CAJ | 학술논문

目的评价七氟醚对β淀粉样蛋白(Aβ)诱导的大鼠认知功能障碍及海马组织氧化应激反应的影响.方法雄性成年SD大鼠96只,体重250 ～ β00 g,采用随机数字表法分为4组(n=24):对照组(C组)海马区注射生理盐水2μl,注射后22 d吸入30％氧气4 h;Aβ组海马区注射Aβ1-402μl,注射后22 d吸入30％氧气4 h;1.3％和2.6％七氟醚组(S1组和S2组)海马区注射Aβ1-40 2 μl,注射后22 d分别吸入1.3％和2.6％七氟醚4h.S1组和S2组分别于麻醉后1、3、7d,C组和Aβ组于相应时点行Morris水迷宫实验,记录游泳速度、逃避潜伏期和原平台象限探索时间比.各时点行为学测试结束后,处死大鼠,取血样,测定血清S100β蛋白浓度;取海马组织,测定SOD活性和MDA含量.结果与C组比较,Aβ组各时点逃避潜伏期延长,原平台象限探索时间比减少,血清S100β蛋白浓度升高,海马SOD活性降低,MDA含量升高(P＜0.05);与Aβ组比较,S1组上述各指标差异无统计学意义(P＞0.05),S2组各时点逃避潜伏期延长,原平台象限探索时间比减少,血清S100β蛋白浓度升高,海马SOD活性降低,MDA含量升高(P＜0.05);与S1组比较,S2组各时点逃避潜伏期延长,原平台象限探索时间比减少,血清S100β蛋白浓度升高,海马SOD活性降低,MDA含量升高(P＜0.05).各组间游泳速度比较差异无统计学意义(P＞0.05)结论吸入2.6％七氟醚4h可加重Aβ诱导的大鼠认知功能障碍,其机制可能与加重脑内氧化应激反应有关.
목적 평개칠불미대β정분양단백(Aβ)유도적대서인지공능장애급해마조직양화응격반응적영향.방법 웅성성년SD대서96지,체중250 ～ β00 g,채용수궤수자표법분위4조(n=24):대조조(C조)해마구주사생리염수2μl,주사후22 d흡입30％양기4 h;Aβ조해마구주사Aβ1-402μl,주사후22 d흡입30％양기4 h;1.3％화2.6％칠불미조(S1조화S2조)해마구주사Aβ1-40 2 μl,주사후22 d분별흡입1.3％화2.6％칠불미4h.S1조화S2조분별우마취후1、3、7d,C조화Aβ조우상응시점행Morris수미궁실험,기록유영속도、도피잠복기화원평태상한탐색시간비.각시점행위학측시결속후,처사대서,취혈양,측정혈청S100β단백농도;취해마조직,측정SOD활성화MDA함량.결과 여C조비교,Aβ조각시점도피잠복기연장,원평태상한탐색시간비감소,혈청S100β단백농도승고,해마SOD활성강저,MDA함량승고(P＜0.05);여Aβ조비교,S1조상술각지표차이무통계학의의(P＞0.05),S2조각시점도피잠복기연장,원평태상한탐색시간비감소,혈청S100β단백농도승고,해마SOD활성강저,MDA함량승고(P＜0.05);여S1조비교,S2조각시점도피잠복기연장,원평태상한탐색시간비감소,혈청S100β단백농도승고,해마SOD활성강저,MDA함량승고(P＜0.05).각조간유영속도비교차이무통계학의의(P＞0.05)결론 흡입2.6％칠불미4h가가중Aβ유도적대서인지공능장애,기궤제가능여가중뇌내양화응격반응유관.
Objective To evaluate the effects of sevoflurane on β-amyloid (Aβ)-induced cognitive dysfunction and oxidative stress response of hippocampal tissues in rats.Methods Ninety-six male adlut SpragueDawley rats,weighing 250-300 g,were randomly divided into 4 groups (n =24 each) using a random number table:control group (group C) ; group Aβ ; 1.3 ％ sevoflurane group (group S1) and 2.6 ％ sevoflurane group (group S2).The animals were anesthetized with intraperitoneal.10％ chloral hydrate 350 mg/kg.Cognitive dysfunction was induced by injecting Aβ1-40 2 μ1 into the bilateral hippocampi in Aβ,S1 and S2 groups.The equal volume of normal saline was given in group C.At 22 days after injection,C and Aβ groups were exposed to 30％ oxygen for 4 h,and S1 and S2 groups inhaled 1.3 ％ and 2.6 ％ sevoflurane,respectively,for 4 h.Eight rats were chosen at days 1,3 and 7 after exposure and cognitive function was assessed by Morris water maze test.The swimming speed,escape latency and exploration time at the original platform quadrant were recorded.The rats were then sacrificed after the end of the behavioral test and blood samples were taken for determination of serum S100β protein concentration.Hippocampi were immediately isolated and the homogenate was prepared for determination of superoxide dismutase (SOD) activity and malondialdehyde (MDA) content.Results Compared with group C,the escape latency was significantly prolonged and exploration time at the original platform quadrant was shortened,the serum S100β protein concentration and MDA content were increased,and SOD activity was decreased at each time point in group Aβ (P ＜ 0.05).There were no significant differences in the variables mentioned above between Aβ and S1 groups (P ＞ 0.05).The escape latency was significantly prolonged and the exploration time at the original platform quadrant was shortened,the serum S100β protein concentration and MDA content were increased,and SOD activity was decreased at each time point in group S2 as compared with Aβ and S1 groups (P ＜ 0.05).There was no significant difference in the swimining speed among the 4 groups (P ＞ 0.05).Conclusion Inhalation of 2.6 ％ sevoflurane for 4 h can aggravate the cognitive dysfunction induced by Aβ in rats and aggravation of oxidative stress response may be involved in the mechanism.