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UCP2在硫酸吲哚酚诱导心肌细胞肥大中的作用

, PP. 2277-2282

Keywords: 硫酸吲哚酚,心肌细胞肥大,解偶联蛋白,机制

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Abstract:

目的探讨解耦联蛋白2(uncouplingprotein2,UCP2)在硫酸吲哚酚(indoxylsulfate,IS)诱导心肌细胞肥大中的作用和机制。方法分离培养新生Sprague-Dawley大鼠心肌细胞,0、100、250、500、1000μmol/LIS孵育心肌细胞1h或500μmol/LIS孵育心肌细胞0、15、30、45、60min后,Westernblot检测心肌细胞UCP2蛋白表达变化。UCP2慢病毒转染心肌细胞后,通过α-actinin免疫荧光染色观察细胞大小,3H-亮氨酸掺入法评价蛋白合成速率,Real-timePCR检测肥大相关基因ANF、BNP和β-MHCmRNA的表达,同时利用MitosoxTM探针检测活性氧(reactiveoxygenspecies,ROS)生成情况。结果与对照组相比,IS处理组心肌细胞的UCP2蛋白水平明显下降(P<0.05);与IS处理组相比,UCP2过表达可以明显抑制IS诱导的心肌细胞ROS生成、体积增大、3H-亮氨酸摄入增加及肥大相关基因(ANF、BNP和β-MHCmRNA)的表达增高,差异有统计学意义(P<0.05)。结论IS诱导心肌细胞肥大可能与其下调UCP2表达及促进氧化应激有关,而UCP2过表达或许可以通过抑制氧化应激拮抗IS诱导的心肌细胞肥大。

References

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