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目的研究黄芩苷(BCL)对过氧化氢(H_2O_2)引起新生大鼠原代海马神经细胞氧化损伤的保护作用。方法分离新生大鼠海马神经细胞并进行原代培养,然后将200μmol·L~(-1)H_2O_2加入到3个质量浓度(25,50,100 mg·m L~(-1)BCL)预处理2 h的细胞培养液中,培养24 h后,以四甲基偶氮唑盐(MTT)法检测细胞存活率;用试剂盒测定培养液内超氧化物歧化酶(SOD)的活力、丙二醛(MDA)的含量以及乳酸脱氢酶(LDH)的释放量。结果模型组的细胞存活率(77.01%)与空白组的细胞存活率(100%)比较,差异有统计学意义(P<0.05);低中高3个量质量浓度实验组共同孵育24 h后的细胞存活率与模型组相比均有所增加,中、高2个质量浓度实验组的BCL的细胞存活率分别为87.00%和94.12%,组间比较差异有统计学意义(P<0.05)。高质量浓度实验组的SOD活力为(32.98±6.13)U·m L~(-1),较模型组的(23.56±4.19)U·m L~(-1)明显升高,差异有统计学意义(P<0.05)。中高2个质量浓度实验组的MDA含量分别为(2.98±0.59),(2.81±0.63)nmol·m L~(-1),较模型组的MDA含量(3.96±0.79)nmol·m L~(-1)均显著降低,差异有统计学意义(P<0.05)。中高2个质量浓度实验组的LDH释放量分别为(334.58±101.41),(327.83±92.66)U·L~(-1),较模型组的LDH释放量(519.67±103.78)U·L~(-1)显著降低,差异有统计学意义(P<0.01)。结论 BCL对H_2O_2引起的新生大鼠原代海马神经细胞的氧化应激损伤具有一定的保护作用。
Objective To investigate the protective effect of baicalin (BCL) on the oxidative damage of primary hippocampal neurons induced by hydrogen peroxide (H_2O_2) in neonatal rats. Methods Hippocampal neurons of neonatal rats were isolated and cultured in primary culture. Then, 200μmol·L -1 H 2 O 2 was added into three BCL pretreatment groups (25, 50 and 100 mg · m L -1) for 2 h After cultured for 24 h, the cell viability was detected by MTT assay. The activity of superoxide dismutase (SOD) MDA content and lactate dehydrogenase (LDH) release. Results The cell viability (77.01%) in the model group was significantly higher than that in the blank group (100%) (P <0.05) Cell survival rate increased compared with the model group. The cell viability of BCL in the two medium and high concentration groups was 87.00% and 94.12%, respectively. The difference between the two groups was statistically significant (P <0.05). The activity of SOD in the high-concentration group was (32.98 ± 6.13) U · m L -1, which was significantly higher than that of the model group (23.56 ± 4.19) U · m L -1, the difference was statistically significant Significance (P <0.05). The contents of MDA in the middle and high concentration groups were (2.98 ± 0.59) and (2.81 ± 0.63) nmol · m L -1, respectively, and those in the model group were (3.96 ± 0.79) nmol · m L -1 -1) were significantly lower, the difference was statistically significant (P <0.05). The results showed that the LDH release in the middle and high concentration groups was (334.58 ± 101.41) and (327.83 ± 92.66) U · L -1, respectively. Compared with the model group, the release of LDH was (519.67 ± 103.78) U · L ~ -1) was significantly lower, the difference was statistically significant (P <0.01). Conclusion BCL can protect oxidative stress injury of primary hippocampal neurons induced by H 2 O 2 in neonatal rats.