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为了探索“救脑宁”注射液对中风病的疗效机理 ,将原代培养 8～ 12d的新生大鼠皮层神经细胞进行缺氧缺糖处理 ,观察该药对缺氧缺糖损伤神经细胞的影响。结果表明 :缺氧缺糖组细胞上清液中丙二醛 (MDA)含量、乳酸脱氢酶 (LDH)活性较对照组显著升高 ,细胞超氧化物岐化酶 (SOD)活性和细胞生存率则显著降低 ,救脑宁组MDA、LDH显著低于缺氧缺糖组 ,而SOD活性及细胞生存率则高于缺氧缺糖组 (P <0 0 1)。因此 ,抗脂质过氧化损伤、提高神经细胞对缺氧缺糖的耐受性 ,可能是其疗效机理之一。
In order to explore the therapeutic mechanism of “JiuXingNing” injection on apoplexy, the primary cultured neonatal rat cortical neurons were subjected to hypoxia and glucose deprivation for 8 to 12 days to observe the effect of the drug on neurons damaged by hypoxia and glucose deprivation. . The results showed that the content of malondialdehyde (MDA) and the activity of lactate dehydrogenase (LDH) in the supernatant of hypoxia-glucose deprivation group were significantly higher than those in the control group, and the activity of superoxide dismutase (SOD) and cell survival were increased. The rate was significantly lower. The MDA and LDH of the Jiunaoning group were significantly lower than those of the hypoxia-hypoglycemia group, while the SOD activity and cell survival rate were higher than those of the hypoxia-hypoglycemia group (P<0 01). Therefore, anti-lipid peroxidation damage and increase of the tolerance of nerve cells to oxygen-glucose deprivation may be one of the therapeutic mechanisms.