浆肿瘤坏死因子(TNF)-α和白细胞介素(IL)-1β水平升高。在接下来的实验中,在相同实验模型中使用高剂量和低剂量的6-姜酚和6-姜烯酚代替生姜粉,以研究它们在生姜抗溃疡机制中的作用。6-姜酚和6-姜烯酚均减少了阿司匹林诱导的溃疡形成、黏膜iNOS以及血浆TNF-α和IL-1β水平。总之,生姜粉通过降低黏膜iNOS活性和炎症细胞因子的血浆水平来预防阿司匹林诱导的胃溃疡形成,但不影响胃液或胃酸分泌或黏膜PGE2含量。生姜粉对胃溃疡的这种保护作用可能归因于姜酚和姜烯酚两者。