論著(zhù)
文章編號:1000-8020(2007)04-0445-
EPA、DHA對人單核細胞NO的產(chǎn)生、iNOSmRNA表達及
夏延平 馮翔 陳裕明 蘇宜香
中山大學(xué)公共衛生學(xué)院營(yíng)養系,廣州 510080
摘 要:目的 探討n-3多不飽和脂肪酸(Eicosapentaenoic acid EPA, Docosahexenoic acid DHA)對人單核細胞炎癥因子一氧化氮(Nitric oxide, NO)的分泌和誘導型NO合酶(Inducible NO synthase mRNA, iNOSmRNA)表達的影響,以及EPA、DHA對核轉錄因子
關(guān)鍵詞 :EPA DHA 單核細胞 一氧化氮 誘導型一氧化氮合酶 核轉錄因子-κB
中圖分類(lèi)號:R392.11 文獻標識碼:A
Effects of EPA,DHA on the secretion of NO,expression of iNOSmRNA and DNA-binding activity of NFκB in human monocyte
XIA Yanping, FENG Xiang, CHEN Yuming, SU yixiang
Faculty of Medical Nutrition, School of Public Health, Sun Yat-sen University, Guang zhou 510080, China
Abstract: Objective To study the effect of n-3 polyunsaturated fatty acids(EPA, DHA) on the production of NO,expression of iNOSmRNA and DNA-binding activity of NFκB in human monocyte. Methods: RT-PCR and enzyme reduction method were used to measure the expression of iNOSmRNA and production of NO respectively. The DNA-binding activity of NFκB was assessed by EMSA. Results: EPA, DHA can decrease the production of NO,expression of iNOSmRNA and DNA-binding activity of NFκB between the dosage of 10μg/ml and 20μg/ml in human peripheral blood monocyte in vitro. Conclusion: EPA, DHA have inhibitory effects on NO production,iNOSmRNA expression and DNA-binding activity of NFκB in monocyte. It indicates EPA, DHA suppress the production of inflammatory mediators via the NFκB signal transduction pathways in human monocyte, accordingly suppress inflammatory responses.
Keywords: EPA DHA monocyte NO iNOSmRNA NFκB
論著(zhù)
文章編號:1000-8020(2007)04- 0443-03
過(guò)量碘對甲狀腺細胞凋亡的影響
深圳市慢性病防治院,深圳 518020
摘要:目的 通過(guò)研究觀(guān)察過(guò)量碘對甲狀腺細胞凋亡相關(guān)基因的影響,
關(guān)鍵詞:細胞凋亡 過(guò)量碘 Fisher大鼠甲狀腺濾泡上皮細胞
中圖分類(lèi)號:R152.4+1 文獻標識碼:A
Study on the effect of iodine excess on cell apoptosis in rat thyroid cells (FRTL)
XU Jian,LIU Xiaoli,YANG Xuefeng,LI Lanying,et al.
Shenzhen Center for Disease Control and Prevention, Shenzhen 518020, China
Abstract:Objective To explore the mechanism of iodine over-treatment to FRTL cell on the cell apoptosis through observing the cell apoptosis related gene. Methods The cells were treated with potassium iodide (0, 5, 10, 50 and 100mmol/L). After treatment 24 hours, the cells were collected and analyzed by flow cytometry. The mRNA levels of fas,fasL,Bcl-2 and Bax of 50mmol/L and 100mmol/L groups were determined with real-time PCR. Results Compared with the normal control group, the rates of cell apoptosis of 10,50 and 100mmol/L iodine groups increased significantly. Compared with the normal control group, the mRNA levels of fasL and Bax in 10 and 50mmol/L iodine groups increased significantly while the level of Bcl-2 decreased significantly. There was no significant difference fas mRNA levels between the normal control group and 10mmol/L iodine group, but the fas mRNA level in 50mmol/L iodine group increased significantly. Conclusion The excessive iodine treatment increased the apoptosis of FRTL cells which might be related to gene expressions of fas, fasL, Bcl-2 and Bax.
Key words:cell apoptosis, iodine excess , FRTL