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用新生Wistar大鼠大脑皮层进行神经细胞培养 ,将培养 8d的神经细胞置于模拟“缺血”状态下 ,5h后神经细胞发生肿胀 ,胞内乳酸脱氢酶 (LDH)漏出增加 ,膜流动性下降、脂质过氧化(LPO)含量增加 ;将经过“缺血”损伤神经细胞置 1 8h模拟“再灌注” ,“再灌注”后细胞数目明显减少 ,LDH的漏出、膜流动性下降和LPO增加继续加重 ,说明细胞损伤进一步加重。经过天麻素孵育后的神经细胞“缺血”或“再灌注”后LDH的漏出及LPO含量明显低于损伤组 ,而膜流动性则明显高于损伤组。表明 :天麻素对体外培养神经细胞的缺血再灌注损伤有保护作用
Neurons were cultured in cerebral cortex of neonatal Wistar rats. The neurons cultured for 8 days were placed in a simulated “ischemic” state. After 5 hours, the nerve cells were swollen, the intracellular lactate dehydrogenase (LDH) leakage increased, and membrane fluidity was increased. Decreased, lipid peroxidation (LPO) content increased; nerve cells after “ischemia” injury were set for 18 hours to simulate “reperfusion”, the number of cells was significantly reduced after reperfusion, LDH leakage, membrane fluidity decline, and LPO The increase continues to increase, indicating that cell damage is further aggravated. After the gastro-injection of gastrodin, the leakage of LDH and the content of LPO in the nerve cells after ischemia or reperfusion were significantly lower than those in the injured group, and the membrane fluidity was significantly higher than that in the injured group. It shows that: Gastrodin has protective effects on ischemia-reperfusion injury of cultured neurons in vitro