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目的通过建立血管性痴呆动物模型,探讨和厚朴酚注射用冻干脂质体对血管性痴呆大鼠的神经保护作用机制。方法采用单侧颈动脉结扎阻断法制作血管性痴呆动物模型,将90只雄性大鼠分为假手术组、模型组、曲克芦丁水溶液组、和厚朴酚注射用冻干脂质体高、中、低剂量组(0.15mg·kg-1,0.03mg·kg-1,0.006mg·kg-1)。术后7d进行行为学检测;HE染色法进行病理形态学分析;脑组织匀浆测定自由基代谢水平及单胺类递质活性。结果与假手术组比较,模型组大鼠逃避潜伏期显著延长,大鼠游泳距离和游泳时间显著缩短,通过安全台次数显著减少(P<0.01),丙二醛(MDA)含量明显上升,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性显著降低(P<0.05,P<0.01),脑组织中去甲肾上腺素(NE)、多巴胺(DA)、5-羟色胺(5-HT)、5-羟吲哚乙酸(5-HIAA)含量显著减少(P<0.05,P<0.01),乙酰胆碱酯酶(Ach E)活性明显降低(P<0.05,P<0.01);与模型组比较,和厚朴酚注射用冻干脂质体高、中剂量组与曲克芦丁水溶液组大鼠逃避潜伏期显著缩短(P<0.05,P<0.01),游泳距离和游泳时间显著延长,通过安全台的次数显著增加(P<0.05,P<0.01),脑组织MDA含量显著降低,SOD、GSH-Px活性显著提高(P<0.05,P<0.01),脑组织中NE、DA、5-HT、5-HIAA含量显著增多(P<0.05,P<0.01),Ach E活性明显升高(P<0.05,P<0.01),尤以和厚朴酚注射用冻干脂质体高剂量组作用显著(P<0.05,P<0.01)。结论和厚朴酚注射用冻干脂质体对血管性痴呆大鼠的学习记忆及行为能力具有明显改善作用,其机制可能与减轻氧化应激反应,提高单胺类递质等密切相关。
Objective To establish the animal model of vascular dementia to investigate the neuroprotective mechanism of honokiol freeze-dried liposomes on vascular dementia rats. Methods Animal models of vascular dementia were established by unilateral carotid artery ligation and blocking. 90 male rats were divided into sham operation group, model group, troxerutin aqueous solution group and honokiol injection freeze-dried liposomes (0.15mg · kg-1, 0.03mg · kg-1, and 0.005mg · kg-1). Behavioral tests were performed 7 days after operation. Pathological analysis was performed by HE staining. Free radical metabolism and monoamine neurotransmitter activity were measured in brain homogenates. Results Compared with the sham operation group, the escape latency of model rats was significantly prolonged, the swimming distance and swimming time of rats in the model group were significantly shortened, the number of safety stations significantly decreased (P <0.01), the content of malondialdehyde (MDA) The activities of SOD, GSH-Px in brain tissue were significantly decreased (P <0.05, P <0.01), and NE, DA, The levels of 5-HIAA and 5-HIAA were significantly decreased (P <0.05, P <0.01) and the activities of AchE were significantly decreased (P <0.05, P <0.01) ). Compared with the model group, the escape latency of the rats treated with honokiol injection freeze-dried liposomes was significantly shortened (P <0.05, P <0.01), swimming distance and swimming time (P <0.05, P <0.01). The content of MDA in brain tissue was significantly decreased and the activities of SOD and GSH-Px were significantly increased (P <0.05, P <0.01) DA, 5-HT and 5-HIAA were significantly increased (P <0.05, P <0.01) and AchE activity was significantly higher (P <0.05, P <0.01) The effect of high dose group was significant (P <0.05, P <0.01). Conclusion Honokiol injection of lyophilized liposomes can significantly improve the learning, memory and behavioral abilities of rats with vascular dementia. The mechanism may be related to the reduction of oxidative stress and the increase of monoamine neurotransmitters.