發(fā)布時(shí)間：2018-01-04 12:28

  本文關(guān)鍵詞：鐵代謝紊亂在七氟醚和異氟醚致小鼠認(rèn)知功能障礙中的作用　出處：《河北醫(yī)科大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 鐵代謝障礙 認(rèn)知障礙 麻醉藥 吸入 異氟醚 阿爾茨海默病

【摘要】：目的:本研究擬評價(jià)鐵代謝紊亂在七氟醚和異氟醚致小鼠認(rèn)知功能障礙中的作用。方法:清潔級健康雄性昆明小鼠24只,12月齡,體重45~55 g,采用隨機(jī)數(shù)字表法,將其分為3組(n=8):對照組(Con組)、七氟醚組(Sev組)和異氟醚組(Iso組)。Sev組吸入2%七氟醚6 h,Iso組吸入1.4%異氟醚6 h,載氣為純氧,Con組僅吸入純氧6 h。各組小鼠于麻醉處理前進(jìn)行Morris水迷宮定位航行訓(xùn)練,歷時(shí)5 d,每天4次。麻醉結(jié)束后12 h再次進(jìn)行Morris水迷宮實(shí)驗(yàn),通過攝像機(jī)和計(jì)算機(jī)記錄各組小鼠水迷宮運(yùn)動軌跡,逃避潛伏期和尋找平臺的總路程。隨后,腹腔注射0.4%戊巴比妥鈉(1 ml/100 g)麻醉小鼠,剪開胸腔暴露心臟,使用0.9%氯化鈉對小鼠進(jìn)行血液灌流,剪下頭部,剝?nèi)∧X組織,分離出大腦皮層和海馬組織。采用Western blot法定性檢測各組小鼠皮層和海馬區(qū)鐵代謝相關(guān)蛋白ferritin-L、ferritin-H、TfR1、FPN1、DMT1(+IRE)以及磷酸化Tau蛋白表達(dá)水平,通過化學(xué)發(fā)光凝膠成像儀獲取相應(yīng)的蛋白條帶圖,然后使用Image-Pro Plus 6.0軟件分析各蛋白條帶的積分光密度值。以目的條帶積分光密度值與內(nèi)參蛋白條帶積分光密度值的比值反映目的蛋白的表達(dá)水平。采用SPSS13.0軟件進(jìn)行統(tǒng)計(jì)分析,以上正態(tài)分布的計(jì)量資料以均數(shù)±標(biāo)準(zhǔn)差(？)表示,組間比較采用單因素方差分析,P0.05認(rèn)為差異有統(tǒng)計(jì)學(xué)意義。結(jié)果:1 Morris水迷宮實(shí)驗(yàn)結(jié)果:麻醉處理前,三組小鼠尋找平臺的總路程和逃避潛伏期差異無統(tǒng)計(jì)學(xué)意義(P0.05);與Con組小鼠相比,Sev組和Iso組小鼠尋找平臺的總路程和逃避潛伏期均延長(P0.05)。2鐵代謝相關(guān)蛋白表達(dá)水平的檢測結(jié)果:與Con組相比,Sev組小鼠的大腦皮層及海馬中ferritin-L、ferritin-H、FPN1表達(dá)均上調(diào),TfR1表達(dá)下調(diào)(P0.05),DMT1(+IRE)表達(dá)差異無統(tǒng)計(jì)學(xué)意義(P0.05);與Con組相比,Iso組小鼠大腦皮層和海馬中ferritin-L、ferritin-H、TfR1、FPN1和DMT1(+IRE)的表達(dá)水平差異無統(tǒng)計(jì)學(xué)意義(P0.05)。3磷酸化Tau蛋白表達(dá)水平的檢測結(jié)果:與Con組相比,Sev組和Iso組小鼠大腦皮層和海馬中磷酸化Tau蛋白表達(dá)均上調(diào)(P0.05)。結(jié)論:七氟醚導(dǎo)致小鼠認(rèn)知功能障礙的機(jī)制與鐵代謝紊亂有關(guān),而異氟醚導(dǎo)致小鼠認(rèn)知功能障礙的過程中并沒有鐵代謝異常的發(fā)生。
[Abstract]:Objective: to evaluate the effect of iron metabolism disorder on cognitive dysfunction induced by sevoflurane and isoflurane in mice. The rats were randomly divided into 3 groups: control group (Con group), sevoflurane group (group Sev) and isoflurane group (Iso group) and isoflurane group (group Iso) inhaled sevoflurane for 6 h. The Iso group inhaled 1.4% isoflurane for 6 hours, the carrier gas was pure oxygen for 6 hours only. The mice in each group were trained in Morris water maze navigation for 5 days before anesthesia. Morris water labyrinth experiment was conducted again 12 hours after anesthesia, and the motion track of water maze was recorded by camera and computer. Then, 0.4% pentobarbital sodium (1 ml/100 g) was injected intraperitoneally to anesthetize the mice and cut open the chest cavity to expose the heart. The mice were perfused with 0.9% sodium chloride, the head was cut off and the brain tissue was removed. The cortical and hippocampal tissues were isolated, and the iron metabolism-related protein ferritin-L in cortex and hippocampus of each group was detected qualitatively by Western blot assay. The expression level of DMT1 (IRE1) and phosphorylated Tau protein were obtained by chemiluminescent gel imager. Then use Image-Pro Plus. The integrated optical density of each protein band was analyzed by software 6.0. The expression level of the target protein was reflected by the ratio of the integrated optical density value of the target band to the integral optical density value of the protein band of the internal reference protein. The expression level of the target protein was reflected by SPSS13.0 soft. Statistical analysis was carried out. The measurement data of the above normal distribution are calculated as mean 鹵standard deviation? The results showed that the differences were statistically significant by univariate ANOVA (P0.05). Results: 1 Morris water maze experiment results: before anesthesia treatment. There was no significant difference in the total distance and escape latency between the three groups. Compared with Con group mice. The expression of P0.052iron metabolism-related protein in Sev group and Iso group was significantly longer than that in Con group. The results were as follows: compared with Con group, the total distance and escape latency of mice in Sev group and Iso group were prolonged. In Sev group, the expression of ferritin-Lnferritin-Hfritin-HFPN1 was up-regulated in cerebral cortex and hippocampus of mice, and the expression of TfR1 was down-regulated (P0.05). There was no significant difference in the expression of DMT1 (IRE1). Compared with Con group, ferritin-Lnferritin-HfR1 was found in cerebral cortex and hippocampus of mice in Iso group. There was no significant difference between FPN1 and DMT1 (IREs) in the expression of P0.05.3 phosphorylated Tau protein. The results were as follows: compared with Con group. The expression of phosphorylated Tau protein in cerebral cortex and hippocampus of Sev and Iso mice were up-regulated. Conclusion: the mechanism of cognitive dysfunction induced by sevoflurane is related to iron metabolism disorder. There was no abnormal iron metabolism during the cognitive impairment induced by isoflurane in mice.
【學(xué)位授予單位】：河北醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R614

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