海参肽对小鼠免疫调节及抗疲劳能力的影响

目的观察海参肽对小鼠免疫功能和抗疲劳能力的影响。方法经口给小鼠0．085、0．170、0．500g／kg海参肽,对免疫调节和抗疲劳等10项指标进行测定。结果海参肽对小鼠迟发型变态反应有促进作用,ConA诱导的脾淋巴细胞增殖能力明显增强,溶血空斑数、血清溶血素也显著高于对照组,巨噬细胞对鸡红细胞的吞噬指数及碳廓清指数明显高于对照组。海参肽能明显延长小鼠的负重游泳时间,显著降低运动后小鼠的血尿素氮含量和血乳酸水平,同时提高了肝糖原含量。结论海参肽能够增强小鼠单核巨噬细胞作用及体液免疫和细胞免疫功能,增强小鼠的抗疲劳能力。     

大黄酚抗衰老作用的实验研究

目的 探讨大黄酚对小鼠抗衰老的作用。方法 采用避暗实验，观察大黄酚对学习记忆的影响；通过常压耐缺氧、断头耐缺氧、亚硝酸钠中毒造成的缺氧以及负重游泳实验，观察大黄酚对小鼠缺氧及耐力的影响；以AlCl3造成急性衰老小鼠模型，观察大黄酚对小鼠血中超氧化物歧化酶（SOD）活性的影响。结果 大黄酚能明显改善记忆障碍、提高小鼠耐力、并且能明显提高急性衰老小鼠血中SOD活性。结论 大黄酚具有一定的抗衰老作用。     

野玫瑰根煎剂对老龄小鼠免疫功能的恢复作用及抗衰老效应的实验研究

野玫瑰根煎剂对老龄小鼠免疫功能及抗衰老作用的研究结果表明:野玫瑰根煎剂明显地增强老龄小鼠的血清溶菌酶活性、腹腔巨噬细胞吞噬功能、血清特异性抗体效价和脾脏抗体形成细胞(PFC)O.D值等体液免疫功能及外周血淋巴细胞酸性α—醋酸萘酯酶与E—花环细胞的百分率等细胞免疫功能,而有恢复老龄小鼠的免疫功能作用。同时又能增强血清总抗氧化活性和红细胞内SOD活性,从而具有抗衰老效应。     

复方炎平水提物对淋巴细胞转化和巨噬细胞吞噬的影响

目的探讨复方炎平水提物（YP）对淋巴细胞转化和巨噬细胞吞噬的影响。方法淋巴细胞转化试验（体外试验）测定小鼠淋巴细胞增殖情况，并测定小鼠巨噬细胞吞噬功能。结果YP100μg／ml可同时促进小鼠脾淋巴细胞及小鼠脾细胞伴刀豆蛋白A（ConA）的增殖，并具有剂量依赖性；YP10g/kg连续藩服2w，小鼠腹腔巨噬细胞的吞噬功能明显增强。结论YP可明显增强小鼠免疫功能。     

松果菊苷抗氧化作用研究

目的 研究管花肉苁蓉中松果菊苷(echinacoside,ECH)抗氧化、耐缺氧、抗疲劳等抗衰老作用.方法 以维生素E[VE,100mg/(kg*d)]为对照,观察低、中、高剂量[10mg/(kg*d)、20mg/(kg*d)、40mg/(kg*d)]ECH对正常健康小鼠和D-半乳糖亚急性衰老模型小鼠的影响.测定正常小鼠常压耐缺氧和负重游泳时间,检测衰老小鼠血清中超氧化物歧化酶(SOD)活性,丙二醛(MDA)含量,放射免疫法测定外周血白介素-2(IL-2)含量.计算亚急性衰老模型小鼠的脾指数和胸腺指数.结果 ECH和VE能够延长健康小鼠常压耐缺氧和负重游泳时间(P＜0.01);ECH和VE能提高衰老小鼠血清SOD活性(P＜0.01),降低血清MDA含量(P＜0.01),升高外周血IL-2含量(P＜0.05),增加脾指数(P＜0.01)和胸腺指数(P＜0.01).结论 ECH能拮抗自由基损伤,提高健康小鼠常压耐缺氧和负重游泳时间,增加脾指数和胸腺指数,具有抗氧化,增强免疫力,延缓衰老,抗疲劳作用.     

母牛分支杆菌制剂对免疫功能低下小白鼠的免疫调节作用

不同剂量的母牛分支杆菌制剂应用免疫功能低下的小鼠模型，检测小鼠腹腔巨噬细胞吞噬百分率。吞噬指数及脾淋巴细胞增殖率。结果显示注射不同剂量的母牛发支杆菌制剂小鼠腹腔巨噬细胞吞噬百分率及吞噬指数明显高于未注射该制剂对照组（Ｐ〈０．０１），淋巴细胞增殖率也明显高于对照组（Ｐ〈０．０１或Ｐ〈０．０５），提示母牛分支杆菌制剂能明显激活巨噬细胞免疫功能，对脾淋巴细胞增殖有明显刺激作用，对调节及提高机体免疫应答水     

野玫瑰根煎剂对老龄小鼠免疫功能的恢复作用及抗衰老效应的…

野玫瑰根煎剂对老龄小鼠免疫功能及抗衰老作用的研究结果表明；野玫瑰根煎剂明显地增强老龄小鼠的血清溶菌酶活性，腹腔巨噬细胞吞噬功能，血清特异性抗体效价和脾脏抗体形成细胞Ｏ．Ｄ值等体液免疫功能及外周血淋巴细胞酸性ａ－醋酸萘酯酶与Ｅ－花环细胞的百分率等细胞免疫功能，而有恢复老龄小鼠的免疫功能作用，同时又能增强血清总抗氧化活性和红细胞内ＳＯＤ活性，从而具有抗衰老效应。     

复方三子汤对小鼠免疫功能影响的实验研究

每日给正常小鼠分别灌服不同剂量的复方三子汤,连续30 d,对小鼠的免疫器官重量及ConA诱导的小鼠脾淋巴细胞增殖能力无显著影响且能增强小鼠腹腔巨噬细胞吞噬鸡红细胞的能力。表明复方三子汤对小鼠腹腔巨噬细胞的吞噬功能具有一定的促进作用。     

金花葵花总黄酮对衰老模型小鼠抗氧化和免疫功能的影响

目的 观察金花葵花总黄酮对D-半乳糖所致亚急性衰老小鼠抗氧化和免疫功能的影响.方法 昆明种小鼠分成4组,制备D-半乳糖亚急性衰老小鼠模型,分别用相应剂量的金花葵花总黄酮或生理盐水灌胃;6 w后,测定血清中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氯化物酶(GSH-Px)指标,胸腺、脾指数,MTI法检测淋巴细胞转化刺激指数的变化.结果 模型小鼠与正常小鼠比较,血清中MDA含量升高而SOD、GSH-Px含量下降,胸腺、脾指数以及T、B淋巴细胞增殖活性明显降低;金花葵花总黄酮可明显提高亚急性衰老小鼠血清SOD、GSH-Px含量,并使MDA含量降低,并明显提高胸腺、脾指数和T、B淋巴细胞增殖能力.结论 金花葵花总黄酮可增强衰老小鼠抗氧化和免疫功能抗衰老.     

北五味子粗多糖抗衰老作用的实验研究

目的 观察北五味子粗多糖的抗衰老作用。方法 北五味子粗多糖按100、200、400mg/kg连续灌胃3-7d,观察小鼠的存活时间,连续游泳时间和免疫器官重量试验。大鼠连续灌胃20d,测血清LPO含量和SOD活性。结果 北五味子粗多糖能明显提高小鼠耐氧及抗疲劳能力,增加正常小鼠免疫器官重量,并明显增强小鼠网状内皮系统的吞噬功能。可明显降低老年大鼠血清过氧化脂质（LPO）含量,提高超氧化物歧化酶（SOD）活性,结论 北五味子粗多糖具有抗衰老作用。     

江苏地产白首乌C21甾苷抗衰老作用研究

目的研究江苏地产白首乌C21甾苷(C21 steroidal glycoside,CSG)抗氧化、耐缺氧、抗疲劳等抗衰老作用。方法以维生素E[VE,100mg/(kg.d)]为对照,观察CSG低、中、高剂量组[10mg/(kg.d)、20mg/(kg.d)、40mg/(kg.d),即CL、CM、CH组]对小鼠常压耐缺氧试验,负重游泳试验和D-半乳糖(D-gal)亚急性衰老模型小鼠的影响。测定小鼠常压耐缺氧和负重游泳时间,取血清、心、肝、脑组织,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性,硫代巴比妥酸法测定丙二醛(MDA)含量,ELISA法检测端粒酶活性。结果与正常对照组相比,CSG和VE能够延长健康小鼠常压耐缺氧和负重游泳时间,提高D-gal模型小鼠血清、心、肝、脑SOD活性,降低MDA含量;中、高剂量CSG组小鼠血清端粒酶活性升高;CSG低、中、高剂量组及VE组小鼠心脏端粒酶活性均升高(P<0.01);CSG及VE对小鼠肝及脑组织端粒酶活性无影响。结论CSG能拮抗自由基损伤,提高健康小鼠常压耐缺氧和负重游泳时间,提高D-gal衰老模型小鼠血清、心、肝、脑组织SOD活性,减少MDA含量,提高心脏组织中端粒酶活性。具有抗氧化、延缓衰老、抗疲劳作用。     

毛花黄芪总甙对小鼠抗衰老作用的研究

目的 研究毛花黄芪总甙对D-半乳糖（D-gal)所致衰老小鼠学习记忆、抗氧化和免疫功能的影响。方法 D-gal连续注射,造成实验性衰老小鼠模型,通过跳台和避暗实验,并通过测定血清中超氧化物歧化酶（SOD）和丙二醛（MDA）水平,观察毛花黄芪总甙对小鼠学习记忆和抗氧化能力的影响;通过测小鼠免疫器官重量,碳粒廓清速率,迟发超敏反应（DNCB）及体外conA诱导淋巴细胞转化能力,观察药物对衰老小鼠免疫功能的影响。结果 在跳台和避暗试验中,毛花黄芪总甙能显著提高衰老小鼠免疫器官重量,碳粒廓清速率,迟发超敏反应（DNCB）及体外conA诱导淋能上能下细胞转化能力的降低均具有较明显的恢复作用。结论 毛花黄芪总甙能增强衰老小鼠学习记忆力和抗氧化能力,并有较强的免疫增强作用,因此具有较强的抗衰老作用。     

金属硫蛋白抗D-半乳糖拟衰老效应的研究

目的：观察外源性金属硫蛋白（MT）是否具有抗体内自由基损伤及抗衰老效应的能力。方法：采用小白鼠皮下注射D－半乳糖造成的亚急性衰老模型，以阿尼西坦作为阳性对照观察皮下注射不同剂量MT对小鼠在T－型游泳迷宫作业能力的影响及小鼠心、肝、脑组织中丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性。结果：MT可明显改善小鼠的学习记忆能力。MT在1．4mg.kg^-1.d^-1剂量时已表现出比阳性对照药物阿尼西坦（30mg.kg^-1.d^-1)时更明显的治疗效应（正确数获得率），同时MT在7．0mg.kg^-1.d^-1时可明显降低MDA含量及提高SOD活性。结论：MT作为内源性活性氧清除对D－半乳糖的致衰老效应有很好的对抗作用。     

松花粉对D-半乳糖衰老模型小鼠学习记忆功能的影响及机制研究

目的探讨松花粉对脑衰老的作用及其相关机制。方法以100mg/kg D-半乳糖皮下注射建立小鼠衰老模型,灌胃给予模型小鼠高、中、低三个剂量(500mg/kg、1000mg/kg、1500mg/kg)的松花粉,并以非酶糖基化抑制剂盐酸氨基胍(AG)为阳性对照,连续给药8周后,采用跳台法测定小鼠的学习记忆能力。处死小鼠获取血清及脑组织,检测晚期糖基化终末产物(AGE)水平,超氧化物歧化酶(SOD)活力、MDA水平以及炎症因子IL-6和TNF-α水平等衰老相关指标。结果跳台法检测模型组较正常组潜伏期显著缩短,5min内错误次数显著增加(P<0.05),而松花粉处理后能显著逆转这一变化(P<0.05),高剂量组效果最佳;同时,松花粉处理组能显著抑制模型组血清及脑组织中AGE水平及IL-6、TNF-α水平的升高(P<0.05),提高血清及脑组织SOD活力(P<0.05)并下调MDA水平(P<0.01)。结论松花粉能显著改善衰老模型小鼠的学习记忆功能,并上调抗氧化活性和降低衰老相关的炎症介质水平,抑制体内非酶糖基化可能是其发挥延缓衰老作用的机制之一。     

Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin

Cellular senescence arrests the proliferation of mammalian cells at risk for neoplastic transformation, and is also associated with aging. However, the factors that cause cellular senescence during aging are unclear. Excessive reactive oxygen species (ROS) have been shown to cause cellular senescence in culture, and accumulated molecular damage due to mitochondrial ROS has long been thought to drive aging phenotypesin vivo. Here, we test the hypothesis that mitochondrial oxidative stress can promote cellular senescence in vivo and contribute to aging phenotypes in vivo, specifically in the skin. We show that the number of senescent cells, as well as impaired mitochondrial (complex II) activity increase in naturally aged mouse skin. Using a mouse model of genetic Sod2 deficiency, we show that failure to express this important mitochondrial anti-oxidant enzyme also impairs mitochondrial complex II activity, causes nuclear DNA damage, and induces cellular senescence but not apoptosis in the epidermis. Sod2 deficiency also reduced the number of cells and thickness of the epidermis, while increasing terminal differentiation. Our results support the idea that mitochondrial oxidative stress and cellular senescence contribute to aging skin phenotypes in vivo.     

L-肉毒碱对D-半乳糖衰老模型小鼠的作用

目的：观察L-肉毒碱对D-半乳糖所致衰老小鼠的影响，探讨L-肉毒碱的抗衰老作用机制。方法：采用穿梭法、跳台法、自主活动测定法和水迷宫法检测各组小鼠学习记忆行为；并测定脑中丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性，全面考察L-肉毒碱的抗衰老作用。结果：与模型组比较，给L-肉毒碱组动物穿梭箱实验中电击时间减少；跳台实验中错误次数减少；自主活动次数增加；水迷路实验中潜伏期缩短。同时脑组织中MDA含量降低，SOD活力提高。结论：L-肉毒碱能改善D-半乳糖所致衰老小鼠的多项体征。     

Lentivirus-mediated superoxide dismutase1 gene delivery protects against oxidative stress-induced liver injury in mice.

BACKGROUND: The exposure of liver to hepatotoxins, and their subsequent metabolism, results in increased reactive oxygen species (ROS), one of the major culprits in causing both acute liver cell injury and chronic liver diseases. The aim of this present study is to investigate the protective effects of lentiviral vector-mediated copper-zinc superoxide dismutase (LV-SOD1) gene transfer against ROS-induced cytotoxicity in Hep G2 cells and liver injury in mice. METHODS: In vitro SOD1 efficacy was tested against two ROS-generating systems: hypoxanthine/xanthine oxidase (HX/XO) and hydroxyethyl radicals (HER), whereas in vivo SOD1 efficacy was evaluated in carbon tetrachloride (CCl4)-induced liver injury in C57BL/6 mice. RESULTS: LV-SOD1 transduction in Hep G2 cells resulted in a significant increase in SOD activity in cell lysates, and it significantly decreased the toxicity induced by HX/XO and HER. High SOD1 expression in the liver was achieved via portal vein injection of LV-SOD1 in mice and these high levels were observed for 30 days, the length of the experiment to date. SOD1 overexpression significantly decreased the toxicity and restored liver function in the CCl4-treated mice. CONCLUSIONS: These findings demonstrate for the first time that LV transduction led to the long-term expression of fully functional transgene expression in both in vitro and in vivo systems.     

Melatonin protects against oxidative stress caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the mouse nigrostriatum

We tested the hypothesis that melatonin acts as a powerful hydroxyl radical (*OH) scavenger in vivo in the brain, and interferes with oxidative stress caused by the parkinsonian neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We investigated the effect of melatonin on in vitro *OH production employing a Fenton-like reaction in test tubes, and ex vivo *OH generation in isolated mitochondria induced by 1-methyl-4-phenyl pyridinium (MPP+), as well as on in vivo *OH formation in the mouse striatum following systemic administration of MPTP. We also measured reduced glutathione (GSH) levels, and superoxide dismutase (SOD) activity in the nucleus caudatus putamen (NCP) and substantia nigra (SN), 7 days following MPTP and/or melatonin administration. Melatonin caused a significant and dose-dependent inhibition of the production of *OH in the in vitro, ex vivo and in vivo experimental conditions. Melatonin caused no changes in monoamine oxidase-B activity, in vitro in mitochondrial P2 fractions or in vivo following systemic administration. MPTP treatment in mice caused a significant depletion of GSH, and increased the specific activity of SOD both in SN and NCP on the seventh day. MPTP-induced GSH depletion was dose-dependently blocked in SN and NCP by melatonin. Higher doses of melatonin exhibited a synergistic effect on MPTP-induced increase in the SOD activity in the SN. These results suggest that while GSH inhibition is a direct consequence of *OH generation following neurotoxin administration, the increase in SOD activity is a compensatory mechanism for removing superoxide radicals generated as the result of MPTP. Our results not only point to the potency of melatonin in blocking the primary insults caused by MPTP, but also provide evidence for triggering secondary neuroprotective mechanisms, suggesting its use as a therapeutic agent in neurodegenerative disorders, such as Parkinson's disease.     

Mice heterozygous for a defect in mitochondrial trifunctional protein develop hepatic steatosis and insulin resistance

BACKGROUND & AIMS: Little is known about the role of mitochondrial beta-oxidation in development of nonalcoholic fatty liver disease (NAFLD). Mitochondrial trifunctional protein (MTP) catalyzes long-chain fatty acid oxidation. Recently, we generated a mouse model for MTP deficiency and reported that homozygous (MTPa-/-) mice suffer neonatal death. In this study, we investigated effects of heterozygosity for the MTP defect on hepatic oxidative stress, insulin resistance, and development of NAFLD in mice. METHODS: We evaluated liver histopathology, serum alanine aminotransferase (ALT), glucose, fatty acids, and insulin levels in MTPa+/- and MTPa+/+ littermates. Insulin resistance was evaluated using glucose tolerance test (GTT) and insulin tolerance test (ITT). Liver tissues were used to measure triglyceride and fatty acid content, activity of superoxide dismutases (SOD) and glutathione peroxidase (GPx), glutathione (GSH), and cytochrome P-450 2E1 expression. RESULTS: Aging but not young MTPa+/- mice developed hepatic steatosis with elevated ALT, basal hyperinsulinemia, and increased insulin area under curve (AUC) on GTT compared with MTPa+/+ littermates. In response to insulin challenge, aging MTPa+/- mice had slower rate of glucose disappearance and increased glucose AUC. Significant hepatic steatosis and insulin resistance developed concomitantly in the MTPa+/- mice at 9-10 months of age. Aging MTPa+/- mice had higher antioxidant activity of total SOD and GPx, lower GSH, and increased expression of cytochrome P-450 2E1, consistent with increased hepatic oxidative stress. CONCLUSIONS: Heterozygosity for beta-oxidation defects predisposes to NAFLD and insulin resistance in aging mice. Impairment of mitochondrial beta-oxidation may play an important role in pathogenesis of NAFLD.     

快速老化鼠和自然衰老鼠中超氧化物歧化酶的比较研究

目的通过比较快速老化鼠（SAM—P／8）和昆明种自然衰老鼠中超氧化物歧化酶（SOD）表达情况，探讨两种衰老鼠之间异同及SOD在衰老过程中所起的作用。方法选用快速老化鼠（SAM—P／8）3月龄和6月龄各10只，昆明种小鼠3月龄和15月龄各10只，采用生物化学方法检测SOD蛋白活性和MDA含量；免疫组化对SOD蛋白的表达定位；蛋白印迹法检测SOD蛋白的含量变化；RT—PCR方法检测SOD基因的表达变化。结果两种衰老小鼠肝脏中SOD基因表达，SOD蛋白表达和活性均呈增龄性降低，MDA含量均呈现增龄性增加。结论快速衰老鼠和自然衰老鼠的SOD变化趋势相同，SOD在衰老过程中起了重要作用。