山楂叶原花青素对模拟缺血再灌注损伤新生大鼠心肌细胞的保护作用

[Protective effect of hawthorn leaf procyanidins on cardiomyocytes of neonatal rats subjected to simulated ischemia-reperfusion injury].

作者信息

Li Peng, Wang Jiannong, Lu Shujie, Fu Jianhua, Liu Jianxun

机构信息

Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2009 Jan;34(1):96-9.

PMID:19382461

Abstract

OBJECTIVE

To study the direct effect of hawthorn leaf procyanidins on cardiomyocytes subjected to ischemia-reperfusion injury and elucidate their therapeutic mechanism on ischemic heart diseases.

METHOD

Cultured cardiomyocytes of neonatal rats were subjected to anoxia-reoxia injury which simulated the ischemia-reperfusion injury in vivo, and hawthorn leaf procyanidins were applied. The therapeutic effect was valued by LDH leakage and MTT test. For a further mechanism study, contents of MDA and activities of SOD in cardiomyocytes were measured.

RESULT

Hawthorn leaf procyanidins in 24-60 mg x L(-1) significantly and dose-dependently inhibited LDH leakage (compared with the model group, all P<0.01 ) and cell viability decrease (compared with model group, 24-48 mg x L(-1) groups all P<0.05; 60 mg x L(-1) group, P<0.01) in cardiomyocytes induced by anoxia-reoxia injury. Furthermore, hawthorn leaf procyanidins in 24-60 mg x L(-1) significantly inhibited the increase of MDA content (compared with the model group, all P<0.01) and the decreased of SOD activity (compared with the model group, 24 mg x L(-1) group, P<0.05; other groups all P<0.01) in cardiomyocytes undergoing anoxia-reoxia injury.

CONCLUSION

Hawthorn leaf procyanidins have a significant therapeutic effect on the simulated ischemia-reperfusion injury of cultured neonatal rat cardiomyocytes, which may relate to their anti-oxidation effects. And the direct protective effect of hawthorn leaf procyanidins on cardiomyocytes subjected to ischemia-reperfusion injury may be one of the key mechanisms of its therapeutic effect on ischemic heart diseases.

摘要

目的

研究山楂叶原花青素对遭受缺血再灌注损伤的心肌细胞的直接作用，并阐明其对缺血性心脏病的治疗机制。

方法

将培养的新生大鼠心肌细胞进行缺氧复氧损伤以模拟体内缺血再灌注损伤，并应用山楂叶原花青素。通过乳酸脱氢酶（LDH）释放和MTT试验评估治疗效果。为进一步研究机制，检测心肌细胞中丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性。

结果

24 - 60mg·L⁻¹的山楂叶原花青素能显著且剂量依赖性地抑制缺氧复氧损伤诱导的心肌细胞中LDH释放（与模型组相比，均P < 0.01）以及细胞活力下降（与模型组相比，24 - 48mg·L⁻¹组均P < 0.05；60mg·L⁻¹组，P < 0.01）。此外，24 - 60mg·L⁻¹的山楂叶原花青素能显著抑制缺氧复氧损伤心肌细胞中MDA含量的增加（与模型组相比，均P < 0.01）以及SOD活性的降低（与模型组相比，24mg·L⁻¹组，P < 0.05；其他组均P < 0.01）。