球形脂联素通过NF-κB通路抑制血管紧张素II诱导的心肌肥大
diponectin ininhibits cardiac hypertrophy induced by angiotensin II through NF-κB pathway
研究球状脂联素（gobular adiponectin，gAd）抑制血管紧张素II（angiotensin II, AngII）诱导的大鼠心肌细胞肥大的信号转导途径。[3H]-亮氨酸掺入法和实时PCR结果显示，AngII刺激后可以心肌细胞内蛋白合成及心房利钠肽 (atrial natriuretic peptide，ANP) mRNA的表达水平分别增加98%和270%(P<0.01)，5μg/ml的gAd预处理使AngII引起的蛋白合成及mRNA的表达分别降低24%和32%。AngII刺激细胞后核转录因子(nuclear factor κB, NF-κB)在细胞核内的表达量显著增加(P <0.05)，其转录活性及DNA结合活性也明显上升；给予gAd预处理后，NF-κB的核转位、转录及结合活性均出现显著的下调(P <0.05)。这些结果表明，gAd通过下调NF-κB的活性抑制AngII诱导的心肌细胞肥大。
o characterize the inhibitory effect of gobular adiponectin (gAd) on nuclear factor κB (NF-κB) nuclear translocation activation, the transcription activity and DNA-binding ability induced by angiotensin II (AngII) during cardiac hypertrophy. By using [3H]-leucine incorporation and real-time polymerase chain reaction (Real-time PCR), we found that [3H]-luecine incorporation into NRVMs and the expression of atrial natriuretic peptide (ANP) mRNA were increased in 98% and 270% after AngII (10-7 mol/L) stimulation for 48h. Pretreatment NRVMs with gAd for 60 min reduced the increased protein synthesis (P < 0.05) and mRNA expression (P < 0.01) induced by AngII. gAd pretreatment could also inhibit NF-κB translocation, transcription activity and DNA binding ability induced by AngII (P < 0.05). These results suggeste that gAd inhibits cardiac hypertrophy through suppressing NF-κB activation.
李丽、凡栋、吴立玲、周允、崔晓兵、王程
基础医学生理学分子生物学
心肌肥大球状脂联素核转录因子ngII
globular adiponectincardiac hypertrophynuclear factor κBangiotensin II
李丽,凡栋,吴立玲,周允,崔晓兵,王程.球形脂联素通过NF-κB通路抑制血管紧张素II诱导的心肌肥大[EB/OL].(2010-12-31)[2025-08-17].http://www.paper.edu.cn/releasepaper/content/201012-1430.点此复制
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