单羧酸转运蛋白2在急性心力衰竭模型大鼠大脑皮质中的表达变化
Changes of MCT2 expression in cerebral cortex of rats with acute heart failure
目的 观察急性心力衰竭（acute heart failure,AHF）时，大脑皮质区（cerebral cortex）神经元单羧酸转运蛋白2（monocarboxylate transporters2, MCT2）的表达变化，以探讨MCT2参与大脑缺血缺氧时能量代偿的机制。 方法 静脉注射1.5%戊巴比妥钠制作AHF大鼠模型；通过记录左室内压峰值（LVSP）和左室内压最大上升速率（+dp/dt max）变化曲线，以判断模型是否成功；应用免疫组化（IHC）和免疫印迹法（WB）检测AHF模型大鼠大脑皮质区MCT2的表达变化。 结果 与正常组相比，模型大鼠大脑皮质区MCT2阳性神经元的数量及积分光密度（integral optical density，IOD）在5 min时明显升高，到10 min时有所下降，但仍然高于正常水平，具有统计学意义（P＜0.05）；而假手术组与正常组相比无统计学意义（P＞0.05）。WB结果与IHC变化趋势一致。 结论 在AHF状态下，大脑皮质神经元MCT2的表达增强，提示MCT2参与了大脑缺血缺氧时进行自我代偿的过程。
Objective To observe the changes of monocarboxylate transporters 2( MCT2) expression in the rat cerebral cortex under the stimulation of acute heart failure syndrome, so as to detect the alterations of energy metabolism of the cerebral cortex under the condition of acute heart failure, and to provide experimental basis for the best rescue time of acute heart failure. Methods The model was established by intravenous injection of 1.5% pentobarbital sodium.To estimate whether acute heart failure model was successful or not, the left ventricular systolic pressure（LVSP）and increased rate of left ventricular pressure maximum（+dp/dt max）were recorded. Immunohistochemical staining(IHC) and Western blot(WB) were used to explore the alteration of MCT2 expression in rat cerebral cortex. Results Compared with the normal group, the number and the integral optical density（IOD）of MCT2-positive neurons were increased in the cerebral cortex of the acute heart failure model，reaching the highest level on 5 min and declined on 10 min, but still higher than those in the control group (P<0.05). Conclusion Our results involved that MCT2 is enhanced under the case of acute heart failure, which might indicate that MCT2 is involved in the process of self-compensation in the absence of cerebral ischemia.
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