维生素E对阿尔茨海默病模型鼠学习记忆能力的影响

目的观察维生素E对阿尔茨海默病(AD)模型小鼠学习记忆能力的改善作用及其机制。方法采用D-gal与NaNO2联合腹腔注射方法建立AD模型小鼠,在造模同时及模型建立后两个时间点灌胃给予维生素E(28,280IU.kg-1)观察疗效,实验结束后水迷宫检测各组小鼠的逃避潜伏期的变化,化学比色法检测脑组织AChE、SOD活性、MDA含量;免疫组织化学方法检测大脑皮层Aβ、NF-κB表达的变化。结果造模同时给予维生素E可使D-gal与NaNO2联合诱导的AD模型鼠的逃避潜伏期缩短([F(3,56)=6.959]onday1;[F(3,56)=6.689]onday2;[F(3,56)=17.379]onday3;[F(3,56)=13.391]onday4;P<0.05),AChE活性降低([F(3,28)=29.431],P<0.05),SOD活性提高([F(3,28)=7.372],P<0.05),MDA含量降低([F(3,28)=11.235],P<0.05);同时可明显降低AD模型鼠脑组织中Aβ、NF-κB的表达(P<0.05)。模型建立后给予维生素E未发现上述变化。结论维生素E可预防化学诱导的AD模型小鼠学习记忆能力损伤,可能机制与提高SOD活性、降低MDA含量、降低AChE活性、降低脑组织中Aβ、NF-κB的表达等相关。     

川芎嗪对阿尔采末病模型小鼠学习记忆能力的影响及其机制初探

目的观察川芎嗪(tetramethylpyrazine,TMP)对AD模型小鼠学习记忆能力的改善作用及其机制。方法采用D-gal与NaNO2联合腹腔注射和AlCl3灌胃两种造模方法建立AD模型小鼠,灌胃给予TMP(100mg.kg-1)观察疗效,检测各组小鼠的逃避潜伏期、脑组织AChE、SOD活性、MDA含量及大脑皮层Aβ、NF-κB表达的变化。结果TMP可使D-gal与NaNO2联合诱导的AD模型鼠与AlCl3诱导的AD模型鼠的逃避潜伏期缩短(P<0.05);②TMP可使D-gal与NaNO2联合诱导的AD模型鼠与AlCl3诱导的AD模型鼠脑组织中,AChE活性分别降低16%和19%;使SOD活性分别提高50%和39%;使MDA含量分别降低27%和34%;上述检测结果与对照组比较差异均有显著性(P<0.05);③TMP可明显降低两种AD模型鼠脑组织中Aβ、NF-κB的表达(P<0.05)。结论TMP可改善化学诱导的AD模型小鼠学习记忆能力障碍,可能与提高SOD活性、降低MDA含量、降低AChE活性、降低脑组织中Aβ、NF-κB的表达等有关。     

枸杞多肽对D-半乳糖诱导小鼠的抗衰老作用及其可能机制

目的研究枸杞多肽对D-半乳糖（D-gal）衰老模型小鼠的影响及其可能作用机制。方法ICR小鼠60只,随机分为正常对照组、衰老模型组、枸杞多肽200,400,800mg/（kg.d）剂量组和100mg/（kg.d）维生素E（VitE）组。除正常组外均采用D-gal10mg/kg颈背部皮下注射,每日1次,连续注射5周,同时枸杞多肽和VitE组按20ml/（kg.d）灌胃给药。观察各组小鼠的行为学及学习记忆改变,并于5周后检测小鼠血清、心脏、肝脏、脑组织中超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量及端粒酶活性。结果与正常对照组相比,衰老模型组小鼠体重增加明显减少,小鼠跳台错误次数明显增多,小鼠血清、心脏、肝脏和脑SOD和端粒酶活性降低,MDA含量增加（P〈0.01）。与模型组相比,枸杞多肽组和VitE组小鼠体重增加升高（P〈0.01）,小鼠跳台错误次数减少（P〈0.05）,小鼠血清、心脏、肝脏和脑组织SOD活性升高,MDA含量减少（P〈0.05）;枸杞多肽200mg/（kg.d）剂量组及VitE组小鼠血清端粒酶活性有升高的趋势,但差异不显著;400和800mg/（kg.d）剂量组小鼠血清和心脏端粒酶活性升高（P〈0.01）,VitE组小鼠心脏端粒酶活性也明显升高;而各治疗组小鼠肝脏和脑组织端粒酶活性无明显变化。结论枸杞多肽对D-gal诱导衰老模型小鼠有抗衰老作用,其机制可能与提高小鼠血清、心脏、肝脏和脑组织SOD活性,减少MDA含量,以及提高血清和心脏端粒酶活性有关。     

冠舒滴丸对衰老模型大鼠脑组织的保护作用

目的：研究冠舒滴丸对衰老模型大鼠脑组织氧化损伤的保护作用。方法：大鼠腹腔注射D一半乳糖以复制衰老模型。60只Wistar大鼠分为正常对照（等容生理盐水）组、模型（等容生理盐水）组、维生素E（27mg／kg）组与冠舒滴丸高、中、低剂量（800、400、200mg／kg）组,灌胃给药,每天1次,连续8周。测定大鼠血清超氧化物歧化酶（SOD）活性与丙二醛（MDA）含量,大鼠脑组织匀浆SOD活性与MDA、脂褐素（LPF）含量,并对大鼠脑组织进行病理学观察。结果：与正常对照组比较,模型组大鼠血清SOD活性显著减弱,MDA含量显著减少,大鼠脑组织匀浆SOD活性显著减弱,MDA、LPF含量显著减少（P〈0．01）;模型组大鼠神经元与胶质细胞排列紊乱,部分神经元萎缩变性,局灶性神经元核固缩,小胶质细胞增生;与模型组比较,冠舒滴丸高、中剂量组大鼠血清SOD活性显著增强,MDA含量显著增加,大鼠脑组织匀浆sOD活性显著增强,MDA、LPF含量显著减少（P〈0．01或P〈0．05）,大鼠神经元及胶质细胞排列较为规则,细胞大小及形态较为正常,脑膜无充血水肿,未见炎细胞浸润。结论：冠舒滴丸对衰老模型大鼠脑组织氧化损伤有一定的保护作用。     

海带多糖对应激小鼠肾组织抗氧化能力的影响

目的：研究海带多糖对实验性应激小鼠肾组织抗氧化能力的影响。方法：随机将40只小鼠分为正常组、对照组、低剂量给药组和高剂量给药组，每组10只。采用皮下注射肾上腺素加耐力游泳法复制应激小鼠模型，测定小鼠肾组织丙二醛（MDA）、一氧化氮（NO）含量和超氧化物歧化酶（SOD）、一氧化氮合成酶（NOS）活性。结果：与对照组比较，高低剂量组海带多糖均能降低MDA的含量（P〈0．05），增加NO的含量（P〈0．05），并能提高SOD和NOS的活性（P〈0．05）。结论：海带多糖能够提高肾组织抗氧化能力。     

鸡骨草总黄酮对小鼠实验性肝损伤的保护作用

目的研究鸡骨草总黄酮（total flavones of Abrus carhorliensis Hance．,TFA）对小鼠实验性肝损伤的保护作用,并初步探讨其机制。方法采用四氯化碳（CCl。）致小鼠急性肝损伤制备模型,测定小鼠血清中ALT、AST的活性和肝组织中MDA含量、SOD、GSH—Px活性。同时计算肝脏系数和进行病理组织学检查、评分。结果TFA100,80mg·kg^-1能显著降低急性肝损伤小鼠血清中ALT、AST活性（P〈0．05）,肝组织中MDA的生成和肝脏系数（P〈0．05）;升高组织中SOD、GSH—Px活性（P〈0．05）。亦可明显改善肝脏的病理损伤程度。结论TFA对肝损伤有保护作用,其机制可能与抑制氧自由基生成有关。     

六味地黄健脑方对AD小鼠学习记忆及脑组织SOD、MDA含量的影响

目的：观察六味地黄健脑方对阿尔茨海默病（AD）小鼠学习记忆能力及其脑组织超氧化物歧化酶（SOD）、微量丙二醛（MDA）含量的影响。方法：采用D-半乳糖联合氯化铝构建AD小鼠模型。疗程结束时,跳台实验观察各组对AD小鼠记忆能力的影响,测定脑组织中SOD活性和MDA的含量。结果：治疗组均可显著提高小鼠学习记忆能力及脑组织匀浆中SOD活性,降低潜伏时间及MDA含量,但以中药组作用较明显。结论：六味地黄健脑方可增强AD小鼠学习记忆的能力。     

莲房原花青素对D-半乳糖衰老小鼠脑组织抗氧化的作用

目的：探讨莲房原花青素（lotus seedpod procyanidins,LSPC）对D-半乳糖衰老小鼠脑组织抗氧化系统的影响。方法：雄性健康昆明种小鼠60只,随机分为对照组、衰老模型组、ESPC低剂量组（15mg·ml^-1）、LSPC中剂量组（30mg·ml^-1）和LSPC高剂量组（60mg·ml^-1）。采用小鼠皮下注射D-半乳糖（120mg·kg^-1·d^-1）,连续注射8周,建立小鼠衰老模型,ISPC组造模同时灌胃给予ISPC,qd,连续给药8周。化学比色法检测5组小鼠脑组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）和丙二醛（MDA）含量。结果：衰老模型组与对照组相比,小鼠脑组织SOD和GSH—Px活性明显降低,MDA含量明显增高（P〈0．01）。与衰老模型组相比较,LSPC能明显提高衰老小鼠脑组织中SOD活性和GSH—Px活性（P〈0．01）,能减少MDA含量（P〈0．01）。结论：LSPC对D-半乳糖所致衰老小鼠具有明显的抗氧化作用。     

脑益康对阿尔茨海默病模型小鼠学习记忆的影响

目的 :观察脑益康对阿尔茨海默病 (Alzhei mer’sdisease ,AD)模型小鼠学习记忆的影响 ,并探讨其改善学习记忆的机制。方法 :采用D 半乳糖 (D Gal)和亚硝酸钠 (NaNO2 )腹腔注射建立小鼠AD模型 ,通过迷宫刺激器和水迷宫实验检测小鼠学习记忆能力 ;生化方法检测小鼠脑组织内超氧化物歧化酶 (SOD)活性和丙二醛 (MDA)含量 ;透射电镜观察小鼠海马神经细胞的超微结构。结果 :模型对照组小鼠学习记忆能力下降 ,SOD活性降低 ,MDA含量升高 ;而与模型对照组比较 ,脑益康小、中、大剂量组(2 .4、7.2、2 4g·kg-1·d-1)均可显著改善模型小鼠的学习记忆能力 ,提高脑内SOD活性 ,降低脑内MDA含量 (P <0 .0 1或P <0 .0 5 ) ,阻抑海马神经细胞的退行性变化。结论 :脑益康可改善D 半乳糖和亚硝酸钠所致AD模型小鼠的学习记忆能力。     

蒙成药阿那日-4对小鼠乙醇及应激反应引起胃溃疡的影响

目的探讨蒙成药阿那日-4对小鼠乙醇及应激反应引起胃溃疡的影响。方法分别建立小鼠乙醇及应激性胃溃疡模型,检测小鼠胃浆中的超氧化物歧化酶（SOD）、丙二醇（MDA）、一氧化氮（NO）含量及比较胃图片溃疡指数来观察蒙成药阿那日-4对两个模型的影响。结果蒙成药阿那日-4对乙醇致胃溃疡小鼠,3个剂量给药组与模型组比较显著增高SOD及NO含量（P〈0．05）、中剂量给药组显著降低MDA含量（P〈0．05）,3个剂量给药组的溃疡指数显著降低（P〈0．05）,抑制率分别为13．4％,28．1％,59．2％;对应激反应引起的胃溃疡小鼠,与模型组比较,低剂量组SOD含量显著提高（P〈0．01）;中剂量组MDA显著降低（P〈0．05）,低、中、高剂量组NO含量显著提高（P〈0．01）、溃疡指数显著降低（P〈0．01）,抑制率分别为31．4％,51．0％,44.3％。结论蒙成药阿那日-4对小鼠乙醇及应激反应引起的胃溃疡有一定的治疗作用,这与抗氧化、增高胃浆中的NO含量有关。     

Effects of GBEE on memory impairment induced by scopolamine in mice and activity of AChE in cerebral cortex

OBJECTIVE The fruit of Ginkgo biloba L.is also known as Ginkgo nuts. Ginkgo has the effect of warming the lung, boosting qi, downbear phlegm, dispersing toxin, kil ing worms and etc, which also recorded in ancient books on tumor treatment. The scientific name of succulent skin is exocarp in Gingko nuts. Research shows that GBEE(Ginkgo biloba exocarp extracts) has anti-tumor,anti-aging and immune promoting activity. As an M receptor blocker, scopolamine can block the excitatory effect of acetylcholine on M receptors, causing learning and memory dysfunction. It can partially simulate some features of the cholinergic system of Alzheimer disease(AD). The learning and memory impairment model of scopolamine is the classic screening model for AD drug research. In this paper, the effects of GBEE on scopolamine induced learning and memory impairment in mice and its mechanism were preliminarily studied. METHODS GBEE was prepared by the patented method(patent: ZL201610916394.4). Infrared Spectroscopy(IR) analysis shows that the proteoglycan in GBEE is ester linkage. The total content of proteoglycan in GBEE was 62.6%-64.8%, which was measured by phenol sulfuric acid method and brilliant blue method. Pre-column derivatization high-performance liquid chromatography(HPLC) detection showed that the proteoglycan in GBEE contains 6 kinds of monosaccharides including mannose, rhamnose, galacturonic acid, glucose, galactose, arabinose and 14 kinds of amino acids including aspartic acid, glutamic acid, glycine,serine, threonine, alanine, proline, valine, methionine,isoleucine, leucine, phenylalanine, tryptophan and lysine.60 ICR mice, half male and half female, 6-8 weeks old and weight(18-22) g, were randomly divided into six groups: blank control group(normal saline), model group(normal saline), positive drug group( donepezi 1.25 mg·kg-1)and GBEE low-does(50 mg·kg-1), medium-does(100 mg·kg-1) and high-does(200 mg·kg-1) groups. The drug were infused to stomach of mice once a day for 14 d,after that model of learning disorder and dysmnesia were made by intraperitoneal injection of scopolamine hydrobromide(3 mg·kg-1) in six groups except the blank control group on days 15-19. Morris water maze experiment was performed by using the mice′s instinct of escaping from the water to find rest platform. The mean escape latency(s), in other words, the time needed for searching platform was detected on days 15-18, the time in platform annulus(s) was detected on day 19. Each test was performed 30 min after intraperitoneal injection and 1 h after intragastric administration. The mean escape latency(s) and the time in platform annulus(s) were correlated with the memory ability of mice, the former was negatively correlated, the latter was positively correlated, so as to evaluate the changes of learning and memory ability of each group of mice. After the behavioral experiment, the brain tissues of mice were taken out immediately, and the cerebral cortex and hippocampus were cut and stored in the refrigerator at-80℃ with the help of the mouse brain mold. During the test, the brain homogenate was prepared by ultrasonic method, and the activity of acetylcholin esterase(AChE) in the cerebral cortex and hippocampus of each group of mice was measured according to the instructions of AChE test box. RESULTS Scopolamine can significantly prolong the mean escape latency(s) of Morris water maze experiment in mice, and shorten the time in platform annulus(s), which is statistically significant compared with the control group(P<0.05,P<0.01). The results showed that scopolamine caused the decrease of learning and memory ability in the model group. The time required to search for the platform in mice of positive drug group and the GBEE of the three dose groups was significantly reduced on the third and fourth days of Morris water maze experiment test. Except for the GBEE low-dose group, the comparison with the model group was statistically significant(P<0.05, P<0.01). On day 19, positive medicine and three dose groups GBEE can significantly extend the time in platform annulus(s), compared with model group(P<0.05,P<0.01), the effect of medium-dose GBEE group is better than that of high dose, close to the positive drug, the results showed that it could improve the learning and memory ability of scopolamine-induced memory impairment modle mice. While the memory ability of the scopolamine model group was decreased, AChE activity in the cerebral cortex of the mice was significantly increased compared with the control group(P<0.05). Donepezil and GBEE in each dose could reduce Ach E activity in the cerebral cortex of the mice. Except for the high-dose GBEE group, there were significant differences between the other groups and the model group(P<0.05). The results of AChE activity in hippocampi need to be repeated further because of the large difference. CONCLUSION GBEE can improve the learning and memory ability of scopolamine induced memory impairment model mice,and the mechanism may be related to reducing the activity of cerebral AChE and reducing the inactivation of cholinergic neurotransmitter ACh in memory impairment mice.AD is a kind of neural degenerative disease, which can easily be seen in the middle-aged and old people, the early disease mainly for hypomnesis, dysmnesia and so on, accompanied by the reduction of acetylcholine(ACh), the increasing of AChE activity. Early stage of AD is the best treatment stage, by improving the memory function, which can effectively prevent the further development of AD, slow disease progression and reduce disease severity. This study shows that GBEE has certain potential in the treatment of AD, which lays a foundation for further research on the effect and mechanism of GBEE on AD.     

夏天无总生物碱对痴呆大鼠学习记忆障碍及中枢胆碱能神经系统功能的影响

目的　观察夏天无总生物碱 (Xiatianwutotalalkaloids,XA)对喹啉酸损毁海马所致大鼠学习记忆障碍和中枢胆碱能神经系统功能的影响。方法　采用双侧海马CA1区微注射喹啉酸造成大鼠学习记忆障碍模型 ,在造模前 1wk至造模后 3wk内 ,大鼠每天igXA 0 2 5 ,0 5 ,1mg·kg-1。采用三等分Y迷宫测定大鼠学习记忆能力 ,并采用比色法检测海马乙酰胆碱酯酶 (acetylcholinesterase ,AChE)活性和大脑皮层乙酰胆碱 (acetylcholine ,ACh)含量的变化。结果　大鼠双侧海马内微注射喹啉酸可引起大鼠学习记忆功能障碍 ,海马中AChE活性下降 ,大脑皮层ACh含量减少 ;XA可显著改善喹啉酸诱导的痴呆大鼠学习记忆功能障碍 ,同时明显抑制模型大鼠海马的AChE活性 ,提高大脑皮层ACh含量。结论　XA可改善喹啉酸损毁海马造成的痴呆大鼠学习记忆功能障碍 ,而其机制可能与抑制脑AChE活性 ,从而提高ACh含量 ,增强中枢胆碱能系统的功能有关。     

当归芍药散二氯甲烷提取部位对D-半乳糖致衰老小鼠学习记忆能力的影响

目的研究当归芍药散二氯甲烷提取部位(DSP)对D-半乳糖(D-gal)致小鼠学习记忆能力障碍及神经毒性的改善作用。方法 ICR小鼠随机分为空白组,模型组,维生素E组,当归芍药散二氯甲烷提取部位低、高剂量组。空白组以外各组皮下注射D-半乳糖(50mg.kg-1.d-1)50d制备小鼠亚急性衰老模型。用跳台法和Morris水迷宫法评价小鼠的学习记忆能力,测定小鼠血清中总超氧化物歧化酶(T-SOD)、丙二醛(MDA)、谷胱甘肽过氧化酶(GSH-Px)活性和脑组织匀浆中谷胱甘肽/氧化型谷胱甘肽(GSH/GSSG)比值、Na+-K+-ATPase活性和淀粉样蛋白β(Aβ)含量。结果当归芍药散二氯甲烷提取部位能够显著提高衰老小鼠的学习记忆能力(P<0.05或P<0.01),提高衰老模型小鼠血清SOD、GSH-Px及脑组织Na+-K+-ATP酶活性,并升高GSH/GSSG比值,减少血清MDA(P<0.05或P<0.01);减少脑内Aβ含量(P<0.05)。结论当归芍药散二氯甲烷提取部位能够改善D-半乳糖衰老模型小鼠的学习记忆障碍,其作用可能与提高脑组织的抗氧化能力、降低中枢神经毒性有关。     

二苯乙烯苷对慢性脑缺血大鼠学习记忆的影响

目的观察何首乌有效成分二苯乙烯苷(TSG)对慢性脑缺血大鼠学习记忆能力的影响,并探讨其可能机制。方法雄性SD大鼠双侧颈总动脉永久性结扎制备慢性脑缺血致痴呆模型。术前2周起,分别给TSG30,60及120mg·kg-1·d-1,ig,连续11周。术后8周时,分别用Morris水迷宫实验和避暗实验检测大鼠的空间学习记忆能力和被动回避学习记忆能力。术后9周时,采用生化方法检测海马乙酰胆碱酯酶(AChE)活性,免疫组化方法检测海马蛋白磷酸酶2A(PP-2A)和微管相关蛋白2(MAP-2)的表达。结果慢性脑缺血模型组大鼠空间和被动回避学习记忆能力明显降低,海马AChE活性显著升高,PP-2A和MAP-2表达明显减少。TSG给药10周可显著改善慢性脑缺血引起的学习记忆能力降低;给药11周明显抑制海马AChE活性增高,并增加PP-2A和MAP-2的表达。结论TSG可改善慢性脑缺血大鼠的学习记忆能力,其机制可能与抑制海马AChE活性,增加海马PP-2A和MAP-2的表达有关。     

Expression and activity of cytochromes P450 2E1, 2A, and 2B in the mouse ovary: the effect of 4-vinylcyclohexene and its diepoxide metabolite.

4-Vinylcyclohexene (VCH), an occupational chemical, causes destruction of small preantral follicles (F1) in mice. Previous studies suggested that VCH is bioactivated via cytochromes P450 (CYP450) to the ovotoxic, diepoxide metabolite, VCD. Whereas hepatic CYP450 isoforms 2E1, 2A, and 2B can metabolize VCH, the role of ovarian metabolism is unknown. This study investigated expression of these isoforms in isolated ovarian fractions (F1, 25-100 microm; F2, 100-250 microm; F3, >250 microm; interstitial cells, Int) from B6C3F1 mice dosed daily (15 days; ip) with vehicle, VCH (7.4 mmol/kg/day) or VCD (0.57 mmol/kg/day). Ovaries were removed and either isolated into specific ovarian compartments for mRNA analysis, fixed for immunohistochemistry, or prepared for enzymatic assays. mRNA and protein for all isoforms were expressed/distributed in all ovarian fractions from vehicle-treated mice. In the targeted F1 follicles, VCH or VCD dosing increased (p < 0.05) mRNA encoding CYP2E1 (645 +/- 14% VCH; 582 +/- 16% VCD), CYP2A (689 +/- 8% VCH; 730 +/- 22% VCD), and CYP2B (246 +/- 7% VCH) above control. VCH dosing altered (p < 0.05) mRNA encoding CYP2E1 in nontargeted F3 follicles (168 +/- 7%) and CYP2A in Int (207 +/- 19%) above control. Immunohistochemical analysis revealed the greatest staining intensity for all CYP isoforms in the Int. VCH dosing altered (p < 0.05) staining intensity in Int for CYP2E1 (19 +/- 2.4% below control) and CYP2A (39 +/- 5% above control). Staining intensity for CYP2B was increased (p < 0.05) above control in granulosa cells of small preantral (187 +/- 42%) and antral (63 +/- 8%) follicles. Catalytic assays in ovarian homogenates revealed that CYP2E1 and CYP2B were functional. Only CYP2E1 activity was increased (149 +/- 12% above control; p < 0.05) by VCH dosing. The results demonstrate that mRNA and protein for CYP isoforms known to bioactivate VCH are expressed in the mouse ovary and are modulated by in vivo exposure to VCH and VCD. Interestingly, there is high expression of these isoforms in the Int. Thus, the ovary may contribute to ovotoxicity by promoting bioactivation of VCH to the toxic metabolite, VCD.     

D-半乳糖衰老模型大鼠肝脏形态学及抗氧化能力变化的研究

目的:观察D-半乳糖致衰大鼠肝脏形态学改变及氧化水平和抗氧化能力的变化。方法:采用D-半乳糖所致衰老模型大鼠,做肝组织HE染色光镜观察,测定C a2 -ATP酶活性,肝线粒体M DA含量、PLA2活性。结果:衰老模型大鼠肝组织形态学发生明显变化,肝脏C a2 -ATP酶活性显著降低(P<0.01),肝线粒体M DA含量、PLA2活性显著升高(P<0.01)。结论:D-半乳糖致衰大鼠可作为研究衰老的模型。     

两种黔产淫羊藿总黄酮对痴呆大鼠学习记忆的影响

目的研究黔产粗毛淫羊藿与黔岭淫羊藿淫羊藿总黄酮(TFE)对D-gal-AlCl3联合造模大鼠学习记忆能力的影响。方法联用D-gal-AlCl3 12周造模,同时按剂量100、50 mg.(kg.d)-1,分组po给TFE。采用Morris水迷宫实验检测其空间记忆能力;应用生化技术检测脑、血AChE活性;以免疫组化技术检测脑Bcl-2/Bax水平。结果 D-gal-AlCl3造模形成了大鼠学习记忆障碍;TFE能改善D-gal-AlCl3致痴呆大鼠学习记忆能力,降低脑、血组织中AChE的活性,明显升高bcl-2并降低Bax水平。以粗毛淫羊藿改善记忆能力效果为优。结论粗毛淫羊藿对痴呆大鼠记忆能力,脑细胞凋亡具有更明显保护作用。提示淫羊藿苷(ICA)是TFE中增强记忆的主要物质基础。     

三氧化二砷治疗鸡卵蛋白诱导日本大耳白兔类风湿关节炎的初步观察

目的：探讨三氧化二砷对鸡卵蛋白诱导日本大耳白兔致类风湿关节炎模型的滑膜组织核因子NF-κB（p65）表达活性及血清中白细胞介素-1（IL-1）、肿瘤坏死因子-α（TNF-α）水平的影响。方法48只日本大耳白兔随机分为模型组、正常对照组、三氧化二砷低剂量组（1．0 mg·kg－1·d－1）、三氧化二砷中剂量组（2．0 mg·kg－1·d－1）、三氧化二砷高剂量组（4．0 mg ·kg－1·d－1）、醋酸泼尼松龙组（10 mg·d－1）,每组8只。成功建立卵蛋白诱导关节炎模型后,分别给药2周;采用酶联免疫吸附法（ELISA）检测兔外周血中的 IL-1、TNF-α,免疫组化实验方法检测核因子（NF-κB）（p65）在各组动物模型中的表达情况。结果卵蛋白诱导法可以成功诱导兔的关节炎,模型组外周血中的 IL-1、TNF-α含量较正常对照组升高（P＜0．05）;三氧化二砷各剂量组兔的关节炎症状有不同程度改善,IL-1、TNF-α含量较模型组降低（P＜0．05）;免疫组化结果显示,模型组关节滑膜的NF-κB（p65）表达较正常组增强（P＜0．05）,而三氧化二砷各剂量组关节滑膜的NF-κB（p65）表达随砷剂剂量的增加表达减弱,但仍然强于正常对照组（P＜0．05）。结论三氧化二砷对实验性类风湿关节炎日本大耳白兔模型有治疗作用。其机制可能与抑制了滑膜细胞中NF-κB（p65）活性和表达,降低了炎性因子IL-1、TNF-α的水平有关。