吸煙被視為造成牙周病的一項危險因子，其會造成牙周囊袋加深、牙周附連喪失、齒槽骨破壞及牙齒搖動增加等症狀。nicotine是煙草中最主要的生物鹼，其對牙周組織的破壞已被廣泛地研究，但鮮少有研究探討nicotine 對細胞訊息傳遞的影響，最近吾等發現尼古丁會誘發人類牙齦造纖維母細胞cycloxygenase-2 (COX-2) mRNA 與protein 的表達前列腺素(prostaglandin) E2 與發炎和免疫反應過程中扮演相當重要的角色，PGE2 位於細胞膜上的受體皆與G-protein 結合，分別是EP1、EP2、EP3、EP4 四種subtypes，迄今鮮少有研究探討尼古丁與PGE2 受體的訊息傳遞路徑的影響。所以本研究欲以組織培養法，培養人類牙齦造纖維母細胞來探討尼古丁對PGE2 的影響。人類牙齦造纖維母細胞會表達EP1, EP2, andEP4。尼古丁會促進EP1╱4 表達。吸煙被造成牙周組織的影響可能是經由EP1╱4訊息傳遞路徑。 It has long been recognized that there is an association between the use of tobacco and periodontal disease. Nicotine, the most abundant tobacco alkaloid, is considered the most important etiologic factor in cigarette smoking. Recently, our study has shown that nicotine can induce COX-2 mRNA and protein expression in human gingival fibroblasts. As far as we know, little is known about whether chemical interaction can modulate nicotine-induced PGE2 receptors expression. In this study, we will culture human gingival fibroblast cell line HGF-1 to investigate the effect of nicotine by EP1~4 pathways. HGF was found to express EP1, EP2, and EP4. Nicotine was found to elevate EP1 and EP4 in a dose-dependent manner (p<0.05). Taken together, the activation of EP1╱4 expression by nicotine suggests a potential role for nicotine in the pathogenesis of smoking-associated periodontal disease.
