郁金防治急性缺氧小鼠脑损伤的机制

目的 探讨郁金对急性缺氧小鼠脑损伤的保护作用及其机制.方法 用郁金水煎剂低、中、高剂量(10、20、40 g/kg)连续灌胃6 d,利用常压密闭耐缺氧和断头实验复制小鼠急性缺氧模型,检测脑组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)及一氧化氮(N0)含量;利用bcl-2、caspase-3抗体进行脑组织免疫组化染色.结果 与模型组比较,各剂量组均能不同程度地提高缺氧小鼠脑组织SOD活性,减少其MDA和NO含量,使caspase-3蛋白表达下调而bcl-2表达上调.结论 郁金水煎剂减轻急性缺氧小鼠脑组织损伤的机制可能与其减轻氧化应激损伤及抑制脑细胞凋亡有关.     

番茄红素对寰枢椎失稳老龄小鼠记忆的影响

Objective To observe the effect of Lycopene on the improvement of memory abilities by cumulating lactic acid for long time in atlas dentata vertebrae senile mice. Methods Totally 30% lactic acid 30μL one time every week was injected into the place between the first and the second cervical vertebrae for 3 weeks. Forty mice were randomized into five groups:young control group, model group, VitE group(50 mg/kg), control group,and two therapeutic groups of lycopene which was intragastric at the doses of 5, 2.5 mg/kg once everyday. The changes of memory in mice were observed with water-maze test and step-down avoidance test. The activities of acetylcholine esterase(AchE), and the content of acetylcholine, (Ach) in encephalon were tested. HE staining in mice brain, including the cortex and hippocampus was demonstrated. Results Compared with model group. Lycopene high dose could significantly shortened the latency period and wrong times in water-maze test (P ＜0.01 ), In stepdown avoidance test, the reaction period was shortened significantly ( P ＜ 0.01 ) and the latency period was shortened significantly. The activities of ChE decreased (P ＜0.01 ) and the content of ACh increased in the Lycopene high doses group(P＜0.01 ). The therapeutic groups of lycopene had less pathological change of cellular necrosis,neuron loss in hippocampal CAI than the model group. Conclusion Lycopene has a certain protective and improving effect on the decline of memory ability and cervical lesion induced by lactic acid in atlanto-axial joint cumulating.     

颈椎稳定性异常老龄小鼠脑海马神经细胞中Bcl-2和Bax的表达

目的：探讨颈椎失稳老龄小鼠脑海马神经细胞凋亡相关基因Bcl-2和Bax的表达,阐明颈椎失稳所致老龄小鼠记忆和学习能力下降的机制。方法：选取ICR小鼠20只,随机分为模型组和对照组,每组10只,分组后模型组采用颈椎乳酸堆积法制备小鼠颈椎稳定性异常病理模型,对照组未经任何处理。水迷宫实验检测小鼠学习和记忆能力;HE染色观察脑海马神经细胞形态学变化;TUNEL染色观察脑海马神经细胞凋亡情况;RT-PCR和免疫组织化学法检测小鼠脑海马组织Bcl-2、Bax mRNA和蛋白的表达情况。结果：与对照组比较,模型组小鼠水迷宫实验游全程时间和错误次数显著增加(P<0.01);HE染色,与对照组比较,模型组小鼠脑海马神经细胞排列稀疏,死亡细胞明显增多;TUNEL染色,与对照组（7.52%±0.99%）比较,模型组脑海马凋亡细胞数（29.63%±1.63%）明显增多（P<0.01）;RT-PCR和免疫组织化学染色,模型组小鼠脑海马神经细胞Bcl-2表达明显减弱,Bax表达明显增强。结论：颈椎稳定性异常导致的小鼠脑海马神经细胞Bcl-2表达下调,Bax表达上调,可能是促进其细胞凋亡的主要机制之一。     

郁金对CCl4所致急性肝损伤小鼠肝脏的免疫调节作用

目的:观察单味郁金(Curcumae)水煎剂对四氯化碳（CCl4）所致急性肝损伤小鼠肝细胞免疫调节作用,为开发利用单味郁金水煎剂防治急慢性肝损伤提供实验依据。方法: ICR小鼠48只,雌雄各半,随机分为空白对照组,模型组,阳性药物组以及郁金高、中、低剂量组,每组8只。阳性药组以甘利欣22.5 mg/kg腹腔注射,每天1次;郁金高、中、低剂量组分别以12 、6、3 g/kg灌胃,每天1次;空白对照组及模型组等体积蒸馏水灌胃,每天1次;连续给药7 d,第7天给药后11 h;再以0.2%CCl4橄榄油溶液(10 mL/kg)腹腔注射（空白对照组除外）,复制急性肝损伤模型。造模后24　h处死,计算肝指数;肝组织HE染色观察病理变化; RT-PCR 法检测IL-1β及TNF-a mRNA表达水平;免疫组织化学法观察IL-18蛋白表达水平。结果：与模型组比较,各给药组肝指数明显下降（P<0.05）。HE染色显示：模型组小鼠肝小叶组织结构紊乱、肝窦充血明显、炎细胞浸润明显、肝组织呈局灶性细胞变性或死亡;而各给药组上述病理变化明显减轻。与模型组比较,郁金给药组小鼠肝组织IL-1β及TNF-α mRNA表达水平及IL-18蛋白表达水平均明显下调（P<0.05）。结论:单味郁金水煎剂可能通过抑制肝组织细胞因子IL-1β、IL-18和TNF-α的表达,调节小鼠肝脏免疫功能而减轻CCl4所致的急性肝损伤。     

郁金水煎剂对四氯化碳致急性肝损伤小鼠肝细胞p53和caspase-3表达的影响及其对肝损伤的保护作用

目的:探讨单味郁金水煎剂对四氯化碳(CCl4)致急性肝损伤小鼠肝细胞凋亡基因p53和caspase-3蛋白表达的影响,阐明郁金对肝损伤保护作用的机制。方法:ICR小鼠60只,随机分为空白对照组(等体积生理盐水)、模型组(等体积生理盐水)、郁金低剂量组(2.5g·kg-1)、郁金中剂量组(5.0g·kg-1)、郁金高剂量组(10.0g·kg-1)和阳性药组(甘利欣22.5mg·kg-1);连续给药7d后,除空白对照组外各组小鼠均通过CCl4复制小鼠急性肝损伤模型。计算肝指数,测定血清丙氨酸氨基转移酶(ALT)活性,HE染色观察肝组织形态学变化;RT-PCR法检测肝细胞p53基因转录情况;免疫组织化学法检测肝细胞caspase-3蛋白表达。结果:与空白对照组比较,模型组小鼠肝指数明显增加(P<0.05);与模型组比较,各给药组小鼠肝指数明显降低(P<0.05)。与空白对照组比较,模型组小鼠血清ALT增高(P<0.01);与模型组比较,阳性药组及郁金高、中剂量组小鼠血清ALT明显降低(P<0.05)。肝脏形态学变化,肉眼观察,空白对照组小鼠肝脏呈现粉红色,质软而富有弹性,模型组小鼠肝脏明显肿大、呈微黄色,表面可见散在点状及片状黄褐色斑点,质脆,各给药组小鼠肝脏大小、颜色及质地均界于空白对照组与模型组之间,且表面无明显黄褐色斑点;镜下观察,空白对照组小鼠肝脏结构正常,模型组小鼠细胞呈明显局灶性气球样变、水样变性和死亡,而阳性药组和郁金中、高剂量组小鼠与模型组比较肝组织上述病灶数量减少。与空白对照组比较,模型组小鼠肝细胞p53基因转录明显增强(P<0.05);与模型组比较,郁金高剂量组小鼠肝细胞p53基因转录显著减弱(P<0.05)。与模型组比较,郁金给药组小鼠肝细胞caspase-3蛋白表达减弱。结论:郁金对CCl4致小鼠急性肝损伤有一定的拮抗作用,其机制之一可能与下调凋亡基因p53和caspase-3蛋白的表达、阻碍肝细胞凋亡有关。     

寰枢椎周围软组织损伤对老龄小鼠脑衰老进程的影响

目的观察老龄小鼠寰枢椎肌肉、韧带、筋膜损伤对其脑衰老进程的影响。方法利用手术损伤小鼠寰枢椎周围软组织。利用跳台试验检测小鼠学习、记忆能力；组织切片HE染色观察脑海马神经元数量；免疫组织化学染色观察β-淀粉样多肽（Aβ）、caspase-3的表达；试剂盒检测血清NO及脑组织SOD、MDA的变化。结果与对照组相比，跳台试验：模型组小鼠反应期明显延长，潜伏期明显缩短，错误次数显著增加（P〈0．01）；HE染色可见模型组脑海马神经元数量明显减少，大脑皮层嗜神经现象明显；免疫组化：模型组脑海马区Aβ、caspase-3阳性细胞数均明显增加；生化指标检测结果：模型组小鼠脑组织MDA含量显著增加（P〈0．05），SOD活性明显下降（P〈0．01）；其血清NO含量也显著增加（P〈0．05）。结论寰枢椎软组织损伤促进老龄小鼠脑细胞凋亡，导致其学习、记忆功能明显减退，加速了脑衰老的进程。     

女贞子调节糖脂代谢紊乱化学成分及作用机制研究进展

女贞子为木犀科植物女贞Ligustrum lucidum Ait.的干燥成熟果实.女贞子中的多糖、三萜、环烯醚萜以及黄酮类化合物能够通过增强胰岛素敏感性、改善胰岛素抵抗、保护胰岛β细胞;调控激活腺苷酸活化蛋白激酶(AMPK)、蛋白激酶B(AKT)、蛋白酪氨酸磷酸酶1B(PTP1B)信号通路;调节免疫、抑制炎症因子的释放...     

人参二醇皂苷和番茄红素对寰枢椎失稳所致老龄小鼠学习记忆障碍的影响

目的：比较人参二醇皂苷（panaxadiol saponins,PDS）、番茄红素（lycopene）对寰枢椎失稳老龄小鼠记忆的影响。方法：小鼠寰枢椎周围注射30%乳酸溶液复制小鼠颈椎失稳致慢性脑损伤模型。水迷宫测试小鼠学习、记忆能力;碱羟胺比色法测定脑组织乙酰胆碱（Ach）含量,试剂盒检测脑组织胆碱酯酶（AchE）活性;免疫组化观察小鼠脑海马区β-淀粉样蛋白表达。结果：与模型组比较,PDS组小鼠游全程时间缩短、错误次数减少(P＜0.01),而lycopene组小鼠学习、记忆能力有提高趋势;PDS组和lycopene组脑AchE活性降低（P＜0.01）,Ach含量增加（P＜0.01）,且见脑海马CA1区β-淀粉样蛋白表达减弱;两用药组间差异不显著。结论：PDS与lycopene对长期乳酸堆积引起的老龄小鼠寰枢椎失稳所致脑损伤均具有一定的保护作用,可改善小鼠学习记忆能力和脑的代谢。     

番茄红素对寰枢椎失稳老龄小鼠记忆的影响

Objective To observe the effect of Lycopene on the improvement of memory abilities by cumulating lactic acid for long time in atlas dentata vertebrae senile mice. Methods Totally 30% lactic acid 30μL one time every week was injected into the place between the first and the second cervical vertebrae for 3 weeks. Forty mice were randomized into five groups:young control group, model group, VitE group(50 mg/kg), control group,and two therapeutic groups of lycopene which was intragastric at the doses of 5, 2.5 mg/kg once everyday. The changes of memory in mice were observed with water-maze test and step-down avoidance test. The activities of acetylcholine esterase(AchE), and the content of acetylcholine, (Ach) in encephalon were tested. HE staining in mice brain, including the cortex and hippocampus was demonstrated. Results Compared with model group. Lycopene high dose could significantly shortened the latency period and wrong times in water-maze test (P ＜0.01 ), In stepdown avoidance test, the reaction period was shortened significantly ( P ＜ 0.01 ) and the latency period was shortened significantly. The activities of ChE decreased (P ＜0.01 ) and the content of ACh increased in the Lycopene high doses group(P＜0.01 ). The therapeutic groups of lycopene had less pathological change of cellular necrosis,neuron loss in hippocampal CAI than the model group. Conclusion Lycopene has a certain protective and improving effect on the decline of memory ability and cervical lesion induced by lactic acid in atlanto-axial joint cumulating.     

番茄红素对寰枢椎失稳老龄小鼠记忆的影响

目的 观察番茄红素（Lycopene）对寰枢椎失稳老龄小鼠记忆的影响.方法 10月龄ICR雌性小鼠40只,雌雄各半,完全随机分为5组：正常对照组、模型组、维生素E组、番茄红素高5 mg/kg、低（25 mg/kg）剂量组,每组8只.利用水迷宫、跳台实验测试小鼠记忆能力 碱羟胺比色法测定脑组织乙酰胆碱含量,试剂盒检测脑组织胆碱酯酶（AchE）活性 苏木素-伊红（HE）染色法观察小鼠脑海马CA1区神经元细胞形态变化.结果 水迷宫实验中模型组游全程时间（116.7±8.7）s,错误次数（16.0±2.8）次,番茄红素高剂量组小鼠游全程时间缩短为（107.9±21.8）s、错误次数（6.6±3.9）次显著减少（P＜0.01） 跳台实验,番茄红素高剂量组的反应期（68.3±22.7）s,与模型组（123.4±68.6）s相比明显缩短（P＜0.01）,其高、低剂量组的错误次数均明显减少（P＜0.01） 番茄红索高剂量组AchE活性（8.6±1.8）U/mg与模型组（17.7±2.6）U/mg相比显著降低（P＜0.01）,而番茄红素低剂量组间差异无统计学意义,番茄红素高、低剂量组乙酰胆碱含量显著升高（P＜0.01） HE染色可见番茄红素高剂量组小鼠海马CA1区锥体细胞形态基本规则,只见少数散在核固缩细胞.结论 番茄红素对寰枢椎长期乳酸堆积的老龄小鼠记忆能力具有一定的改善作用.