低氧胁迫对鲢心肌细胞凋亡及其调控基因Bax、Bcl-2表达的影响

为了解低氧胁迫对鲢心脏的损伤及其机制,检测了不同低氧条件下鲢血清肌酸激酶(CK)活力和心肌细胞凋亡情况及凋亡调控基因Bax、Bcl-2的表达。结果显示:低氧胁迫下血清CK活性显著升高,表明低氧实验中鲢心肌细胞可能受到了损伤;TUNEL检测显示低氧胁迫鲢心肌细胞发生了凋亡,且随着氧浓度的下降凋亡指数升高,组间差异极显著;qPCR显示,鲢心肌Bax基因和Bcl-2基因变化趋势相反,Bax基因随着处理时间的延长,氧浓度的下降,表达量升高,Bcl-2基因表达量降低,且实验结束时与常氧对照值(Normoxia group,NO)比较差异显著。结果表明,低氧胁迫通过升高鲢心肌Bax基因表达、降低Bcl-2基因表达,导致心肌细胞凋亡,从而造成鲢心脏损伤甚至鱼死亡。

Effects of hypoxia stress on cardiomyocyte apoptosis and the control for Bax,Bcl-2 expressions in Hypophthalmichthys molitrix

Serum CK activity, cardiomyocyte apoptosis and the expression of apoptosis-regulatory gene Bax, Bcl-2 under different hypoxia stress treatments were detected to elucidate silver carp heart injure and its mechanism under hypoxia stress.Serum enzyme test results show that serum CK activity was significantly increased with density of oxgen decrease in water, which indicated that the myocardial cells may be damaged in hypoxia treatments.TUNEL detection results showed that hypoxia stress aggravated the apoptosis of cardiomyocyte and the apoptosis index increased with the decrease of oxygen density, the differences in different groups were significant.The result of qPCR showed that the changes of Bax and Bcl-2 gene expressions were opposite.Compared to normoxia group, Bax gene expression increased and the Bcl-2 gene expression decreased significantly with oxgen density decrease.The results showed that hypoxia stress could up-regulate Bax gene ex-pression and down-regulate the expression of Bcl-2 gene, promote cardiomyocyte apoptosis and damaged heart to cause silver carp death.