纳米硒对小鼠氧化损伤的保护作用

采用给小鼠颈后皮下注射D 半乳糖水溶液,同时灌胃不同浓度的纳米硒混悬液,10d后测定血浆中脂质过氧化物(LPO)、谷胱甘肽过氧化物酶(GSH PX)和超氧化物歧化酶(SOD)的活性.结果表明,D 半乳糖可使小鼠血浆LPO含量显著升高(P<0 05),GSH PX和SOD活性显著降低(P<0 05);给予纳米硒后血浆中LPO含量显著降低(P<0 05),而SOD和GSH PX活性显著升高(P<0 05).说明D 半乳糖可导致小鼠氧化损伤,纳米硒可通过提高GSH PX和SOD的活性保护D 半乳糖所致小鼠的氧化损伤.     

地参多糖对D-半乳糖所致衰老小鼠的抗氧化作用研究

[目的]研究地参多糖(LLP)对D-半乳糖所致衰老小鼠的抗氧化作用。[方法]取昆明种小白鼠50只,随机分为5组。除正常对照组外,其余各组每天于颈背皮下注射D-半乳糖80 mg/kg,连续42 d,造成亚急性衰老模型。在注射D-半乳糖的同时,试验组每天分别灌胃给予地参多糖(LLP)300、200和100 mg/kg,正常对照组及模型对照组给予等量生理盐水。末次给药12 h后,分离血清及肝组织,分别测定各组小鼠衰老相关生化指标。[结果]LLP能拮抗D-半乳糖所致的小鼠衰老,使小鼠血清及肝组织SOD和GSH-Px活性明显回升,MDA的水平下降。[结论]LLP具有一定的抗氧化和抗衰老作用。     

酸樱桃汁对D-半乳糖致衰老小鼠学习记忆功能的影响

目的检测酸樱桃汁对D-半乳糖致衰老小鼠模型学习记忆功能的影响.方法颈背部皮下注射D-半乳糖120 mg/（kg·d^-1）连续56 d建立亚急性衰老模型,同时灌胃给予不同剂量的酸樱桃汁进行治疗,治疗8周后,分别采用跳台实验、Morris水迷宫检测小鼠的学习记忆能力.结果跳台法检测结果显示：酸樱桃汁能延长D-半乳糖致衰老模型小鼠的潜伏期,减少错误次数;Morris水迷宫实验结果显示：酸樱桃汁能使D-半乳糖致衰老模型小鼠平均潜伏期明显缩短,跨过平台次数显著增加.结论酸樱桃汁能有效提高D-半乳糖致衰老小鼠的学习记忆能力.     

左卡尼汀对D-半乳糖致衰老小鼠抗氧化作用的研究

为了研究左卡尼汀(L-carnitine,LC)对D-半乳糖所致衰老小鼠的抗氧化作用,试验将50只小鼠随机分成5组,即空白对照组、模型组和左卡尼汀治疗组[0.25、0.50、1.00 g/(kg.d)],采用D-半乳糖复制亚急性衰老小鼠模型,试验6周后处死小鼠,测定其血浆、脑组织及肝脏中的超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量。试验结果显示,左卡尼汀能显著提高衰老小鼠血清、脑组织及肝脏中的SOD、GSH-Px活性,降低MDA含量,且呈剂量依赖性。表明左卡尼汀有一定的抗衰老作用,其机制可能与抗氧化作用有关。     

中剂量螺旋藻多糖和银杏提取物的联合抗衰老作用研究

[目的]研究中剂量螺旋藻多糖和银杏提取物的联合抗衰老作用。[方法]每天对试验小鼠颈下注射D-半乳糖125 mg/kg,连续42d,建立衰老模型。给药组小鼠每天灌服100 mg/kg螺旋藻多糖、银杏叶及复合药液,观察中剂量复合螺旋藻多糖和银杏叶有效成分对D-半乳糖致衰老小鼠的作用,并测定免疫器官重量、血清SOD活性和心肌、脑丙二醛（MDA）含量等相关衰老指标。[结果]螺旋藻多糖和银杏提取物均能有效对抗D-半乳糖所致小鼠衰老,二者的复合药效要强于单一药效。[结论]该研究为螺旋藻多糖和银杏提取物的联合抗衰老作用提供了试验依据。     

Antioxidant Efficacy of Protein Hydrolysates from Large Yellow Croaker (Pseudosciaena crocea) in D-galactose-Induced Aging Mice

The antioxidant efficacy of protein hydrolysates prepared from large yellow croaker (Pseudosciaena crocea) by enzymatic hydrolysis using neutral protease was evaluated in D-galactose-induced aging mice. Animals were divided into normal and model control groups, and low-, middle-, and high-dose groups (50, 100, and 300 mg/kg; LYCHs), as well as tocopherol (VE) and antagonistic (LYCHs + VE) groups. The study was carried out for 30 days. Administration of D-galactose induced oxidative damage with a significant rise (p < 0.01) in malondialdehyde and a reduction in several endogenous antioxidant enzymes and glutathione (GSH). Treatment with large yellow croaker protein hydrolysates stimulated an increase in superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities, increased levels of reduced glutathione, and decreased malondialdehyde, compared with the model control group. Additionally, hepatocellular damage was evaluated by measuring aspartate aminotransferase and alanine aminotransferase levels. These results demonstrate the protective role of large yellow croaker protein hydrolysates in D-galactose-induced oxidative stress, as well as their potential as nutraceuticals or adjuvant agents for disease prevention.     

Effects of aluminum on the reduction of neural stem cells,proliferating cells,and differentiating neuroblasts in the dentate gyrus of D-galactose-treated mice via increasing oxidative stress

Aluminum (Al) accumulation increases with aging, and long-term exposure to Al is regarded as a risk factor for Alzheimer''s disease. In this study, we investigated the effects of Al and/or D-galactose on neural stem cells, proliferating cells, differentiating neuroblasts, and mature neurons in the hippocampal dentate gyrus. AlCl₃ (40 mg/kg/day) was intraperitoneally administered to C57BL/6J mice for 4 weeks. In addition, vehicle (physiological saline) or D-galactose (100 mg/kg) was subcutaneously injected to these mice immediately after AlCl₃ treatment. Neural stem cells, proliferating cells, differentiating neuroblasts, and mature neurons were detected using the relevant marker for each cell type, including nestin, Ki67, doublecortin, and NeuN, respectively, via immunohistochemistry. Subchronic (4 weeks) exposure to Al in mice reduced neural stem cells, proliferating cells, and differentiating neuroblasts without causing any changes to mature neurons. This Al-induced reduction effect was exacerbated in D-galactose-treated mice compared to vehicle-treated adult mice. Moreover, exposure to Al enhanced lipid peroxidation in the hippocampus and expression of antioxidants such as Cu, Zn- and Mn-superoxide dismutase in D-galactose-treated mice. These results suggest that Al accelerates the reduction of neural stem cells, proliferating cells, and differentiating neuroblasts in D-galactose-treated mice via oxidative stress, without inducing loss in mature neurons.     

玉米幼芽提取物对衰老小鼠心肌自由基代谢和超微结构的影响

小鼠颈背部皮下注射D-半乳糖生理盐水溶液(125 mg/(kg.d))诱导其衰老,同时分别灌胃10,20和40 mg/(kg.d)玉米幼芽提取物(Extract of maize plumule,EMP),每日1次,连续处理42 d后,测定心肌组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)和一氧化氮(NO)的含量,并用透射电镜观察心肌细胞超微结构,研究EMP对D-半乳糖致衰老小鼠心肌自由基代谢和超微结构的影响。结果表明,与对照组相比,D-半乳糖能明显的降低小鼠心肌组织中的SOD、CAT和GSH-Px活性,提高MDA、NO含量;与衰老模型组比较,20 mg/kg EMP处理组小鼠心肌组织的SOD、CAT和GSH-Px活性均极显著升高,MDA和NO含量均极显著降低;与对照组相比,衰老模型组小鼠的心肌Z线变宽、模糊,肌原纤维断裂、溶解、凝集,线粒体肿胀、空泡化、嵴消失;20 mg/kg EMP处理组的以上病变均有明显的改善。这表明20 mg/kg的EMP具有增强衰老小鼠心肌抗氧化酶活性,改善心肌自由基代谢,保护心肌细胞超微结构的作用。     

美拉德反应修饰改善猪血浆蛋白抗氧化肽功能特性的研究

研究主要探讨美拉德反应修饰对猪血浆蛋白抗氧化肽功能特性的影响。采用D-半乳糖对猪血浆蛋白抗氧化肽进行美拉德修饰,蛋白质和糖的比例为1??3(W/W),在90℃水浴中分别加热0、1和6 h,得到美拉德反应产物(MRPs),测定其溶解性、表面疏水性、乳化性及乳化稳定性、起泡性及起泡稳定性。结果表明,经美拉德反应修饰后猪血浆蛋白抗氧化肽的功能特性有明显改善,其溶解性、乳化及乳化稳定性、起泡及起泡稳定性均随反应时间增加而逐渐增大(P0.05),表面疏水性则随反应时间增加而降低(P0.05)。同时,MRPs功能特性随体系中p H的改变而显著变化(P0.05)。因此,采用美拉德修饰改善猪血浆蛋白抗氧化肽功能特性,可使其广泛应用于食品加工业。     

白茶体外抗氧化与体内抗衰老作用的研究

为比较不同原料来源白茶的体外抗氧化和体内抗衰老作用并探究其作用机制,本研究制备白毫银针（Baihaoyinzhen, YZ）、白牡丹（Baimudan, MD）和寿眉（Shoumei, SM）的提取物,检测其主要功效成分含量及其体外抗氧化活性。通过诱导D-半乳糖衰老小鼠模型,探究其体内抗衰老作用。结果显示,YZ提取物的主要功效成分含量均高于MD和SM提取物,SM提取物的茶多酚和总黄酮含量高于MD提取物。在体外,相同浓度下YZ提取物抗氧化能力最强,MD和SM提取物差异不明显。在体内,YZ提取物在抑制肝脏脂质过氧化方面表现出显著优势（P<0.05）,SM提取物在提高血清抗氧化酶活性方面具有显著优势（P<0.05）,但未表现出剂量依赖关系。3种白茶提取物上调了小鼠肝脏抗氧化酶与抗衰老基因的表达,表现出剂量依赖性,有效地改善了机体氧化应激状态,且对小鼠均未表现出肝脏毒性作用。