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目的:探讨梓醇对脑缺血大鼠恢复早期脑能量代谢的影响。方法:线栓法建立SD大鼠右侧大脑中动脉永久性缺血模型(pMCAO),于术后3d开始给药,术后14d取材,测定各组大鼠脑组织中钠、钾-三磷酸腺苷酶(Na+、K+-ATPase)和钙、镁-三磷酸腺苷酶(Ca2+、Mg2+-ATase)活性。结果:模型组与假手术组比较,Na+、K+-ATPase和Ca2+、Mg2+-ATPase活性明显降低,表明模型组在术后14d未自行恢复到正常水平。模型组与各给药组比较,Na+、K+-ATPase和Ca2+、Mg2+-ATPase活性差异均具有显著意义。结论:梓醇抑制脑缺血大鼠细胞凋亡的机理与Na+、K+-ATPase和Ca2+、Mg2+-ATPase升高有关。
Objective: To investigate the effect of catalpol on brain energy metabolism in early recovery of cerebral ischemia rats. Methods: The right middle cerebral artery occlusion model (pMCAO) of SD rats was established by thread occlusion. The rats were administered 3d on the 3rd day after operation. The rats were sacrificed 14 days after the operation to determine the changes of sodium, potassium-ATPase (Na +, K + -ATPase) and calcium, magnesium-ATPase (Ca2 +, Mg2 + -ATase) activity. Results: The activities of Na +, K + -ATPase, Ca2 + and Mg2 + -ATPase in the model group were significantly lower than those in the sham operation group, indicating that the model group did not return to normal level on the 14th day after operation. Compared with the other groups, the activity of Na +, K + -ATPase, Ca2 + and Mg2 + -ATPase in model group were significantly different. Conclusion: The mechanism of catalpol inhibiting apoptosis in cerebral ischemia rats is related to the increase of Na +, K + -ATPase, Ca2 + and Mg2 + -ATPase.