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目的探讨梓醇对永久性脑缺血损伤大鼠恢复早期运动感觉功能和能量代谢的影响及作用机制。方法线栓法制备大鼠大脑中动脉永久性局灶性缺血模型,除假手术组外,缺血动物于术后3 d随机分成模型组、梓醇小剂量组、梓醇中剂量组、梓醇大剂量组、天保宁组,并于造模后3~14 d灌胃给予相应的药物。在术后3、9、14 d 3个时间点分别观察动物的横木行走功能和揭除胶布的潜伏期,并在术后14 d行为学检测完成后断头处死动物,取材,测定脑组织中乳酸和丙酮酸的含量、钠钾-三磷酸腺苷酶(Na+,K+-ATPase)和钙镁-三磷酸腺苷酶(Ca2+,Mg2+-ATPase)活性。结果模型组大鼠横木行走能力和揭除胶布的潜伏期都随着时间的延长而逐渐的改善,但在14 d的观察期结束时仍然有大部分动物未恢复到正常的水平,而给药组能明显的促进缺血大鼠横木行走能力和揭除胶布的潜伏期的改善,尤其以梓醇中、大剂量组最为显著(P<0.05,P<0.01);且各给药组均能显著降低脑组织中乳酸的含量,增加丙酮酸的含量,增强Na+,K+-ATPase和Ca2+,Mg2+-ATPase活力,与模型组比较有显著性差异(P<0.05,P<0.01)。结论梓醇可加快大鼠永久性脑缺血后运动感觉功能的恢复,其可能的机制是改善了能量耗竭症状。
Objective To investigate the effect and mechanism of catalpol on recovery of early motor function and energy metabolism in permanent cerebral ischemia injury rats. Methods The model of permanent focal cerebral ischemia in the middle cerebral artery was established by suture method. The ischemic animals were randomly divided into model group, catalpol low dose group, catalpol medium dose group, Catalpol large dose group, Tianbaoning group, and in the modeling 3 ~ 14 d after administration of the corresponding drug. At 3, 9, and 14 days after operation, the function of horizontal walking and the incubation period of adhesive tape were observed respectively. Animals were sacrificed on the 14th day after the completion of behavioral testing. The animals were sacrificed and the contents of lactate And the content of pyruvate, the activities of Na +, K + -ATPase and Ca2 +, Mg2 + -ATPase. Results In the model group, the walking ability of the crossbar and the tape release latency gradually improved over time, but most of the animals did not return to the normal level at the end of the 14-day observation period. (P <0.05, P <0.01), and significantly decreased in each treatment group (P <0.05, P <0.01) Compared with the model group, the content of lactic acid, the content of pyruvate and the activity of Na +, K + -ATPase, Ca2 + and Mg2 + -ATPase in brain tissue were significantly different (P <0.05, P <0.01). Conclusion Catalpol can accelerate the recovery of motor sensory function after permanent cerebral ischemia in rats, and its possible mechanism is to improve the symptoms of energy depletion.