梓醇对缺糖缺氧诱导PC12细胞损伤的保护作用研究

目的探讨梓醇对抗缺糖缺氧诱导的PCI2细胞损伤作用。方法梓醇预处理PCI2细胞，加入含连二亚硫酸钠的无糖Earle’s液制备损伤模型，检测细胞存活率，乳酸脱氢酶、超氧化物歧化酶、谷胱甘肽过氧化物酶、丙二醛水平，检测细胞内游离Ca2＋浓度。结果与模型组比较，梓醇可剂量依赖性的提高细胞存活率（P〈0．01），减少乳酸脱氢酶漏出率（P〈0．05或〈0．01），提高超氧化物歧化酶、谷胱甘肽过氧化物酶活性，拮抗丙二醛水平升高，降低细胞内游离Ca2＋浓度（P〈0．05或〈0．01）。结论梓醇对缺糖缺氧诱导的PCI2细胞损伤具有保护作用，作用机制可能与其清除自由基和抑制钙超载有关。

Protective effects of catalpol on PC12 cell injury induced by oxygen-glucose deprivation

Objective To investigate the protective effects of catalpol on PC12 ceils damage induced by oxygen-glucose deprivation. Methods PC12 cells were pretreated with catalpol, then exposed to sodium hyposulfite to establish cell injury model. The cell survival rates were detected by MTI＂ assay. The activities of LDH, SOD, GSH-Px and MDA levels were detected by colorimetry,and free Ca2＋ concentration within cell was detected by fluorescence probe. Results As compared with model group, catalpol could enhance significantly survival rate of PC12 cell in a dose-dependent manner （ P 〈 0.01） ,and could reduce the efflux of LDH from damaged cell and increase the activities of SOD, GSH-Px, however,which could decrease MDA levels and intracellular Ca2 ＋ concentration （ P 〈 0.05 or P 〈 0.01 ）. Conclusion Catalpol can protect PC12 cells from oxygen glucose deprivation injury, and its action mechanism may be related with removing free radical and inhibiting calcium overload.