青年科学工作者论坛2007年第4期

沈秀华  蔡威  汤庆娅 冯一 吴江

上海新华医院营养中心 上海交通大学医学院营养系 ，上海200092

 

摘要 ：目的 观察营养性肥胖大鼠氧应激、抗氧化能力的改变。方法 ：20只断乳的SD雄性大鼠（75-80g）随机分两组，每组10只。膳食诱导肥胖组（DIO组）喂饲高脂饲料，对照组喂饲基础饲料，10周后取血及睾周、肾周脂肪组织。用ELISA法检测血浆8-表氧-前列腺素2α（8-epi-PGF2α）、二硫代双硝基苯甲酸法测血浆抗氧化酶GPX（谷胱甘肽过氧化物酶）活性、黄嘌呤氧化酶法测血浆SOD（超氧化物歧化酶）活性，HPLC（高效液相色谱仪）测血浆维生素E并经血脂校正。同时测血浆空腹血糖、胰岛素、三酰甘油（TG）、总胆固醇(TCHL)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)等糖脂代谢指标。结果 高脂喂养10周后，DIO组的各项肥胖指标（体重、腹部脂肪/体重、Lee’s指数）均高于对照组（P<0.01）；血浆8-epi-PGF2α增高，SOD和GPX 活性、经血脂校正后的血浆维生素E 水平显著显著降低（P<0.05）。另有脂代谢紊乱，空腹血糖与胰岛素也显著高于对照组。结论高脂喂养肥胖大鼠模型显示血脂升高并伴有胰岛素抵抗；氧应激水平增高而抗氧化能力下降。

关键词：肥胖，大鼠，氧应激

中图分类号：  R151.2  R589.2        文献标识码：A

 

SHEN Xiuhua, CAI Wei，TANG Qingya ,FENG Yi,et al.

 Department of Nutrition,  School of Medcine, Shanghai Jiao Tong University,

 Clinical Nutrition Center, Shanghai XinHua Hospital,Shanghai 200092 , China

 

Abstract   Objective:To evaluate the levels of antoxidative  indexes , lipid metabolism and glycometabolism in high fat diet-induced obese rats .Methods: A rat model of high diet-induced obesity  was established by feeding weaning male Sprague-Dawley rats with high-fat diet for 10 weeks. Plasma 8-epi-prostaglandin-F₂ (8-epi-PGF₂), α-tocopherol, superoxide dismutase activity (SOD), and glutathione peroxidase activity (GPx) were detected. Parameters of lipid metabolism and glycometabolism were also tested using standard methods.Results: After 10 weeks, the high fat diet-induced obesity and lipid metabolism and glycometabolism disorders of  obese rats (n=10) were found. In comparison with the control group (n=10) plasma 8-epi-PGF₂ levels of  obese rats were more higher , while plasma adjusted α-tocopherol (divided by plasma lipids), SOD and GPX activities of  obese rats were more lower. Conclusions: Obesity induced by high-fat feeding involves increased oxidative stress and decreased antioxidant capacity.

Keywords: obesity, rat ,oxidative stress

论著 
文章编号：1000-8020（2007）04-0445-04 

EPA、DHA对人单核细胞NO的产生、iNOSmRNA表达及NFκB活性的影响    

夏延平 冯翔 陈裕明 苏宜香

中山大学公共卫生学院营养系，广州 510080  

摘 要：目的 探讨n-3多不饱和脂肪酸(Eicosapentaenoic acid EPA, Docosahexenoic acid DHA)对人单核细胞炎症因子一氧化氮（Nitric oxide, NO）的分泌和诱导型NO合酶（Inducible NO synthase mRNA, iNOSmRNA）表达的影响，以及EPA、DHA对核转录因子（Nuclear factor,NFκB）与DNA结合活性的影响。方法：硝酸还原酶法测定NO的含量，RT-PCR技术分析iNOSmRNA表达水平，凝胶电泳迁移实验检测NFκB与DNA的结合活性。结果：EPA、DHA在10μg/ml～20μg/ml浓度范围内能够降低体外培养的人外周血单核细胞NO的分泌和iNOSmRNA的表达并降低NFκB的DNA结合活性。结论：EPA、 DHA能够抑制单核细胞炎症因子NO的产生，减少iNOSmRNA的表达，并通过抑制信号转导途径中NFκB与DNA的结合活性这一通路来抑制炎症因子分泌，产生抑制炎症作用。

关键词 ：EPA  DHA  单核细胞  一氧化氮  诱导型一氧化氮合酶 核转录因子-κB

中图分类号：R392.11   文献标识码：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

论著 
文章编号：1000-8020（2007）04- 0443-03

过量碘对甲状腺细胞凋亡的影响

徐健 刘小立 杨雪锋1李兰英2 孙云2 孙秀发1

深圳市慢性病防治院，深圳  518020 

摘要：目的  通过研究观察过量碘对甲状腺细胞凋亡相关基因的影响，探讨过量碘促进甲状腺细胞凋亡的机制。方法  选取FRTL细胞系为研究对象，正常对照组培养基内不加碘，过量碘组分别含碘（碘化钾）1、5、10、50和100mmol/L，培养24h，流式细胞术测定调亡细胞的比例，荧光定量PCR法测定5、10、50mmol/L碘剂量组fas、fasL、Bcl-2和Bax的mRNA水平。结果  与正常对照组比较，10、50、100mmol/L碘剂量组FRTL细胞凋亡率显著升高（P<0.05）。5mmol/L碘组各项指标与正常对照组比较无显著性差异。10mmol/L、50mmol/L碘组fasL和Bax mRNA水平较正常对照组显著升高（P<0.05），Bcl-2 mRNA水平较正常对照组显著下降（P<0.05）。10mmol/L碘组fas与正常对照组比较无显著性差异，50mmol/L碘组fas较正常对照组显著升高（P<0.05）。结论  过量碘可通过调节fas、fasL、Bcl-2及Bax的表达而促进影响甲状腺细胞凋亡的发生。

关键词：细胞凋亡   过量碘  Fisher大鼠甲状腺滤泡上皮细胞

中图分类号：R152.4+1               文献标识码：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