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作 者:吴丽琼[1] 张辛燕[2] 孙正[1] 张敏[1] 关晓兵[1]
机构地区:[1]北京首都医科大学口腔医学院牙周粘膜科,100050 [2]北京首都医科大学口腔医学院研究所,100050
出 处:《北京口腔医学》2011年第4期181-185,共5页Beijing Journal of Stomatology
基 金:国家自然科学基金(30872879);北京市自然科学基金(7093121);北京市中医局资助项目(JJ2007-020)
摘 要:目的观察姜黄素和乳香酸对人口腔鳞癌细胞系Tca8113增殖和凋亡的影响及对炎症代谢通路中Cox-2、5-Lox的作用。方法培养人口腔鳞癌细胞系Tca8113,采用不同浓度的姜黄素和乳香酸及二者联合处理Tca8113细胞24、48、72 h。MTT方法检测对细胞增殖的影响,AnnexinV-FITC/PI染色法流式细胞仪检测对细胞凋亡的影响,RT-PCR及W estern-b lotting法检测对Cox-2、5-Lox表达的影响。结果姜黄素和乳香酸均能抑制Tca8113细胞增殖,呈现一定的浓度和时间依赖关系。姜黄素和乳香酸均能促进Tca8113细胞凋亡,呈现一定的浓度依赖关系。两种药物联合应用抑制细胞增殖和促进凋亡的作用明显强于单独作用。姜黄素能抑制炎症代谢通路中限速酶Cox-2、5-Lox的表达,乳香酸可以抑制5-Lox表达,且有一定的剂量相关性,两者联合应用时对Cox-2、5-Lox的表达均有抑制作用,尤其是对5-Lox通路的抑制,联合应用较单独应用作用显著增强。结论姜黄素和乳香酸均能抑制口腔鳞癌细胞Tca8113的增殖,促进凋亡。姜黄素能抑制炎症代谢通路中Cox-2和5-Lox的表达。乳香酸能抑制5-Lox表达,天然植物药姜黄素和乳香酸可能通过抑制花生四烯酸代谢通路发挥口腔癌的化学预防作用。Objective To investigate the effect of curcumin and acetyl-11-keto-beta-boswellic acid (AKBA) on proliferation and apoptosis of oral squamous carcinoma cell (OSCC) line Tca8113 and on Cox-2 and 5-Lox. Methods OSCC line Tea8113 were cultured and treated with low to high doses of curcumin and AKBA separately or in combination for 24, 48, 72 h. The cells proliferation was measured by MTT assay. Cells apoptosis was examined by flow cytometer with Annexin-V FITC/PI staining. The expression of Cox-2 and 5-Lox was detected by RT-PCR and Western-blotting. Results Both curcumin and AKBA could inhibit the proliferation of Tca8113 cells in a dose-dependent and time-dependent manner. Curcumin and AKBA could induce OSCC line apoptosis in a dose-dependent manner. The cells growth inhibition and apoptosis inducing effect with combined treatment of the two compounds was much better than that of either single agent. The RT-PCR and Western-blotting showed that curcumin could inhibit the expression of Cox-2 and 5-Lox, AKBA inhibited the expression of 5-Lox, and the combined treatment of the two agents decreased the expression of 5-Lox more significantly than that of either one. Conclusion Curcumin and AKBA may serve as chemopreventive agents in oral squamous cells carcinoma by inhibiting arachidonic acid (AA) metabolism pathway.
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