黄芩素对过氧化氢致PC12细胞损伤的保护作用研究

目的:研究黄芩素(BAI)对过氧化氢(H2O2)损伤的神经细胞的保护作用。方法:用体外细胞培养法,预先孵育24h,以500μmol·L-1H2O2复制大鼠肾上腺髓质嗜铬瘤分化细胞株(PC12)不可逆氧化损伤模型,观察BAI对其影响,并在损伤时分为移除药物和不移除药物2种情况进行分析;通过MTT微量比色法测定细胞活度,并测定培养液中乳酸脱氢酶(LDH)的含量。结果:预先给予BAI作用24h后,在造模时不论是否移除药物,BAI对损伤细胞均有显著的保护作用,尤以不移除药物的效果更为显著。镜下观察,BAI组细胞形态出现一定程度上的边缘模糊,单个细胞体积变大,有少许细胞融合的状态发生;MTT法测定细胞活度升高,培养液中LDH含量降低,与模型组比较差异显著。结论:BAI能显著减轻PC12细胞损伤,其作用机制可能在氧化-抗氧化环节,与BAI能够减轻呼吸链阻断造成的自由基堆积、抗氧化和清除自由基的能力有关。

Neuroprotective Effect of Baicalein on H2O2 - induced PC12 Injury

OBJECTIVE： To observe the neuroprotective effect of Baicalein on H2O2- induced PC12 injury. METHODS： The PC12 cells cultured in vitro were preincubated with BAI for 24 h before being duplicated into the irreversible oxidative damages model with 500 μmol · L^ -2 H2O2, then the protective effect of BAI （BAI presence or withdrawal） on these damaged cells in vitro was observed. The cell activity was detected by MTT microcolorimetry, and the lactate dehydrogenase（LDH） level in supernatant was determined as well. RESULTS： After pretreatment with BAI for 24 h, the injury of PC12 cells was significantly lessened in the presence or withdrawal of drugs in modeling, especially in the presence of drugs. Microscopically, PC12 cells can be seen with fuzzy edge and increased size, and cell fusion occurred in the BAI - treated H2O2 injury model. Cell activity increased, LDH level in the medium decreased, which were significantly different as compared with the model group. CONCLUSION ： BAI can significantly reduce the hypoxic - ischemic injury of PC12 cells. Its mechanism may be related to its ability in reducing the accumulation of free radicals induced by blockage of the respiratory chain, antioxidation and free radical scavenging.