Lee Jeong-Sang, Oh Tae-Young, Kim Young-Kyung, Baik Joo-Hyun, So Sung, Hahm Ki-Baik, Surh Young-Joon
College of Pharmacy, Seoul National University, Seoul 151-742, South Korea.
Mutat Res. 2005 Nov 11;579(1-2):214-24. doi: 10.1016/j.mrfmmm.2005.03.027. Epub 2005 Aug 10.
There are multiple lines of compelling evidence from epidemiologic and laboratory studies supporting that frequent consumption of green tea is inversely associated with the risk of chronic human diseases including cancer. The chemopreventive and chemoprotective effects of green tea have been largely attributed to antioxidative and anti-inflammatory activities of its polyphenolic constituents, such as epigallocatechin gallate. The present study was designed to evaluate the efficacy of green tea polyphenols in protecting against alcohol-induced gastric damage and to elucidate the underlying mechanisms. Intragastric administration of ethanol to male Sprague-Dawley rats caused significant gastric mucosal damage, which was accompanied by elevated expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) as well as transient activation of redox-sensitive transcription factors, such as NF-kappaB and AP-1, and mitogen-activated protein kinases (MAPKs). Oral administration of the green tea polyphenolic extract (GTE) significantly ameliorated mucosal damages induced by ethanol and also attenuated the ethanol-induced expression of COX-2 and iNOS. Inactivation of MAPKs, especially p38 and ERKl/2, by GTE might be responsible for inhibition of ethanol-induced expression of COX-2 and iNOS.
流行病学和实验室研究提供了多条令人信服的证据,支持经常饮用绿茶与包括癌症在内的慢性人类疾病风险呈负相关。绿茶的化学预防和化学保护作用很大程度上归因于其多酚成分(如表没食子儿茶素 gallate)的抗氧化和抗炎活性。本研究旨在评估绿茶多酚对酒精诱导的胃损伤的保护作用,并阐明其潜在机制。对雄性Sprague-Dawley大鼠进行胃内乙醇给药会导致显著的胃黏膜损伤,同时伴有环氧合酶-2(COX-2)和诱导型一氧化氮合酶(iNOS)表达升高,以及氧化还原敏感转录因子(如NF-κB和AP-1)和丝裂原活化蛋白激酶(MAPKs)的短暂激活。口服绿茶多酚提取物(GTE)可显著改善乙醇诱导的黏膜损伤,并减弱乙醇诱导的COX-2和iNOS表达。GTE对MAPKs(尤其是p38和ERK1/2)的失活可能是抑制乙醇诱导的COX-2和iNOS表达的原因。