利多卡因对缺氧大鼠脑细胞丙二醛及乳酸水平的影响

Lidocaine effects on increasing levels of malondiadehyde and lactate in rats cortex brain cells cultured under anoxic condition

目的:探索利多卡因对缺氧脑细胞保护作用的途径。方法:选用出生24小时以内的Wistar大鼠乳鼠,分离其大脑皮层细胞进行培养,用MTT方法观察细胞在缺氧条件下培养24小时及48小时后OD值的变化,然后将细胞分为正常培养组,缺氧培养组,缺氧培养十利多卡因组,分别测定培养48小时后培养液中乳酸及丙二醛的含量。结果:大鼠大脑皮层细胞在缺氧培养24小时后,其存活率同正常培养组相比无显著差别;缺氧培养48小时后,其存活率显著下降。缺氧培养48小时后,大鼠脑细胞培养液中丙二醛和乳酸水平显著升高,而利多卡因组的升高则不明显。结论:利多卡因有抑制由缺氧引起的大脑皮层细胞丙二醛和乳酸水平升高的作用。

Objective: To determine the mechanism of protective effects of lidocaine on brain during ischemia. Method: Wistar rats within 24h after birth were enrolled. The brain cortex cells were separated and then cutured under normal or anoxic condition. The OD value of these cells were detected with rapid colorimetric assay after they were cultured 24h and 48h. According to the above values, other cells were cultured in different condition and divided intc three groups: control group(N) cultured under normal condition (37℃, 5%CO_2+95%air); anoxic group(A) and anoxic+ lidoeaine group(L) cultured under anoxic condition(37℃, 5%CO_2+95%N_2). 6.9×10^(-5)mol/L lidocaine was added to the medium in group L. Cells of these three groups were cultured under different condition for 48h, then malondiadehyde and lactate levels of each group were measured. Result: The survival cells of anoxic group were significantly lower than that of control group after cultured for 48h, the malondiadehyde levels were as follows (nmol/ml): group N(4.93 ±0.43, n=12), group A(5.56±0.34, n=12), group L(4. 80±0.25, n=11); the lactate levels (mmol/L): group N(8.05±1.64, n=21), group A (11.86±2.58, n=22), group L(9.96±1.88, n=21), Conclusion: Lidocaine may protect brain from ischemia through inhibiting malondiadehyde and lactate production induced by anoxia.