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肝X受体抑制乳鼠心肌细胞缺氧/复氧损伤

殷然 王梦洪 郑泽琪 彭锦添 夏莺

中国病理生理杂志2011,Vol.27Issue(9):1671-1675,5.
中国病理生理杂志2011,Vol.27Issue(9):1671-1675,5.DOI:10.3969/j.issn.1000-4718.2011.09.002

肝X受体抑制乳鼠心肌细胞缺氧/复氧损伤

Liver X receptors attenuate anoxia/reoxygenation injury in neonatal rat cardiomyocytes

殷然 1王梦洪 1郑泽琪 1彭锦添 1夏莺2

作者信息

  • 1. 南昌大学第一附属医院心内科,江西省高血压病研究所
  • 2. 江西省人民医院干部病房,江西,南昌330006
  • 折叠

摘要

Abstract

AIM: To investigate the effect of liver X receptors ( LXRs ) on anoxia/reoxygenation injury in cultured neonatal rat cardiomyocytes and to explore the underlying cellular signaling pathway.METHODS: Neonatal rat cardiomyocytes were cultured and treated with anoxia/reoxygenation in the absence or presence of T0901317 ( an agonist of LXRs ) at various doses (1,5 and 10 μmol/L ).LDH and CK were detected by colorimetry 24 h after reoxygenation.The relative transcription levels of proinflammatory factors, such as tumor necrosis factor α( TNF - α ), interleukin - 6( IL - 6 ) and monocyte chemoattractant protein - l( MCP - 1 ),were quantified by real - time PCR.H9c2 cells were infected with adenoviral vectors containing constitutively - active forms of LXRα and LXRβ, then underwent anoxia/reoxygenation procedure.The activity of NF - κB in the cells was detected by luciferase assay.RESULTS: Treatment with T0901317 significantly suppressed anoxia/reoxygenation - induced increases in LDH and CK ( P <0.05 ).Transcription levels of proinflammatory factors in T0901317 treatment groups were significantly lower than those in control group ( P <0.05 ).Adenovirus -mediated overexpression of constitutively - active LXRs suppressed anoxia/reoxygenation - induced NF - κB activity in H9c2 cells.CONCLUSION: LXRs are negative regulators of myocardial ischemia - reperfusion injury.

关键词

X受体,肝/心肌缺血/再灌注损伤/细胞培养

Key words

X receptors,liver/ Myocardial ischemia - reperfusion injury/ Cell culture

分类

医药卫生

引用本文复制引用

殷然,王梦洪,郑泽琪,彭锦添,夏莺..肝X受体抑制乳鼠心肌细胞缺氧/复氧损伤[J].中国病理生理杂志,2011,27(9):1671-1675,5.

基金项目

国家自然科学基金资助项目(No.81000071) (No.81000071)

中国病理生理杂志

OA北大核心CSCDCSTPCD

1000-4718

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