从生化和免疫角度探讨胎窘方对缺氧缺血新生大鼠脑保护的作用机制。在成功建立了缺氧缺血新生大鼠模型的基础上,以西药“洛斯宝”为对照,应用生化免疫的方法,检测模型大鼠灌服胎窘方后血清一氧化氮(NO)、谷氨酸(Glu)、白三烯C4(LTC4)的变化。结果:①对于NO,胎窘方高剂量组与模型组比较,疗效明显(P〈0.05);②对于Glu,胎窘方高、低剂量组及西药组与模型组比较,有非常显著差异(P〈0.01);③对于LTC4,胎窘方高剂量组及西药组与模型组比较,有较好疗效。P〈0.05,P〈0.01;④对于NO、Glu,胎窘方高剂量组与空白组及假手术组均无显著差异(P〉0.05)。说明胎窘方可降低NO的神经毒性,使其正常发挥神经递质作用;降低Glu的损害;降低LTC4缩血管作用,从而起到减轻缺氧缺血后脑损伤的作用。
To explore the protective mechanism of the prescription for fetal distress in neonatal rats with hypoxic-ischemic brain-damage (HIBD) in terms of biochemistry and immunity. The models were made and drenched with the prescription, then the contents of NO, Glu and LTC4 in serum were detected, and Vasobral as control. The results showed that the curative effects of high dose group were better in NO and LTC4 compared with the control group (P〈0.05); and was far better in Glu (P〈0.01). Conclusion: The prescription for fetal distress could cut down the neurotoxicity of NO and induce its normal neurotransmitter effect, decrease the excited harm of Glu, and depress the shrinking blood vessel effect of LTC4, and thereby lessen the degree of HIBD.