脑血康口服液对实验性脑出血大鼠脑内一氧化氮生成的抑制作用

摘要

探讨脑血康口服液(简称脑血康)治疗脑出血急性期的作用机理。立体定位内囊注射含0.4u胶原酶(Ⅶ型)的生理盐水1μl，诱导大鼠脑出血模型。比色法检测血肿周围大脑皮质中一氧化氮(nitric oxide,NO)含量，神经缺损症状积分法检查大鼠神经机能。观察脑血康及一氧化氮合酶抑制剂N-亚硝基-L-精氨酸甲酯(L-NAME)对脑出血大鼠大脑皮质中NO生成及神经机能的影响，并设蒸馏水治疗空白对照及假手术对照。结果：与假手术组比较，蒸馏水组大鼠术后1～7d时大脑皮质中NO生成均显著增加(P＜0.01)，术后4d达峰值(P＜0.01)；蒸馏水组大鼠术后神经缺损症状积分也明显升高(P＜0.05)，术后1d时最高(P＜0.01)，2d时开始改善，7d时接近正常。L-NAME对脑出血大鼠大脑皮质中NO生成的抑制作用强于脑血康(P＜0.05)，但对神经机能改善作用不及后者(P＜0.05)。结论：抑制脑内NO的过度产生，可能是脑血康保护脑出血损伤的作用机理之一。%For the purpose of investigating the therapeutic mechanism of Naoxuekang oral liquid (NXK) in acute period of intracerebral hemorrhge (ICH),nitric oxide(NO) production in the cerebral cortex and neurological deficits of collagenase-induced ICH rats were observed,and distilled water (DW) treatment and sham operation were used separately as placebo and operation controls.The results showed that compared with those of sham-operated rats,the levels of NO in the cerebral cortex of DW-treated rats increased significantly 1d,2d,4d and 7d after operation(P＜0.01) and peaked 4d after operation,the scores of the neurological deficits of DW-treated rats were elevated remarkably(P＜0.05)，peaked 1d after operation,improved 2d after operation and approximately normalized 7d after operation.The inhibitory effects of L-NAME on brain NO production were superior to those of NXK,but the improvement of neurological deficits of the rats treated with NXK was more significant than that of the rats treated with L-NAME.These results suggest that the inhibition of NO production in the cerebral cortex might be one of the possible pharmacological mechanisms of NXK against ICH injury.