丙戊酸对AngⅡ诱导的心肌细胞肥大与HDAC2表达的抑制作用
《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]
- 期数:
- 2009年第5期
- 页码:
- 639-642
- 栏目:
- 基础研究
- 出版日期:
- 2009-07-14
文章信息/Info
- Title:
- Valproic acid inhibits cardiomyocyte hypertrophy and HDAC2 expressions induced by angiotensin II
- Author(s):
- LU Ying1; YANG Shuang2; LI Hu-lun3
- 1.Department of Emergency, 2.Department of Cardiology, Second Affiliated Hospital, 3.Department of Neurobiology, Harbin Medical University, Harbin 150086, Heilongjang, China
- Keywords:
- histone deacetylase 2; angiotensin II; cardiomyocyte; hypertrophy; valproic acid
- 分类号:
- Q556.9
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 目的: 观察组蛋白脱乙酰基酶抑制剂—丙戊酸（valproic acid,VPA）抑制心肌细胞肥大和组蛋白脱乙酰基酶2（histone deacetylase 2，HDAC2）的表达。方法: 常规方法培养原代心肌细胞，分为5组：对照组、肥大组、低浓度VPA组(5×10-6 mol/L)、中浓度VPA组(10-5 mol/L)和高浓度VPA组(2×10-5 mol/L)。给予血管紧张素Ⅱ(AngⅡ)刺激心肌细胞造成肥大后，给予不同浓度的VPA进行干预。AngⅡ作用24 h后,于相差显微镜下观察心肌细胞面积的变化。用RT-PCR检测HDAC2 mRNA的表达；免疫组化染色法检测HDAC2蛋白的表达。结果: 经AngⅡ刺激后，在相差显微镜下可见心肌细胞面积变大，HDAC2 mRNA的水平增高，HDAC2蛋白表达亦增加。给予不同浓度的VPA后，上述指标随着VPA浓度的增加而逐渐下降（P<0.05）。结论: AngⅡ致心肌细胞肥大的过程中伴有 HDAC2表达增加，给予HDAC抑制制后，可使心肌细胞面积减少，HDAC2表达减少，提示VPA可抑制心肌细胞的肥大，HDAC2有可能参与心肌细胞肥大的机制。
- Abstract:
- AIM: To observe the expression of histone deacetylase 2 (HDAC2) in hypertrophic cardiomycytes induced by angiotensin II (AngII) and to study the inhibitory role of valproic acid (VPA). METHODS: Cultured cardiomyocytes were treated with AngII to induce hypertrophy, along with VPA of different concentrations. They were divided randomly into control group, hypertrophic group, and low (5×10-6 mol/L), medium (10-5 mol/L) and high concentration (2×10-5 mol/L) group. Morphological changes of cardiomyocytes were observed under the contrast phase microscope. mRNA levels of HDAC2 were examined by reverse transcriptase polymerase chain reaction (RT-PCR). Protein expressions of HDAC2 were examined by immunohistochemistry. RESULTS: Stimulated by AngII, cardiomyocytes were enlarged under the contrast phase microscope. After stimulation by AngII, the mRNA level of HDAC2 and the protein expression of HDAC2 increased in the hypertrophic cardiocytes. Along with VPA, these data decreased accordingly as the VPA concentrations increased. CONCLUSION: Expression of HDAC2 increased in hypertrophic cardiomyocytes stimulated by AngII. HDAC2 may play a role in cardiocyte hypertrophy. VPA may inhibit cardiomyocyte hypertrophy and HDAC2 expressions.
参考文献/References
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备注/Memo
- 备注/Memo:
- 收稿日期：2008-10-27.基金项目：黑龙江省卫生厅课题项目资助（2005-295） 通讯作者：陆莹，副主任医师，博士，主要从事心肌病发病机制研究Email:lyholly@163.com
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