脂氧素对大鼠心肌缺血再灌注后心梗程度和细胞凋亡的影响

Effects of Lipoxins on ischemia / reperfusion-induced cardiocyte necrosis and apoptosis

目的:观察脂氧素A4(lipoxins,LXA4)对大鼠心肌缺血再灌注后心梗程度和细胞凋亡的影响。方法:36只大鼠随机分成假手术组(S组,n=12)、缺血/再灌注组(I/R组,n=12)和I/R+LXA4治疗组(L组,n=12),分别以HE染色光镜下观察心肌组织病理学变化,通过RT-PCR和Western blot法检测缺血心肌Caspase-3、Bcl-2和Bax的表达水平。结果:L组心肌组织病理学损伤较I/R组减轻。I/R组中基因Bax和Bcl-2的表达均增强,Caspase-3的含量升高(P<0.01)。L组中基因Bax、Caspase-3表达明显减弱,Bcl-2表达增强(P<0.01)。结论:脂氧素通过抑制Caspase-3和Bax活化,增强Bcl-2的表达而对缺血再灌注的心肌有一定保护作用。

Objective To study the effects of Lipoxins （LX）, on ischemia/reperfusion （I/R）-indueed myocardial injury and myocyte apoptosis in rats. Methods 36 Sprague-Dawley rats, weighing 250 - 350 g, were divided randomly into 3 groups in equa number： sham-operated group （S）, myocardial I/R group （I/R） and lipoxin A4 group （L）. Immunohistochemistry（IHC） was used to detect qualitatively and semi-quantitatively the expressions of Caspase-3, Bax and Bcl-2. Results The myocardial damage in group L was significantly reduced. After ischemia, the expressions of Caspase-3, Bax and Bcl-2 were all increased in group I/R. The levels of Bax and Caspase-3 in group L were lower but the level of Bcl-2 was higher as compared to group I/R. Conclusion Lipoxins could inhibit I/R- induced myocardial apoptosis by inhibiting Caspase-3 and Bax expressions and enhancing Bcl-2 expression.