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作 者:官滨斌[1] 王丽静[1] 刘小莺[1] 刘礼斌[1]
机构地区:[1]福建医科大学附属协和医院内分泌科,福建省内分泌研究所,福州350001
出 处:《福建医科大学学报》2012年第3期165-168,共4页Journal of Fujian Medical University
基 金:福建省卫生厅青年科研课题(2009/1/17)
摘 要:目的观察内质网应激(ERs)抑制剂牛磺熊脱氧胆酸(TUDCA)对ERs诱导剂衣霉素(TM)介导的3T3-L1脂肪细胞胰岛素抵抗(IR)的干预效果,探讨脂肪细胞IR与ERs的关系。方法体外培养3T3-L1前脂肪细胞,并将其诱导分化为成熟的脂肪细胞。以MTT比色法检测不同干预条件下脂肪细胞存活情况、以葡萄糖氧化酶法(GOD)法检测不同干预条件下脂肪细胞葡萄糖消耗情况,利用Western blot检测不同干预条件下ERs关键信号蛋白(P-IRE、IRE)的表达差异。结果 (1)5μg/mL TM作用5h后可使胰岛素刺激的3T3-L1脂肪细胞葡萄糖消耗量降低19.7%(P<0.05),而1mmol/L TUDCA预处理24h后均可缓解TM的抑制作用。(2)Westernblot显示,5μg/mL TM作用5h明显增加P-IRE的表达,而经1mmol/L TUDCA预处理24h后可减少P-IRE的表达。不同处理因素对总IRE的表达无明显影响。结论 ERs可诱导3T3-L1脂肪细胞发生IR,缓解ERs可减轻IR。Objective In this study we investigated the effect of Tauroursodeoxycholic which was an inhibititor of endoplasmic reticulum stress on endoplasmic reticulum stress inducer tunieamycin media- ted insulin resistance in 3T3-L1 adipocytes. Preliminary study the the correlation between insulin resist- ance and endoplasmic reticulum stress in adipocytes. Methods In vitro 3T3-L1 pre-adipocytes were dif- ferentiated into adipocytes. Cell viability was determined by MTT assay. Glucose oxidase (GOD) assay was used to detecte the glucose consumption and evaluated the insulin sensitivity in different intervention in 3T3-L1 adipocytes. The expression of the key endoplasmic reticulum stress signaling proteins (P-IRE, IRE ) were detected by Western blot. Results (1) Tunicamycin (5 μg/mL for 5 h) inhibited insulin- stimulated glucose consumption by 19.7%(P〈0.05). After intervention by 1 mmol/L Tauroursodeoxy- cholic Acid for 24 h, the inhibition of Tunicamycin could be partly relieved(P〈0.05). (2) Western Blot showed that Tunicamycin(5μg/mL for 5 h) could significantly increase the expression of P-IRE ,whereas pretreatment of 3T3-L1 adipocytes with 1 mmol/L Tauroursodeoxycholic Acid for 24 h could reduce the expression of P-IRE. The expression of IRE was not changed in different groups. Conclusion Endo- plasmic reticulum stress can induce insulin resistance in 3T3-L1 adipocytes. Alleviating the endoplasmic reticulum stress can improve insulin resistance.
关 键 词:内质网应激 3T3-L1脂肪细胞 胰岛素抵抗
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