3,6-(二甲氨基)-二苯骈碘杂六环葡萄糖酸盐对培养的脑皮质神经元和缺血再灌注大鼠脑脂质过氧化的拮抗作用(英文)

目的:观察3,6-(二甲氨基)-二苯骈碘杂六环葡萄糖酸盐对培养的脑皮质神经元和缺血再灌注大鼠脑脂质过氧化的拮抗作用。方法:原代培养大鼠胎鼠脑皮质神经元并制做可逆性不开颅大鼠大脑中动脉梗塞模型,测定培养上清液中乳酸脱氢酶(LDH)的溢出,神经元内和脑匀浆中丙二醛(MDA)含量,脑匀浆超氧化物歧化酶(SOD)活性,脑水肿指数和形态学变化。结果:I-93 10-40μmol·L~(-1)剂量依赖性抑制H_2O_2引起的神经元LDH外漏和MDA升高。I-93 0.5mg·kg~(-1)改善脑组织结构损害,减轻脑水肿,降低脑匀浆中MDA含量并提高SOD活性。结论:I-93通过提高抗氧化酶活性和抑制脂质过氧化对H_2O_2引起的神经毒性和缺血再灌注引起的脑损伤产生保护作用。

Antagonistic effect of 3,6-dimethamidodibenzopyriodonium gluconate on lipid peroxidation in cerebral cortical neuronal cultures and rat brains during focal cerebral ischemia reperfusion

AIM: To study 3,6-dimethamidodibenzopyriodonium gluconate (I-93) antagonistic effects on lipid peroxidation in cerebral cortical neuronal cultures and rat brains during focal cerebral ischemia-reperfusion. METHODS: Cerebral cortical neurons were cultured and rat focal cerebral ischemia-reperfusion model was established by reversible middle cerebral artery occlusion (MCAO) without craniectomy. The efflux of lactate dehydrogenase (LDH) from neurons, content of malondialdehyde (MDA) in neurons and brain homogenate, activity of superoxide dismutase (SOD) in brain homogenate, and index of cerebral edema as well as brain morphology were investigated. RESULTS: I-93 10-40 mumol.L-1 concentration-dependently inhibited efflux of LDH and elevated levels of MDA induced by addition of H2O2(10 mumol.L-1) in vitro. I-93 0.5 mg.kg-1 improved the cerebral morphology, reduced brain edema, decreased MDA content, and enhanced SOD activity in brain homogenate. CONCLUSION: I-93 protects neurons from H2O2-induced neurotoxicity and ischemia-reperfusion mediated damage by increasing the activity of antioxidant enzymes and suppressing the generation of lipid peroxides.