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脂肪因子Apelin-13对3T3-L1脂肪细胞水通道蛋白7基因表达的影响

Effects of Apelin-13 on Aquaporin 7 expression in 3T3-L1 adipocytes
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摘要 目的 探讨脂肪因子Apelin-13对3T3-L1脂肪细胞水通道蛋白7(AQP7)基因表达的影响.方法 体外培养3T3-L1脂肪细胞,以油红O染色鉴定为成熟脂肪细胞后,分为阴性对照组(无干预),不同浓度(10^-9、10^-8、10^-7、10^-6nmol/L) Apelin-13干预组(均干预24 h),阳性对照组(10^-5 nmol/L罗格列酮干预24 h)和10^-7 nmol/L Apelin-13干预不同时间(0、12、24、36、48 h)组.用反转录-聚合酶链反应检测各组细胞AQP7 mRNA表达水平.结果 阴性对照组、10^-9、10^-8、10^-7、10^-6 nmol/L Apelin-13和阳性对照组AQP7表达水平分别为(0.22±0.02)、(0.29±0.07)、(0.36±0.05)、(0.43±0.05)、(0.31±0.06)、(0.32±0.08),阳性对照组与阴性对照组之间差异有统计学意义(P<0.05);与阴性对照组比较,10^-8、10^-7 nmol/L Apelin-13能明显刺激AQP7 mRNA表达(P <0.05);10^-8、10^-7 nmol/L Apelin-13组与阳性对照组比较,10^-7 nmol/L Apelin-13能明显刺激AQP7 mRNA表达(P<0.05);10^-8、10^-7 nmol/L Apelin-13组间差异无统计学意义.在时间组中,10^-7 nmol/L Apelin-13的0、12、24、36、48 h各组灰度比值分别为(0.27±0.09)、(0.43±0.07)、(0.55±0.10)、(0.42±0.08)、(0.33±0.09),12、24、36 h组AQP7 mRNA表达较0h组能明显刺激AQP7 mRNA表达(P<0.05),作用24 h表达最高;但12、24、36h3组之间AQP7mRNA表达差异无统计学意义.结论 Apelin-13在一定程度上能增加3T3-L1脂肪细胞AQP7 mRNA表达的水平,并分别以10^-7 nmol/L和24 h为最佳作用浓度和时间. Objective To investigate a dependent manner of adipocykine Apelin-13 on Aquaporin (AQP7) gene expression in 3T3-L1 adipocyte.Methods The fully differentiated 3T3-L1 adipocytes identified by red oil O staining were divided into groups including negative control group,Apelin-13 treated groups with concentrations of 10^-9,10^-8,10^-7,10^-6 nmol/L for24 h and with concentration of 10^-7 nmol/L for0,12,24,36 and 48 h and positive control group treated with rosiglitazone for 24 h with the concentration of 10^-5 nmol/L.The expression of AQP7 mRNA was measured according to the reverse trans cription-polymerase reaction.Results The expressions of AQP7 mRNA in the negative control group,Apelin-13 treated groups with concentration of 10^-9,10^-8,10^-7,10^-6 nmol/L and positive control group were (0.22 ± 0.02),(0.29 ± 0.07),(0.36 ± 0.05),(0.43 ± 0.05),(0.31 ± 0.06) and (0.32 ± 0.08) respectively.There were significant differences between positive control group and negative control group (P 〈 0.05); compared with negative control group,10 8,10 7 nmol/L Apelin-13 significantly stimulated AQP7 mRNA expression (P 〈 0.05) ; 10 8,10^-7 nmol/L Apelin-13 group compared with positive control group,10 7 nmol/L Apelin-13 significantly stimulated AQP7 mRNA expression (P 〈0.05); there showed no statistical difference between 10^-8 and 10^-7 nmol/L Apelin-13 group.In the time group,the garg-scale ratio of 0,12,24,36,48 h of 10^-7 nmol/L Apelin-13 were (0.27 ±0.09),(0.43 ± 0.07),(0.55 ± 0.10),(0.42 ± 0.08),(0.33 ± 0.09) respectively.12,24,36 h group compared with 0 h group significantly stimulated AQP7 mRNA expression (P 〈 0.05),and the highest expression at 24 h ; but there were no significant differences between the 12,24,36 h group.Conclusion To some extent,Apelin-13 increases AQP7 mRNA expression in 3T3-L1 adipocytes with the excellence concentration of 10^-7 nmol/L treatment for 24 h.
出处 《中国医药》 2014年第4期570-574,共5页 China Medicine
基金 国家自然科学基金(81300310) 广东省自然科学基金(10151503102000019)
关键词 脂肪因子Apelin 3T3-L1脂肪细胞 水通道蛋白7 肥胖 Apelin 3T3-L1 adipocyte Aquaporin 7 Obesity
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参考文献15

  • 1Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes [ J ]. Nature, 2006,444 (7121) :840-846.
  • 2Hibuse T, Maeda N, Funahashi T, et al. Aquaporin 7 deficiency is associated with development of obesity through activation of adi- pose glycerol kinase [ J ]. Proc Natl Acad Sci U S A, 2005,102 (31) :10993-10998.
  • 3Castan-Laure|| I, Dray C, Attan6 C, et a|. Ape|in, diabetes, and obesity[J]. Endocrine, 2011,40( 1 ) : 1-9.
  • 4陈馥,郭梅,陈永松,李卫平.棕榈酸诱导3T3-L1脂肪细胞肥大模型的建立[J].汕头大学医学院学报,2012,25(1):21-23. 被引量:1
  • 5Yue P, ]in H, Xu S, et al. Apelin decreases lipolysis via G(q), G(i) , and AMPK-Dependent Mechanisms J ]. Endocrinology, 2011,152( 1 ) :59-68.
  • 6Kishida K, Shimomura 1, Nishizawa H, et al. Enhancement of the aquaporin adipose gene expression by a peroxisome proliferator-ac- tivated receptor gamma [ J ]. J Biol Chem, 2001,276 ( 51 ) :48572- 48579.
  • 7Spalding KL, Arner E, Westemmrk PO, et al. Dynamies of fat eell turnover in humans [J ]. Nature, 2008,453 (7196) :783-787.
  • 8Spalding KL, Arner E, Westermark PO, et al. Dynamics of fat cell turnover in humans [ J 1- Nature, 2008,453 ( 7196 ) : 783- 787.
  • 9Trayhurn P, Wtd IS. Adipokines: itfflanation anti the pleiotropierole of white adipose tissue [ J ]. Br J Nutr, 2004,92 ( 3 ) : 347- 355.
  • 10Higuchi K, Masaki T, Gotoh K, et al. Apelin, an APJ receptor ligand, regulates body adiposity and favors the messenger ribonu- cleic acid expression of uncoupling proteins in mice[J]. Endocri- nology, 2007,148 ( 6 ) : 2690-2697.

二级参考文献10

  • 1SINGH A S, MULDER C, TWISK J W, et al. Tracking of childhood overweight into adulthood: a systematic review of the literature[J]. Ohes Rev, 2008, 9(5): 474-488.
  • 2KAHN S E, HULL R L, UTZSCHNEIDER K M. Mechanisms linking obesity to insulin resistance and type 2 diabetes [J]. Nature, 2006, 444(7121)- 840-846.
  • 3JU J H, YOON H S, PARK H J, et al. Antl-obesity and an- tioxidative effects of purple sweet potato extract in 3T3-L1 adipocytes in vitro[J]. J Med Food, 2011, 14(10): 1097- 1106.
  • 4STUDENT A K, HSU R Y, LANE M D. Induction of fatty acid synthetase synthesis in differentiating 3T3-Ll preadipocytes[J]. J Bid Chem, 1980, 255(10): 4745- 4750.
  • 5COUSIN S P, HttQL S R, WREDE C E, et al. Free fatty acid-induced inhibition d glucose and insulin-like growth factor I-induced deoxyribonucleic acid synthesis in the pancreatic beta-cellline INS-1[J]. Endocrinology, 2001, 142(1): 229- 240.
  • 6TAKAHASHI K, YAMAGUCHI S, SHIMOYAMA T, et al. JNK- and IkappaB-dependent pathways regulate MCP-1 but not adiponectin release from artificially hypertrophied 3T3-L1 adipocytes preloaded with palmitate in vitro[J]. Am J Physiol Endocrinol Metab, 2008, 294(5): E898-909.
  • 7KIM S K, KONG C S. Anti-adipogenic effect of dioxinodehydroeckol via AMPK activation in 3T3-L1 adipocytes[J]. Chem Biol Interact, 2010, 186(1): 24-29.
  • 8GREEN H, MEUTH M. An established pre-adipose cell line and its differentiation in culture[J]. Cell, 1974, 3(2): 127- 133.
  • 9TAMORI Y, MASUGI J, NISHINO N, et aI. Role of peroxi- some proliferator-activated receptor-gamama in maintenance of the characteristics of mature 3T3-L1 adipocytes [ J ]. Diabetes, 2002, 51(7): 2045-2055.
  • 10张崇本.脂肪细胞的分化及调控[J].生理科学进展,2004,35(1):7-12. 被引量:31

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