摘要
目的在离体水平，探讨黄芩苷对缺氧缺糖／再灌注（OGD／RP）诱导的脑片及神经元损伤的保护作用及机制。方法小鼠离体脑片OGD／RP模型中，以2，3，5-三苯基氯化四氮唑（TFC）产物白腊评价脑片活性；原代培养大鼠皮层神经元OGD／RP模型中，以噻唑蓝（MTT）还原和乳酸脱氢酶（IDH）活性测定神经元活性变化，用2，7一二氯荧光素二乙酸盐（DCF-DA）测定细胞内自由基水平。观察不同时间给予黄芩苷对损伤的保护作用。结果在脑片，全程给药和OGD时给予黄芩苷0.01—1μmol·L^-1，再灌注时给予黄芩苷0．1～1μmol·L^-1，可显著减轻损伤。在神经元，全程给予黄芩苷0．1～1μmol·L^-1可减轻神经元损伤，并降低神经元内自由基水平升高。结论黄芩苷对OGD／RP损伤有浓度依赖性保护作用，再灌注时给药亦有效，其作用至少部分与抗自由基有关。
OBJECTIVE： To investigate the protective effect of baicalin on oxygen-glucose deprivation/reperfusion （OGD/RP）-induced injury and possible mechanism in mouse brain slices and rat cortical neurons, METHODS In mouse brain slices, the viability after OGD/RP was assessed by the formation of formazn,a red product of 2,3,5-trihenylterzolium chloride （TTC）. In primary cultured rat cortical neurons,the neuronal viability and damage after OGD/RP were assessed by MTT reduction and LDH release, and the intracellular free radicals were measured with 2,7-dichlorofluorescein diacetate （DCF-DA）. The effect of baicalin at different times on OGD/RP injury at various concentrations was evaluated. RESULTS In mouse brain slices, baicalin significantly attenuated OGD/RP injury at 0.01 - 1 μmol· L^-1 when baicalin was added throughout the experiment or during OGD, and at 0.1 - 1 μmol· L^-1 with baicalin was added during reperfusion. In rat cortical neurons, baicalin protected the neurons from OGD/RP injury, and inhibited the elevation of intracellular free radicals at 0.01 - 1 μmol· L^- 1 when baicalin was added throughout the expriment. CONCLUSION Baicalin had concentration-dependently protective effect on OGD/RP injury in vitro, even when being administrated during reperfusion, this effect may be, at least partly, mediated by the inhibition of intracellular free radicals.
出处
《中国药学杂志》
CAS
CSCD
北大核心
2006年第16期1234-1237,共4页
Chinese Pharmaceutical Journal
基金
国家自然科学基金资助项目(30271498)
关键词
黄芩苷
脑缺血
缺氧缺糖/再灌注
脑片
神经元
baicalin
cerebral ischemia
oxygen- glucose deprivation/reperfusion （OGD/RP）
brain slices
neuron
