基础医学与临床 ›› 2013, Vol. 33 ›› Issue (9): 1150-1154.

• 研究论文 • 上一篇    下一篇

HO-1/CO系统抑制AngII诱导的大鼠心肌细胞凋亡

谷颖,王爱红,陈东昌,鹿克风   

  1. 山东大学附属省立医院
  • 收稿日期:2012-09-27 修回日期:2012-12-28 出版日期:2013-09-05 发布日期:2013-08-28
  • 通讯作者: 鹿克风 E-mail:lukefeng@medmail.com.cn
  • 基金资助:
    山东省自然科学基金;山东省卫生厅科研基金

Heme oxygenase - 1 / carbon monoxide system inhibits angiotensin II induced apoptosis of myocardial cells

  • Received:2012-09-27 Revised:2012-12-28 Online:2013-09-05 Published:2013-08-28

摘要: 目的 探讨血红素氧合酶-1/一氧化碳(HO-1/CO)系统对血管紧张素II(AngII)诱导的大鼠心肌细胞凋亡的影响。方法 原代培养新生Wistar大鼠心肌细胞,随机分为:对照组、AngII组、AngII+氯化血红素(hemin)(HO-1诱导剂)组和AngII+锌原卟啉-9(ZnppIX)(HO-1抑制剂)组。用Real Time-PCR及Western blot检测心肌细胞HO-1 mRNA和蛋白的表达,比色法测定细胞培养上清液中碳氧血红蛋白(COHb)含量,流式细胞仪检测细胞凋亡。结果 AngII组心肌细胞HO-1mRNA、蛋白、COHb含量和细胞凋亡均明显高于对照组(P<0.05),AngII+hemin组HO-1mRNA、蛋白、COHb含量进一步升高(P<0.05),而细胞凋亡回降(P<0.05),但仍高于对照组(P<0.05),AngII+ZnPPIX组仅细胞凋亡显著升高(P<0.05),其它指标无显著变化。结论 HO-1/CO系统对AngII诱导的心肌细胞凋亡具有抑制作用。

关键词: 关键词:血红素氧合酶-1, 内源性一氧化碳, 心肌细胞, 凋亡

Abstract: Objective To investigate the influence of heme oxygenase -1/carbon monoxide (HO-1/CO) system on apoptotic myocardial cells induced by angiotensin II (AngII) . Methods Primary culture of myocardial cells in neonatal Wistar rat, randomly divided cells into four groups. Respectively with Real Time - PCR and Western blot analyzed HO -1 mRNA and protein expression, colorimetric method was used for determination of cell culture supernatant fluid medium carbon oxygen hemoglobin content; flow cytometry instrument was used to detect cells apoptosis rate. Results AngII group of myocardial cell HO -1 mRNA, protein, COHb content and cell apoptosis were significantly higher than those in the control group (P < 0.05), AngII+hemin group HO -1 mRNA, protein and COHb content further raise (P < 0.05), while apoptosis rollback (P < 0.05), but still higher than those of the control group (P < 0.05), and AngII+ZnPPIX group only apoptosis significantly increased (P < 0.05), other index no significant change. Conclusion HO-1/CO system attenuate the myocardial cells apoptosis induced by AngII.

Key words: key words:heme oxygenase-1, Endogenous carbon monoxide, Myocardial cells, apoptosis

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