本文選題：鹽酸美金剛 + 血管性癡呆�。� 參考：《中國老年學(xué)雜志》2014年04期

【摘要】：目的觀察鹽酸美金剛干預(yù)對血管性癡呆(VD)大鼠海馬區(qū)腦源性神經(jīng)營養(yǎng)因子(BDNF)表達(dá)以及氧化應(yīng)激水平的影響。方法選取60只健康雄性Wistar大鼠為研究對象,隨機分為模型組,對照組,觀察組,每組各20只。模型組、觀察組均采用持久雙側(cè)頸總動脈結(jié)扎方法制作血管性癡呆大鼠模型,對照組不做結(jié)扎處理,術(shù)后8 w模型組給予羥甲基纖維素鈉干預(yù),觀察組給予鹽酸美金剛干預(yù),連續(xù)4 w后對各組大鼠進行水迷宮試驗,然后處死,檢測并比較3組大鼠腦海馬區(qū)BDNF表達(dá)及氧化應(yīng)激指標(biāo)丙二醛(MDA)、超氧化物歧化酶(SOD)水平的差異,分析鹽酸美金剛的干預(yù)效果。結(jié)果對照組水迷宮測試時間為(92.8±37.6)s,模型組為(154.6±38.7)s,觀察組為(117.4±34.2)s,3組間差異具有統(tǒng)計學(xué)意義(P0.05)。對照組大鼠海馬區(qū)神經(jīng)元細(xì)胞正常,模型組海馬區(qū)神經(jīng)元細(xì)胞數(shù)量降低,觀察組海馬區(qū)形態(tài)學(xué)變化介于對照組與模型組之間。經(jīng)病理圖像分析軟件分析以及SOD、MDA的光密度(OD)值測定,3組大鼠海馬區(qū)BDNF平均灰度值以及MDA、SOD表達(dá)水平有顯著差異(P0.05)。結(jié)論鹽酸美金剛可清除海馬區(qū)氧自由基,減輕組織損傷,并上調(diào)海馬區(qū)BDNF的表達(dá)保護神經(jīng)元細(xì)胞。
[Abstract]:Objective to observe the effect of MJ on the expression of brain-derived neurotrophic factor (BDNF) and the level of oxidative stress in hippocampus of rats with vascular dementia (VD). Methods 60 healthy male Wistar rats were randomly divided into three groups: model group, control group and observation group. The model group and the observation group were all treated with permanent bilateral common carotid artery ligation method to make vascular dementia rats. The control group was not treated with ligation, the model group was treated with sodium hydroxymethyl cellulose at 8 weeks after operation, and the observation group was treated with methadone hydrochloride. After 4 weeks, the rats in each group were tested by water maze test, and then killed. The expression of BDNF and the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in the hippocampus of the three groups were detected and compared. Results the test time of water maze in the control group was 92.8 鹵37.6 s, that in the model group was 154.6 鹵38.7 s, and that in the observation group was 117.4 鹵34.2 Ms. The difference was statistically significant (P 0.05). The hippocampal neurons in the control group were normal and the number of neurons in the hippocampal area in the model group was decreased. The morphological changes of the hippocampal area in the observation group were between the control group and the model group. There were significant differences in the mean gray value of BDNF and the expression level of BDNF in hippocampal area of the three groups by the analysis of pathological image analysis software and the optical density and ODV value of SDD. Conclusion MJ can scavenge the oxygen free radicals in the hippocampus, reduce tissue damage, and up-regulate the expression of BDNF in the hippocampal area to protect the neuronal cells.
【作者單位】： 鄭州大學(xué)第一附屬醫(yī)院;
【分類號】：R965;R749.1

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