彭红艳姬秋和△ 周洁邢影高彬曹宏伟刘涛.利拉鲁肽下调游离脂肪酸作用下βTC3 细胞PERK 的表达[J].,2012,12(13):2448-2450 |
利拉鲁肽下调游离脂肪酸作用下βTC3 细胞PERK 的表达 |
The Down-regulation Effect of Liraglutide (Lira) on the Expression ofDouble-stranded RNA-dependent Protein Kinase-like EndoplasmicReticulum Kinase (PERK) in βTC3 Cells Induced by Free Fatty Acids (FFA) |
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DOI: |
中文关键词: 游离脂肪酸 PERK 利拉鲁肽 内质网应激 |
英文关键词: Free fatty acid Double-stranded RNA-dependent protein kinase-like endoplasmic reticulum kinase Liraglutide Endoplasmic
reticulum stress |
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中文摘要: |
目的:探讨游离脂肪酸(FFA)作用下胰岛βTC3 细胞双链RNA 依赖性蛋白样内质网激酶(PERK)的表达以及利拉鲁肽(Lira)
对其表达的干预作用。方法:以βTC3 细胞为研究对象,分为对照组和FFA 组(0.125,0.25,0.5 及1 mmol/L)孵育24 h,Western
blot 方法检测PERK 的表达。然后,分为对照组,FFA 组,和FFA+Lira 组(0.5 mg/L 和1 mg/L),Lira 预孵育6 h 后,1 mmol/L FFA
继续孵育24 h,Western blot 检测PERK 的表达。结果:①不同浓度FFA 孵育24 h 后,与对照组相比,1 mmol/L FFA 组PERK 表达
增加(P<0.05)。②与1 mmol/L FFA 组相比,0.5mg/L Lira+1 mmol/L FFA 和1 mg/L Lira+1 mmol/L FFA 组PERK 表达减少(P<0.05),
两组之间有统计学差异(P<0.05)。结论:FFA 作用能够上调βTC3 细胞PERK 的表达,而Lira 在一定程度上逆转FFA 水平异常导
致的βTC3 细胞PERK 表达上调,减轻内质网应激反应。 |
英文摘要: |
Objective: To investigate the expression of PERK in βTC3 cells exposed to different concentrations of FFA and the
intervention effect of Lira on the expression of double-stranded RNA-dependent protein kinase-like endoplasmic reticulum kinase
(PERK) induced by FFA. Methods: βTC3 cells were treated with different concentrations of FFA (0, 0.125, 0.25, 0.5 and 1.0 mmol/L).
Western Blot analysis was used to determine the expression of PERK in βTC3 cells after 24 hours. Afterwards, βTC3 cells were preincubated
with different concentrations of Lira(0, 0, 0.5, 1 mg/L)for 6 hours, and different concentrations of FFA(0,1, 1, 1 mmol/L)were
then added and the cells were incubated for another 24 hours. The expression of PERK was detected. Results: ①After the cells were incubated
with FFA of different concentrations for 24 hours, compared with the control group, the expression of PERK in βTC3 cells in the
group with 1 mmol/L FFA increased (P<0.05). ②Compared with that in the group with 1 mmol/L FFA, the expression of PERK decreased
(P<0.05) in the group with 0.5 mg/L Lira+1 mmol/L FFA and the group with 1 mg/L Lira+1 mmol/L FFA, and there was statistical
difference between the two groups (P<0.05). Conclusion: The expression of PERK in βTC3 cells is up-regulated by administration of
FFA of certain concentration, while Lira can reverse this response to some extent, partly inhibiting endoplasmic reticulum stress. |
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