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青年科學(xué)工作者論壇2007年第4期

論著(zhù)
文章編號:1000-8020(2007)04-0443-03
營(yíng)養性肥胖大鼠氧應激水平的改變
沈秀華  蔡威  湯慶婭 馮一 吳江
上海新華醫院營(yíng)養中心 上海交通大學(xué)醫學(xué)院營(yíng)養系 ,上海200092
 
摘要 :目的 觀(guān)察營(yíng)養性肥胖大鼠氧應激、抗氧化能力的改變。方法 20只斷乳的SD雄性大鼠(75-80g)隨機分兩組,每組10只。膳食誘導肥胖組(DIO組)喂飼高脂飼料,對照組喂飼基礎飼料,10周后取血及睪周、腎周脂肪組織。用ELISA法檢測血漿8-表氧-前列腺素2α(8-epi-PGF2α)、二硫代雙硝基苯甲酸法測血漿抗氧化酶GPX(谷胱甘肽過(guò)氧化物酶)活性、黃嘌呤氧化酶法測血漿SOD(超氧化物歧化酶)活性,HPLC(高效液相色譜儀)測血漿維生素E并經(jīng)血脂校正。同時(shí)測血漿空腹血糖、胰島素、三酰甘油(TG)、總膽固醇(TCHL)、低密度脂蛋白膽固醇(LDL-C)、高密度脂蛋白膽固醇(HDL-C)等糖脂代謝指標。結果 高脂喂養10周后,DIO組的各項肥胖指標(體重、腹部脂肪/體重、Lee’s指數)均高于對照組(P<0.01);血漿8-epi-PGF2α增高,SOD和GPX 活性、經(jīng)血脂校正后的血漿維生素E 水平顯著(zhù)顯著(zhù)降低(P<0.05)。另有脂代謝紊亂,空腹血糖與胰島素也顯著(zhù)高于對照組。結論高脂喂養肥胖大鼠模型顯示血脂升高并伴有胰島素抵抗;氧應激水平增高而抗氧化能力下降。
關(guān)鍵詞:肥胖,大鼠,氧應激
中圖分類(lèi)號:  R151.2  R589.2        文獻標識碼:A
 
Oxidative stress in a rat model of dietary-induced obesity
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{alpha} (8-epi-PGF2{alpha}), 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{alpha} 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

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文章編號:1000-8020200704-0445-04 

EPADHA對人單核細胞NO的產(chǎn)生、iNOSmRNA表達及NFκB活性的影響    

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  

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EPADHA對核轉錄因子Nuclear factor,NFκB)與DNA結合活性的影響。方法:硝酸還原酶法測定NO的含量,RT-PCR技術(shù)分析iNOSmRNA達水平,凝膠電泳遷移實(shí)驗檢測NFκBDNA的結合活性。結果EPADHA10μg/ml20μg/ml濃度范圍內能夠降低體外培養的人外周血單核細胞NO的分泌和iNOSmRNA的表達并降低NFκBDNA結合活性。結論:EPA DHA能夠抑制單核細胞炎癥因子NO的產(chǎn)生,減少iNOSmRNA的表達,并通過(guò)抑制信號轉導途徑中NFκBDNA的結合活性這一通路來(lái)抑制炎癥因子分泌,產(chǎn)生抑制炎癥作用。

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 EPADHA on the secretion of NOexpression 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 NOexpression 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 NOexpression 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 productioniNOSmRNA 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

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文章編號:1000-8020200704- 0443-03

過(guò)量碘對甲狀腺細胞凋亡的影響

徐健 劉小立 楊雪鋒1李蘭英2 孫云2 孫秀發(fā)1

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,探討過(guò)量碘促進(jìn)甲狀腺細胞凋亡的機制。方法  選取FRTL細胞系為研究對象,正常對照組培養基內不加碘,過(guò)量碘組分別含碘(碘化鉀)151050100mmol/L,培養24h,流式細胞術(shù)測定調亡細胞的比例,熒光定量PCR法測定51050mmol/L碘劑量組fasfasLBcl-2BaxmRNA水平。結果  與正常對照組比較,1050100mmol/L碘劑量組FRTL細胞凋亡率顯著(zhù)升高(P<0.05)。5mmol/L碘組各項指標與正常對照組比較無(wú)顯著(zhù)性差異。10mmol/L50mmol/L碘組fasLBax mRNA水平較正常對照組顯著(zhù)升高(P<0.05),Bcl-2 mRNA水平較正常對照組顯著(zhù)下降(P<0.05)。10mmol/L碘組fas與正常對照組比較無(wú)顯著(zhù)性差異,50mmol/L碘組fas較正常對照組顯著(zhù)升高(P<0.05)。結論  過(guò)量碘可通過(guò)調節fasfasLBcl-2Bax的表達而促進(jìn)影響甲狀腺細胞凋亡的發(fā)生。

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 JianLIU XiaoliYANG XuefengLI Lanyinget al.

Shenzhen Center for Disease Control and Prevention, Shenzhen 518020, China

AbstractObjective 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 wordscell apoptosis, iodine excess , FRTL

 

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