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PPARβ激动剂对肥大心肌细胞蛋白合成及IL-1β表达的影响 被引量:1

Regulation of PPARβ activation on protein synthesis and IL-1β expression in hypertrophic cardiomyocytes
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摘要 目的探讨过氧化物酶体增殖物活化型受体β亚型(PPARβ)激动剂对体外肥大心肌细胞蛋白合成及相关炎性因子IL-1β表达的影响。方法体外培养新生大鼠的心室肌细胞,以血管紧张素Ⅱ(AngⅡ)诱导建立心肌细胞肥大模型,将适宜浓度PPARβ激动剂GW0742作用于心肌细胞,用3H-亮氨酸掺入法检测心肌细胞蛋白合成速率,RT-PCR及Western印迹方法分别检测IL-1βmRNA和蛋白水平的表达变化。结果与结论 GW0742在抑制肥大心肌细胞蛋白合成速率的同时,下调其IL-1βmRNA和蛋白的表达,而作为溶剂的DMSO则无此影响,说明GW0742抑制AngⅡ介导的体外心肌细胞肥大,其机制可能与调控炎性因子IL-1β密切相关。 Objective To investigate the effect of activation of peroxisome proliferator-activated receptor β/δ( PPARβ / δ) on protein synthesis and expression of angiotensin( Ang) Ⅱ-induced hypertrophic myocytes( MC) in vitro. Methods Hypertrophy in neonatal rat cardiac MC culture was established with AngⅡ,then the effect of GW0742 on hypertrophy was detected. The synthetic rate of protein in MC was detected by3H-leucine incorporation. mRNA and protein expression of atrial natriuretic IL-1β was measured by reverse transcription-polymerase chain reaction( RT-PCR) and Western-blotting.Results and Conclusion GW0742 could reduce the synthetic rate of protein in hypertrophic MC while down-regulating the mRNA and protein expression of IL-1β,but no changes were observed after treatment with DMSO. The result demonstrated that activation of PPAR beta / delta inhibited cardiac hypertrophy in vitro and this effect might be related to inflammatory factors.
出处 《军事医学》 CAS CSCD 北大核心 2015年第6期453-455,479,共4页 Military Medical Sciences
基金 国家重点基础研究发展计划资助项目(2013CB530804)
关键词 过氧化物酶体增殖物活化型受体 心肌细胞肥大 白细胞介素-1Β 血管紧张素Ⅱ peroxisome proliferator-activated receptor cardiac hypertrophy interleukin-1β angiotensinⅡ
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