运动和饮食因素对脑老化小鼠学习记忆能力影响的行为学观察

目的观察高脂饮食和运动对D-半乳糖(D-gal)致脑老化小鼠学习记忆功能的影响。方法采用D-gal致脑老化复制脑老化小鼠模型,以Morris水迷宫测试小鼠学习记忆功能。结果高脂饲料脑老化模型组与普通饲料脑老化模型限食组、普通饲料脑老化模型加运动组、高脂饲料脑老化模型加运动组、高脂饲料正常组、普通饲料加运动组、普通饲料正常组之间学习记忆功能的差异均有统计学意义(P<0.05);空间探索试验显示,普通饲料脑老化模型限食组与普通饲料脑老化模型组之间的差异有统计学意义(P<0.05)。结论运动和限食可减轻脑老化小鼠学习记忆能力的下降;高脂饮食有促进脑老化的作用。     

限食与运动对D-半乳糖诱导的脑老化小鼠的神经保护作用

目的:探讨限食和运动在抗脑老化中的神经保护作用。方法:雄性ICR小鼠60只,随机分为6组,即脑老化模型组(A组)、脑老化模型限食组(B组)、脑老化模型运动组(C组)、运动组(D组)、限食组(E组)和对照组(F组),每组10只,A、B、C组制备脑老化模型,B、E组限食,C、D组运动训练,分别干预10周后,以Morris水迷宫测试小鼠空间记忆和学习能力,以dUTP缺口末端标记(TUNEL)法测定海马神经元凋亡率。结果:A组逃避潜伏期(EL)大于F组(P<0.05),B、C组EL均小于A组(P<0.05)而与F组无差异,D、E组的EL与F组之间无差异;A组海马神经元凋亡率高于F组(P<0.05),B、C组神经元凋亡率低于A组(P<0.05)而与F组之间无差异,D、E组小鼠神经元凋亡率与F组比较亦无差异。结论:限食、运动具有防止脑老化性学习记忆能力下降的效应,并能有效减轻脑老化性神经元凋亡,但对正常小鼠学习记忆能力和神经元凋亡率无明显影响。     

乌圆补血口服液对拟老年痴呆症小鼠脑乙酰胆碱酯酶的影响

目的：探讨乌圆补血口服液对拟老年痴呆症小鼠的预防和治疗效果.方法：实验于2004-06-10/10-03在右江民族医学院重金属与氟砷毒物研究实验室内进行.选用昆明种小白鼠60只,随机分为正常对照组、模型组、乌圆补血口服液预防组、乌圆补血口服液治疗组、脑复康治疗组,每组12只.除正常对照组外,其他各组均用12 mg/mL的氯化铝蒸馏水溶液,按303 mg/kg灌胃,1次/d,连续115 d,制作拟老年痴呆症小鼠模型.乌圆补血口服液预防组从造模开始就用乌圆补血口服液灌服;造模第8周后,乌圆补血口服液治疗组用乌圆补血口服液灌服治疗,脑复康治疗组用脑复康治疗;正常对照组,模型组用等量生理盐水灌胃,1次/d.分别于造模前,造模第8周,治疗后从鼠尾部取血,采用高铁氰化钾法测定各组大鼠血红蛋白,分离血清,采用酶法、改良赖氏法、脲酶-波氏比色法分别测定各组小鼠血清乙酰胆碱酯酶活力、丙氨酸氨基转移酶活力、尿素含量,实验结束后处死各组小鼠,取大脑和肝脏,冰冻下匀浆,用生理盐水制成10%匀浆,测定脑乙酰胆碱酯酶活力、脑丙二醛和肝丙二醛含量（TBA反应法）,组间比较采用方差分析,t检验,实验数据以x&;#177;s表示,P＜0.05有显著性差异. 结果：实验纳入小鼠60只,全部进入结果分析.①血红蛋白含量的变化：与造模前比较,造模后第8周乌圆补血口服液预防组及脑复康治疗组的血红蛋白含量明显降低（P＜0.01）.治疗后,模型组的血红蛋白含量明显低于造模后第8周（P＜0.01）,脑复康治疗组在造模后第8周时血红蛋白含量明显低于模型组（P＜0.05）.②血清尿素、丙氨酸氨基转移酶、乙酰胆碱酯酶活性活力测定：模型组乙酰胆碱酯酶活性明显高于其他各组[（138.97&;#177;16.52）nkat/L,（128.04&;#177;12.79,120.46&;#177;31.21,117.87&;#177;19.45,114.86&;#177;16.37）nkat/L,（P＜0.05）].各组小鼠血清尿素含量、丙氨酸氨基转移酶活力各组间无显著性差异（P＞0.05）.③脑丙二醛、脑乙酰胆碱酯酶活力和肝丙二醛测定：正常对照组、乌圆补血口服液预防组、乌圆补血口服液治疗组及脑复康治疗组的脑乙酰胆碱酯酶活性明显低于模型组[（12.17&;#177;3.17,16.34&;#177;15.00,15.00&;#177;1.83,14.50&;#177;2.00）nkat/L,（23.00&;#177;2.67）nkat/L,（P＜0.01）].脑、肝丙二醛含量各组比较无显著性差异（P＞0.05）.结论：拟老年痴呆症模型小鼠大脑胆碱能系统受到明显的损害,乌圆补血口服液对其有一定的改善作用.     

乌圆补血口服液对拟老年痴呆症小鼠脑乙酰胆碱酯酶的影响

目的:探讨乌圆补血口服液对拟老年痴呆症小鼠的预防和治疗效果。方法:实验于2004-06-10/10-03在右江民族医学院重金属与氟砷毒物研究实验室内进行。选用昆明种小白鼠60只,随机分为正常对照组、模型组、乌圆补血口服液预防组、乌圆补血口服液治疗组、脑复康治疗组,每组12只。除正常对照组外,其他各组均用12mg/mL的氯化铝蒸馏水溶液,按303mg/kg灌胃,1次/d,连续115d,制作拟老年痴呆症小鼠模型。乌圆补血口服液预防组从造模开始就用乌圆补血口服液灌服;造模第8周后,乌圆补血口服液治疗组用乌圆补血口服液灌服治疗,脑复康治疗组用脑复康治疗;正常对照组,模型组用等量生理盐水灌胃,1次/d。分别于造模前,造模第8周,治疗后从鼠尾部取血,采用高铁氰化钾法测定各组大鼠血红蛋白,分离血清,采用酶法、改良赖氏法、脲酶-波氏比色法分别测定各组小鼠血清乙酰胆碱酯酶活力、丙氨酸氨基转移酶活力、尿素含量,实验结束后处死各组小鼠,取大脑和肝脏,冰冻下匀浆,用生理盐水制成10%匀浆,测定脑乙酰胆碱酯酶活力、脑丙二醛和肝丙二醛含量(TBA反应法),组间比较采用方差分析,t检验,实验数据以x±s表示,P<0.05有显著性差异。结果:实验纳入小鼠60只,全部进入结果分析。①血红蛋白含量的变化:与造模前比较,造模后第8周乌圆补血口服液预防组及脑复康治疗组的血红蛋白含量明显降低(P<0.01)。治疗后,模型组的血红蛋白含量明显低于造模后第8周(P<0.01),脑复康治疗组在造模后第8周时血红蛋白含量明显低于模型组(P<0.05)。②血清尿素、丙氨酸氨基转移酶、乙酰胆碱酯酶活性活力测定:模型组乙酰胆碱酯酶活性明显高于其他各组[(138.97±16.52)nkat/L,(128.04±12.79,120.46±31.21,117.87±19.45,114.86±16.37)nkat/L,(P<0.05)]。各组小鼠血清尿素含量、丙氨酸氨基转移酶活力各组间无显著性差异(P>0.05)。③脑丙二醛、脑乙酰胆碱酯酶活力和肝丙二醛测定:正常对照组、乌圆补血口服液预防组、乌圆补血口服液治疗组及脑复康治疗组的脑乙酰胆碱酯酶活性明显低于模型组[(12.17±3.17,16.34±15.00,15.00±1.83,14.50±2.00)nkat/L,(23.00±2.67)nkat/L,(P<0.01)]。脑、肝丙二醛含量各组比较无显著性差异(P>0.05)。结论:拟老年痴呆症模型小鼠大脑胆碱能系统受到明显的损害,乌圆补血口服液对其有一定的改善作用。     

急性心肌梗死大鼠心肌乙酰胆碱酯酶活性的变化

目的:观察大鼠急性心肌梗死后心肌中乙酰胆碱酯酶活性的变化。方法:实验于2004-10/2005-04在哈尔滨医科大学附属第一医院中心实验室完成。①实验方法:选择雄性Wistar大鼠68只,采用结扎左冠状动脉前降支的方法制备大鼠心肌梗死及假手术(穿线后不结扎冠状动脉)模型。②实验分组:将术后存活的53只心肌梗死大鼠按随机数字表法分为心肌梗死后3,7,30d组各9,10,10只,将假手术大鼠24只做为各组的对照组,每组8只。③实验评估:从各组大鼠梗死中心、梗死周边、室间隔和右室取材,检测不同部位心肌中乙酰胆碱酯酶活性的变化。结果:存活的53只大鼠均进入结果分析。①心肌梗死后3d时,梗死中心区、梗死周边和室间隔中乙酰胆碱酯酶活性明显高于假手术组[分别为(14.12±3.55),(1.50±0.75)μkat/g;(16.59±7.17),(0.92±0.22)μkat/g;(8.64±4.02),(2.43±1.63)μkat/g],差异有显著性意义(t=3.168,3.367,P<0.01,t=2.817,P<0.05)。②心肌梗死后7d时,梗死中心区、梗死周边心肌中乙酰胆碱酯酶活性明显低于心梗后3d组[分别为(7.13±2.50),(14.12±3.55)μkat/g;(7.45±1.42),(16.59±7.17)μkat/g],但仍明显高于假手术组,差异有显著性意义(t=2.732,2.176,P<0.01);室间隔及右室中乙酰胆碱酯酶活性仍明显高于假手术组(P<0.01,P<0.05)。③心梗后30d时,梗死中心区和梗死周边乙酰胆碱酯酶活性较心梗后3d组进一步降低[分别为(4.55±1.17),(7.13±2.50)μkat/g;(5.83±1.55),(7.45±1.42)μkat/g],差异有显著性意义(t=2.653,2.763,P<0.05),梗死周边、室间隔、右心室中乙酰胆碱酯酶活性仍高于假手术组(P<0.05)。结论:心肌梗死后不同部位心肌中乙酰胆碱酯酶的活性具有不同的变化特点,提示心肌中乙酰胆碱酯酶的检测不仅是评价迷走神经活性的指标,可能也是一个较好的评价迷走神经支配的方法。     

电针对大鼠脑缺血再灌注后脑组织内乙酰胆碱酯酶活性的影响

目的：探讨电针穴位对脑缺血再灌注损伤引起的脑海马及大脑皮质内乙酰胆碱酯酶(AChE)活性的影响。方法：采用夹闭大鼠双侧颈总动脉造成的脑缺血再灌注损伤模型，以改良的Ellman法测定AChE。每日电针“百会”、“风池”、“大钟”及“足三里”穴30min 7和14d，疏-密渡频率：2～20Hz，强度2．0A。结果：实验后第7天．大鼠海马及大脑皮质内的AChE活性在缺血再灌注组明显低于假手术组[(234．4&;#177;36．2)，(318．9&;#177;39．O)nmol／s，P&;lt;0．01：(217．9&;#177;41．8)，(269．4&;#177;39．0)nmol／s．P&;lt;0．05)]，而其电针组的AChE活性则基本恢复。第14天，缺血再灌注及其电针组的大脑皮质AChE活性恢复；海马AChE活性在缺血再灌注组仍低于假手术组[(2507&;#177;38．8)，(302．1&;#177;35．5)nmol／L，P&;lt;0．05)]，电针组的AChE活性恢复。结论：脑缺血再灌注所致的脑损伤可能与脑内AChE的活性有关；电针能提高大鼠海马及大脑皮质内的AChE活性，从而对抗脑缺血-再灌注所致的脑损伤作用。     

电针对大鼠脑缺血再灌注后脑组织内乙酰胆碱酯酶活性的影响

目的:探讨电针穴位对脑缺血再灌注损伤引起的脑海马及大脑皮质内乙酰胆碱酯酶(AChE)活性的影响。方法:采用夹闭大鼠双侧颈总动脉造成的脑缺血再灌注损伤模型,以改良的Ellman法测定AChE。每日电针“百会”、“风池”、“大钟”及“足三里”穴30min7和14d,疏-密波频率:2～20Hz,强度2.0A。结果:实验后第7天,大鼠海马及大脑皮质内的AChE活性在缺血再灌注组明显低于假手术组(234.4±36.2),(318.9±39.0)nmol/s,P<0.01;(217.9±41.8),(269.4±39.0)nmol/s,P<0.05),而其电针组的AChE活性则基本恢复。第14天,缺血再灌注及其电针组的大脑皮质AChE活性恢复;海马AChE活性在缺血再灌注组仍低于假手术组(250.7±38.8),(302.1±35.5)nmol/L,P<0.05),电针组的AChE活性恢复。结论:脑缺血再灌注所致的脑损伤可能与脑内AChE的活性有关;电针能提高大鼠海马及大脑皮质内的AChE活性,从而对抗脑缺血-再灌注所致的脑损伤作用。     

血液保存对红细胞胆碱酯酶活性的影响

目的　测定不同保存时间冷藏 (4～ 6℃ )全血中红细胞胆碱酯酶活力 ,以探讨该血液成份用于抢救重症有机磷农药中毒患者的可行性。方法　采用便携式分析仪器 (Biocheck)及其配套使用的试剂 ,分别测定 10名志愿献血者血液在不同保存期全血中红细胞胆碱酯酶 (E AChE)活力。结果　库血随保存时间延长E AChE水平虽有所波动 ,但无显著下降 ,各组间方差分析无显著性差异 (P >0 .0 5 ) ,库存血保存时间与E AChE直线回归方程无显著意义 (P >0 .0 5 )。结论　冷藏全血中红细胞在保存期内 (2 1d) ,其E AChE活力无明显下降 ,提示红细胞悬液可用于抢救重症有机磷农药中毒患者。     

重症肌无力患者血乙酰胆碱酯酶活性测定及其临床意义

目的：探讨乙酰胆碱酯酶活性改变在重症肌无力(MG)发病中的作用。方法：采用三氯化铁显色分光光度比色分析法分别检测50例不同型MG患者与正常人血浆乙酰胆碱酯酶(P-AchE)、红细胞乙酰胆碱酯酶(E-AchE)活性。结果：患者组的P-AchE平均活性和E-AchE活性显著高于对照组，而且与重症肌无力临床类型和病情轻重有关，病情越重，其活性越高。结论：重症肌无力的发病机制除自身免疫因素外，乙酰胆碱酯酶活性改变也是一个重要因素，P-AchE和E-AchE活性测定可作为MG的一项辅助诊断方法。也可作为抗胆碱酯酶药物疗效观察指标。     

有机磷中毒血浆内皮素水平与乙酰胆碱酯酶活性的关系

目的:通过观测正常人和有机磷中毒患者(AOPP)血浆内皮索(ET)和全血乙酰胆碱酯酶(AChE)活性的水平,探讨ET在AOPP发病过程中的变化及意义。方法:用放射免疫法测定血浆ET,用Eliman法测定全血AChE活性。结果:ET轻度组与对照组比较无显著变化(P>0.05),中度和重度组与对照组相比较,均有显著升高(P<0.05或P<0.01),AChE在轻、中、重度组均有显著降低(P<0.01),中度组及重度组ET与AChE之间呈显著负相关(r=-0.61 7,P<0.05,r=-0.692,P<0.01)。结论;AOPP患者血浆ET含量的变化与中毒程度有关,可作为判断预后和中毒程度的指标。     

磁处理水对小白鼠脑胆硷酯酶和单胺氧化酶活性的影响

研究饮用磁处理水对小白鼠全脑胆硷酯酶和单胺氧化酶活性的影响。结果表明，小白鼠饮用磁处理水４０天，脑内的胆硷酯酶活性明显升高，但单胺氧化酶的活性无有意义的改变。由于脑的胆硷酯酶是乙酰胆硷的标识物，故可证明饮用磁处理水可提高脑内的局酰胆硷水平。     

酒精联合高脂饮食对大鼠血脂与脂质过氧化的影响

目的 研究不同浓度的白酒和高脂对大鼠的损伤作用压VitE的保护作用。方法 用灌胃白酒及喂饲高脂饮食的方法，观察脏器系数的改变和血清中MDA、葡萄糖（Glu）、总胆固醇（T-CHO）、甘油三酯（TG）含量变化。结果 肝脏的脏器系数在高荆量酒精、高脂组及高脂联合中剂量酒精组差异有显著性，高脂加中剂量酒精组和中剂量酒精组比较差异有显著性。心脏的脏器系数只在高剂量酒精组有统计学意义，肾脏的脏器系数各组间无显著性差异，MDA含量与肝脏的脏器系数改变趋势一致，VitE使MDA、Glu、T-CHO、TG下降，随着胃饲时间的延长，血清中Glu、T-CHO、TG逐渐递增，差异有显著性。结论 高剂量酒精、高脂及高脂联合中剂量酒精对大鼠肝脏有一定的损伤作用，使血清中葡萄糖、总胆固醇、甘油三酯的含量增高，高脂加重了酒精对肝脏的损伤，而高荆量酒精对心脏也有一定程度的损伤作用，可能与脂质过氧化引起自由基损伤有关，VitE对其损伤作用有一定的保护作用。     

Antioxidant Activity and Lipid-Lowering Effect of Essential Oils Extracted from Ocimum sanctum L. Leaves in Rats Fed with a High Cholesterol Diet

It has been reported that Ocimum sanctum L. (OS) leaves decrease serum lipid profile in normal and diabetic animals. No experimental evidences support the anti-hyperlipidemic and antioxidative actions against hypercholesterolemia. Moreover the identity of the specific chemical ingredients in OS leaves responsible for these pharmacological effects are unknown. Since OS leaves are rich in essential oil (EO). Therefore the present study was conducted to investigate the anti-hyperlipidemic and antioxidative activities of EO extracted from OS leaves in rats fed with high cholesterol (HC) diet. EO was extracted by the hydrodistillation method and the chemical constituents were then identified by Gas Chromatography-Mass Spectrometry. The experiment was performed in Male Wistar rats fed with 2.5 g%(w/w) of cholesterol diet for seven weeks. During the last 3 weeks, rats were daily fed with EO. The results showed that phenyl propanoid compounds including eugenol and methyl eugenol were the major constituents of EO. EO suppressed the high serum lipid profile and atherogenic index as well as serum lactate dehydrogenase and creatine kinase MB subunit without significant effect on high serum levels of aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase in rats fed with HC diet. In addition, EO was found to decrease the high levels of thiobarbituric acid reactive substances (TBARS), glutathione peroxidase (GPx) and superoxide dismutase (SOD) without impacting catalase (CAT) in the cardiac tissue while in the liver, it decreased high level of TBARS without significantly effecting GPx, SOD and CAT. Histopathological results confirmed that EO preserved the myocardial tissue. It can be concluded that EO extracted from OS leaves has lipid-lowering and antioxidative effects that protect the heart against hypercholesterolemia. Eugenol that is contained in EO likely contribute to these pharmacological effects.     

Changes on the Physiological Lactonase Activity of Serum Paraoxonase 1 by a Diet Intervention for Weight Loss in Healthy Overweight and Obese Women

Low caloric diet (LCD) is used for weight loss. Paraoxonase 1 (PON-1) is associated with the antioxidant functions of high-density lipoprotein (HDL). Among limited data on the relationships between obesity and PON-1, there has been no study on the effects of a stand-alone LCD on the physiological lactonase activity of PON-1. We investigated the prospective effects of LCD intervention (2 months) for weight loss on serum PON-1 activities (lactonase, arylesterase [mono-esterase] and tri-esterase) and HDL cholesterol (HDL-C), and their association with low-density lipoprotein cholesterol (LDL-C) in overweight and non-morbidly obese but otherwise healthy women (n = 30; mean age, 50.3 years; mean body mass index [BMI], 28.5 kg/m²). In addition to the data such as BMI, blood pressure, blood glucose and lipids, PON-1 activities were examined between pre- and post-intervention. The intervention reduced all metabolic outcomes, and PON-1 lactonase activity (determined with 5-[thiobutyl]butyrolactone) significantly decreased by 6.1%, paralleled by arylesterase (by 7.3%) and tri-esterase (by 7.8%). In multiple regression analysis, the percent change of PON-1 lactonase was significantly, positively and independently correlated to that of LDL-C (β = 0.51), HDL-C (β = 0.40), and BMI (β = 0.37). Our results showed that the solo diet treatment on weight loss might reduce serum PON-1 lactonase activity with reduced HDL-C and LDL-C. The relationship between the lactonase and LDL-C may be adaptive, plausibly hypothesizing less need for PON-1 activity as an antioxidant property to protect lipoproteins. Further research is needed to confirm this prediction.     

自然衰老大鼠脑线粒体和血小板膜外周型苯二氮 受体结合活性的变化

目的以3月龄青年大鼠为对照,观察24月龄自然衰老大鼠大脑皮层线粒体和血小板膜外周型苯二氮 受体(PBRs)结合数量及亲和力的改变。方法雄性SD大鼠断头取脑,以差速离心法提取大脑皮层线粒体,低渗溶血法制备外周血小板膜。采用放射配基［³H］PK11195单点结合实验测定PBRs特异结合活性,通过受体饱和实验和Scatchard作图得到最大结合容量Bmax值和平衡解离常数Kd值。结果与3月龄组大鼠相比,24月龄组的大脑皮层线粒体及外周血小板膜PBRs特异结合活性均显著上升(P<0-001)。饱和实验结果表明,24月龄组大鼠大脑皮层线粒体PBRs的受体容量(Bmax)升高而受体亲和力明显下降,Kd值显著增高(P<0-001)。结论老龄鼠PBRs容量上升而亲和力下降,可能参与脑老化进程。外周血小板膜［³H］PK11195结合活性与脑内该指标的变化一致。     

衰老小鼠组织端粒酶活性变化及黄精多糖的干预作用

【目的】探讨衰老小鼠组织端粒酶活性的变化及黄精多糖的干预作用。【方法】30只C57/BL/6j小鼠随机分为对照组、衰老组及治疗组;腹壁皮下注射D半乳糖建立动物模型;端粒酶活性测定采用端粒重复扩增微孔板杂交法。【结果】衰老模型组小鼠脑、肝及性腺组织端粒酶活性显著降低(P<0.05),应用黄精多糖治疗后,其脑及性腺组织端粒酶活性显著上升(P<0.05)。【结论】衰老小鼠组织端粒酶活性降低,而黄精多糖可上调其活性的表达。     

High-fat diet intake from senescence inhibits the attenuation of cell functions and the degeneration of villi with aging in the small intestine,and inhibits the attenuation of lipid absorption ability in SAMP8 mice

We examined the effect of a high-fat diet from senescence as a means of preventing malnutrition among the elderly. The senescence-accelerated mouse P8 was used and divided into three groups. The 6C group was given a normal diet until 6 months old. The 12N group was given a normal diet until 12 months old. The 12F group was given a normal diet until 6 months old and then a high-fat diet until 12 months old. In the oral fat tolerance test, there was a decrease in area under the curve for serum triacylglycerol level in the 12N group and a significant increase in the 12F group, suggesting that the attenuation of lipid absorption ability with aging was delayed by a high-fat diet from senescence. To examine this mechanism, histological analysis in the small intestine was performed. As a result, the degeneration of villi with aging was inhibited by the high-fat diet. There was also a significant decrease in length of villus in the small intestine in the 12N group and a significant increase in the 12F group. The high-fat diet from senescence inhibited the degeneration of villi with aging in the small intestine, and inhibited the attenuation of lipid absorption ability.