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目的:研究巴西苏木红素对小鼠脑缺血损伤中能量代谢的影响作用。方法:将40只小鼠随机分为假手术组、脑缺血组、苏木红素5,10 mg.kg-1组,每组10只,构建脑缺血模型。脑缺血手术前3 d开始静脉注射苏木红素,给药剂量依据预试验确定,随后处死小鼠,制备大脑匀浆液。利用HPLC对脑内三磷酸腺苷、二磷酸腺苷、腺苷一磷酸和乳酸含量进行测定,RT-PCR检测脑内单羧酸转运体(MCT1,MCT2)基因水平的表达。结果:小鼠脑缺血20 min后,脑内乳酸含量迅速升高,再灌注1 h内逐渐减低,再灌注24 h后逐渐降低至正常水平。缺血再灌的最初,能荷值迅速显著减低,再灌1 h过程中能荷恢复较快,但再灌24 h后能荷仍未恢复至正常水平。脑缺血过程中,随着脑内乳酸的升高,MCT1和MCT2的表达也随之上调,预先静脉注射苏木红素5 mg.kg-1能上调MCT2 mRNA的表达,与模型组相比差异显著(P<0.05),苏木红素10 mg.kg-1组能上调MCT1和MCT2 mRNA的表达,与模型组相比差异显著(P<0.01)。结论:苏木红素所具有的神经保护作用可能是通过改善能荷水平而实现的。
Objective: To study the effect of hematoxylin on energy metabolism in mice with cerebral ischemia. Methods: Forty mice were randomly divided into sham-operation group, cerebral ischemia group, hematoxylin-5,10 mg.kg-1 group, 10 rats in each group. Venous injection of hematoxylin was started 3 days before the operation of cerebral ischemia. The dosage was determined according to the pre-test, and then the mice were sacrificed to prepare brain homogenates. The contents of adenosine triphosphate, adenosine monophosphate, adenosine monophosphate and lactic acid in the brain were measured by HPLC. The expression of monocarboxylate transporters (MCT1 and MCT2) in the brain were detected by RT-PCR. RESULTS: After cerebral ischemia for 20 min, the content of lactate in brain increased rapidly, gradually decreased within 1 h after reperfusion, and then gradually decreased to normal level 24 h after reperfusion. At the beginning of ischemia-reperfusion, the charge value decreased rapidly and recovered quickly at 1 h after reperfusion. However, the energy charge did not return to normal level at 24 h after reperfusion. In the process of cerebral ischemia, the expression of MCT1 and MCT2 also increased with the increase of lactate in the brain. Pretreatment with hematoxylin 5 mg.kg-1 could up-regulate the expression of MCT2 mRNA, which was significantly different from the model group (P <0.05). The hematoxylin 10 mg.kg-1 group could up-regulate the expression of MCT1 and MCT2 mRNA significantly compared with the model group (P <0.01). Conclusion: The neuroprotective effect of hematoxylin may be achieved by improving the energy charge level.