姜黄素对D-半乳糖致衰老大鼠氧化应激及Nrf2/ARE通路的影响

目的 研究姜黄素对D-半乳糖致衰老模型大鼠氧化应激及Nrf2/ARE通路的影响.方法 将大鼠随机均分为空白组、模型组和姜黄素组于模型组和姜黄素组大鼠每日sc 125 mg· kg-1D-半乳糖造模,姜黄素组大鼠同时ip 10 mg·kg-1姜黄素,空白组大鼠给予生理盐水,连续7周.测定各组大鼠血清中丙二醛(MDA)、肝组织中蛋白质糖基、谷胱甘肽过氧化物(GSH)的含量和血清超氧化物歧化酶(SOD)、全血谷胱甘肽过氧化物酶(GSH-Px)的活性;用Western blot法分析肝组织中Nrf2蛋白和HO-1蛋白的表达水平.结果 与模型组比较,姜黄素组大鼠血清中SOD的活性和MDA、肝中GSH、蛋白质羰基的含量均降低,全血中GSH-Px的活性显著升高,Nfr2和HO-1蛋白的表达水平也明显升高.结论 姜黄素能够缓解D-半乳糖导致的大鼠氧化应激,Nrf2/ARE通路参与了姜黄素的抗氧化活性.     

松花粉对酒精性肝损伤的保护功能研究

目的 研究松花粉对酒精性肝损伤的保护作用.方法 采用酒精复制大鼠肝损伤模型,测定肝组织的丙二醛(MDA)、甘油三脂(TG)及还原型谷光甘肽(GSH)含量;并观察肝脏的病理组织学改变.结果 受试样品大鼠肝组织的MDA、TG含量均低于肝损模型组;而GSH含量高于肝损模型组;各剂量组大鼠肝脏病理改变评分值均低于肝损模型组.结论 松花粉对酒精性肝损伤具有保护功能.     

枸杞多糖对高脂饮食诱导的脂肪肝大鼠模型的影响

目的 观察枸杞多糖(lycium barbarum polysaccharide,LBP)对高脂饮食大鼠非酒精性脂肪肝的影响及可能的机制.方法 32只雄性Wistar大鼠随机分成4组:正常对照组、模型组和LBP高、低剂量组.采用喂高脂饲料复制大鼠非酒精性脂肪肝模型.观察不同处理组大鼠血清ALT、AST、血脂、肝脂质、肝组织超氧化物歧化酶(SOD)活性、还原型谷胱甘肽(GSH)和丙二醛(MDA)的含量以及肝脏病理形态学的变化.结果 与非酒精脂肪肝模型组相比,LBP干预组血清ALT下降,以高剂量组明显(P＜0.05),血清总胆固醇(TCh)和LDL-Ch明显下降(P＜0.05),血清HDL-ch呈升高趋势,但无显著性差异(P＞0.05),肝内甘油三酯和TCh含量下降(P＜0.05),肝内脂肪变性和炎症程度均明显减轻(P＜0.05),肝内MDA含量均显著降低(P＜0.05),肝内SOD活性和GSH含量升高,高剂量组明显(P＜0.05).结论 LBP可明显减轻高脂饮食诱导的大鼠非酒精性脂肪肝,其机制可能与其抗氧化作用有关.     

肉苁蓉多糖对衰老小鼠肺蛋白含量与抗氧化功能关系的影响

使用D 半乳糖造成小鼠实验性衰老模型 ,观察肉苁蓉多糖对实验性衰老小鼠肺胶原蛋白、弹性蛋白含量的影响 ,对肺组织和红细胞中超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)及丙二醛 (MDA)含量的影响。结果　灌服肉苁蓉多糖的衰老小鼠的肺组织及红细胞中SOD、GSH Px活力不同程度提高 ,肺及血浆中丙二醛含量有所降低。同时肺胶原蛋白含量减少 ,弹性蛋白含量增多。结论　肉苁蓉多糖具有抗氧化性损伤和抗肺衰老的作用     

还原型谷胱甘肽对大鼠肝纤维化肝内抗氧化体系的影响

目的 探讨还原型谷胱甘肽（GSH）对大鼠肝纤维化肝内抗氧化体系的影响.方法 将36只雄性SD大鼠随机分为三组：正常组、模型组、GSH组,每组各12只.除正常组外,大鼠造模采用腹部皮下注射四氯化碳法制备大鼠肝纤维化模型,GSH组在造模的同时进行GSH治疗,各组于第14周测定大鼠肝脏中过氧化氢酶（CAT）、超氧化物歧化酶（SOD）、维生素E（VitE）和丙二醛（MDA）.结果 模型组大鼠肝组织中CAT、SOD、VitE明显低于正常组（P＜0.01）,而MDA明显升高（P＜0.01）;GSH组与模型组比较,各组的SOD、CAT、VitE均明显升高,而MDA明显下降,差异均有统计学意义（P＜0.01）.结论 GSH能有效降低大鼠肝纤维化肝内脂质过氧化.     

羧甲基壳聚糖对D-半乳糖诱导氧化损伤模型小鼠肝、脑的保护作用

目的:探索羧甲基壳聚糖(CMC)对D-半乳糖诱导氧化损伤模型小鼠肝、脑的作用。方法:实验分为4组:对照组、CMC组、D-半乳糖模型组、D-半乳糖+CMC组。测定各组小鼠肝、脑超氧化物歧化酶(SOD)、过氧化氢酶(CAT)的活性、丙二醛(MDA)的含量及蛋白质羰基化程度。结果:D-半乳糖可诱导小鼠蛋白质羰基化,诱导小鼠氧化损伤,CMC可使小鼠蛋白质羰基化含量降低,SOD、CAT活性增加,MDA含量降低。结论:CMC对D-半乳糖引起的氧化损伤有一定的保护作用。     

枸杞多糖与丹参酮延缓小鼠皮肤衰老的实验研究

目的比较枸杞多糖与丹参酮对衰老小鼠皮肤的抗衰老作用。方法60只雌性昆明种小鼠,随机分为4组（n=15）：正常对照组皮下注射生理盐水;其余3组每日颈背部皮下注射D-半乳糖[1000mg/（kg·d）]造成小鼠衰老模型,同时各组分别灌胃生理盐水（衰老模型组）、枸杞多糖[200mg/（kg·d）]、丹参酮[1500mg/（kg·d）]。42d后,测定小鼠背部皮肤组织匀浆中超氧化物歧化酶（SOD）活力、过氧化脂质代谢产物丙二醛（MDA）含量和皮肤羟脯氨酸（Hyp）含量。结果枸杞多糖可使衰老模型小鼠皮肤中MDA含量显著降低,较丹参酮组明显;但SOD活力显著升高,不及丹参酮组改变显著;枸杞多糖和丹参酮均可使羟脯氨酸含量升高,且效果相当。结论枸杞多糖与丹参酮都有显著的抗小鼠皮肤衰老作用,枸杞多糖清除皮肤中脂质过氧化代谢产物方面较丹参酮明显,而提高皮肤抗氧化酶活力则不及丹参酮显著,在增强成纤维细胞活性方面两者效果相当。     

山药多糖对小鼠免疫性肝损伤的保护作用

目的 探讨山药多糖对卡介苗(BCG)与脂多糖(LPS)致小鼠免疫性肝损伤的保护作用.方法 将昆明种小鼠分为对照组、模型组、山药多糖高、中、低剂量保护组,第1天,模型组与保护组均尾iv BCG,保护组每天分别按体重30、60、120 mg·kg~(-1)山药多糖ig-次,第12天末次ig 2 h,模型组与山药多糖高、中、低保护组经尾iv LPS.16 h后取小鼠称重,于眼球取血,测定小鼠血清中ALT、AST活性;处死小鼠,计算肝指数和脾脏指数;制备肝匀浆,测定肝组织中MDA、GSH含量及SOD和GSH-Px活性.结果 与模型组比较山药多糖各剂量可降低小鼠肝指数、脾脏指数及降低血清ALT、AST活性(P<0.05);降低MDA的含量,增加GSH含量和GSH-Px活性.结论 山药多糖对BCG和LPS诱导的小鼠免疫性肝损伤有保护作用.     

酒龙胆中总多糖和总环烯醚萜苷保肝作用的研究

目的研究酒龙胆中总多糖和总环烯醚萜苷对四氯化碳(CCl4)所致大鼠急性肝损伤的保护作用。方法将50只大鼠随机分为空白组、模型组、总多糖组、总环烯醚萜苷组和阳性对照药联苯双酯组,给药7 d后,除空白组外,其余各组大鼠腹腔注射2.5%CCl_4植物油溶液(1.5 mL·kg~(-1)),复制急性肝损伤模型。测定各组大鼠血浆中丙氨酸转氨酶(ALT)、天门冬氨酸氨基转移酶(AST)、肿瘤坏死因子α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)、白细胞介素-6(IL-6)以及肝组织超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽(GSH)、谷胱甘肽过氧化物酶(GSH-Px)的含量以及HE染色法观察各组大鼠急性肝损伤程度。结果总多糖和总环烯醚萜苷均能使肝损伤大鼠体内SOD、GSH-Px、GSH的含量升高、MDA的含量降低,其中总多糖的升高或降低作用更优;总多糖可使肝损伤大鼠体内AST、ALT的含量下降,总环烯醚萜苷则几乎没有这些作用;总多糖和总环烯醚萜苷均能使肝损伤大鼠体内TNF-α、MCP-1、IL-6的含量降低,其中总环烯醚萜苷的降低作用更优。肝组织病理切片显示,总多糖和总环烯醚萜苷均一定程度减轻肝脏组织病理性改变,其中总多糖较总环烯醚萜苷作用更强。结论酒龙胆中总多糖、总环烯醚萜苷均对CCl4所致的大鼠急性肝损伤有一定保护作用,其中总多糖较总环烯醚萜苷作用更强。     

女贞子多糖的抗氧化活性研究

目的:研究女贞子多糖的抗脂质过氧化作用.方法:用D-半乳糖造衰老小鼠模型,观察女贞子多糖对衰老模型小鼠抗氧化系统的影响.结果:女贞子多糖均能使衰老模型小鼠肝、肾组织中MDA下降;SOD及GSH-PX活力提高;脑组织中LF下降.结论:女贞子多糖通过清除·OH,提高SOD及GSH-PX活力而发挥抗脂质过氧化作用.     

富硒枸杞抗肾脏衰老作用的形态学定量研究

目的:探讨富硒枸杞抗肾脏衰老的作用。方法:建立小鼠衰老模型,以10%富硒枸杞水煎剂连续灌胃42d,采用光镜,透射电镜,组织化学和B I2000图象分析系统对小鼠肾脏各项形态学指标进行定量分析。结果:富硒枸杞实验组肾小球形态大小,肾小球硬化率,肾组织内微血管指标,肾小球平均细胞数,肾小球基底膜厚度均较老年对照组有显著性差异(P<0.05或P<0.01)。结论:富硒枸杞具有较好的预防或延缓小鼠肾脏衰老的作用。     

Effect of chronic supplementation with methylsulfonylmethane on oxidative stress following acute exercise in untrained healthy men

Objective This study was conducted to assess the effects of chronic daily methylsulfonylmethane (MSM) supplementation on known markers of oxidative stress following acute bouts of exercise in untrained healthy young men. Methods Eighteen untrained men volunteered for this study. Participants were randomized in a double‐blind placebo‐controlled fashion into two groups: MSM (n = 9) and placebo (n = 9). The participants took supplementation or placebo daily for 10 days before running. Participants ran 14 km. The MSM supplementation was prepared in water at 50 mg/kg body weight. The placebo group received water. Serum malondialdehyde (MDA), protein carbonyl (PC) and plasma oxidized glutathione (GSSG) were measured as markers of oxidative stress. The plasma‐reduced glutathione (GSH) level and the GSH/GSSG ratio were determined as markers of plasma antioxidant capacity. Key Findings Acute exercise led to elevated levels of serum MDA, PC and plasma GSSG. MSM supplementation maintained PC, MDA and GSSG at lower levels after exercise than the placebo. The plasma level of GSH and the ratio of GSH/GSSG were significantly higher in the MSM supplemented group. Conclusions These results suggest that chronic daily oral supplementation of MSM has alleviating effects on known markers of oxidative stress following acute bouts of exercise in healthy young men.     

枸杞多糖对D-半乳糖致衰老小鼠肾脏的保护作用的研究

目的:观察枸杞多糖对D-半乳糖致衰老小鼠肾脏的保护作用,并探讨其延缓衰老作用的机理。方法:50只昆明系小鼠随机分为A、B、C、D、E 5组,B组小鼠每日颈背部皮下注射D-半乳糖(1m g/10g体重)建立衰老模型,C、D、E组注射等量的D-半乳糖同时分别以0.5m g/10g体重、1.0m g/10g体重、2.0m g/10g体重三个不同剂量灌服枸杞多糖,42天后取肾脏制备切片,用光镜、电镜观察其的形态变化;测定肾组织SOD的活性及M DA的含量。结果:B组小鼠肾小球形态大小、肾小球的基底膜厚度、内皮细胞窗口分布与A组相比有显著差异,C、D、E组较B组有所改善,E组肾小球无明显变化与A组相近。B组肾组织SOD活性显著低于正常(P<0.01),M DA含量显著高于正常(P<0.01),C、D、E组肾组织SOD活性较B组显著增高(P<0.01),且呈剂量依赖性;M DA含量与B组相比显著降低(P<0.01)。尤其是E组与A组无明显差异(P>0.05)。结论:枸杞多糖具有延缓肾脏衰老的作用,且随剂量的增加,保护作用也增强。其机制可能是通过增强细胞活力、提高体内的SOD活性、改善肾小球滤过屏障功能实现的。     

枸杞多糖防治大鼠酒精性脂肪肝的作用及机制研究

目的:研究枸杞多糖(LBP)对大鼠酒精性脂肪肝(AFL)的防治作用及机制。方法:治疗组大鼠用乙醇灌胃10wk复制慢性AFL模型,再用LBP治疗10wk,以戒酒组为阳性对照,作治疗前后比较;预防组用乙醇和LBP同时灌胃10wk,与模型组比较肝脏病理形态、丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、γ-谷氨酰基转移酶(γ-GT)、谷胱甘肽过氧化物酶(GSH-PX)、超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)、丙二醛(MDA)、肝细胞色素P_(450)2E1(CYP2E1)基因及蛋白表达。结果:LBP能抑制CYP2E1基因及蛋白表达,降低血清ALT、AST、γ-GT含量,提高GSH-PX、SOD活性,增加GSH含量,减少MDA产生,明显改善和预防酒精所致大鼠肝脏脂肪病变。结论:LBP可通过减轻脂质过氧化反应,有效地防治AFL。     

Influence of gender on oxidative stress, lipid peroxidation, protein damage and apoptosis in hearts and brains from spontaneously hypertensive rats

1. Hypertension leads to oxidative stress, lipid and protein damage, apoptosis and impaired cardiac contractile function. However, impact of gender on these hypertension-associated abnormalities has not been elucidated. 2. The present study evaluated the oxidative stress, lipid/protein damage, apoptosis in heart and brain tissues as well as cardiomyocyte contractile function in Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR) of both genders. Oxidative stress, lipid peroxidation, protein damage and apoptosis were assessed by glutathione (GSH) : reduced glutathione (GSSG) ratio, malondialdehyde (MDA) levels, protein carbonyl levels and caspase-3 activity, respectively. Cardiomyocyte contractile function was examined including peak shortening (PS), time-to-PS (TPS), time-to-90% relengthening (TR90) and maximal velocity of shortening/relengthening (+/-dL/dt). The SHR cardiomyocytes displayed reduced PS and +/-dL/dt compared with gender-matched WKY counterparts. Male but not female SHR cardiomyocytes possessed longer resting cell length, normal TPS and prolonged TR90. All mechanical parameters were comparable between male and female WKY rats with the exception of a higher TR90 in females. Hypertension did not significantly affect the GSH : GSSG ratio in the heart and brain tissues of either gender. Brain from female WKY rats displayed a reduced GSH : GSSG ratio. The MDA levels were unchanged and elevated, respectively, in SHR heart and SHR brain tissues from both genders. Protein carbonyl formation and caspase-3 activity were elevated in male but not female SHR hearts. Nonetheless, brain protein carbonyl level and caspase-3 activity were unaffected by hypertension or gender. 3. In summary, these results suggest that gender affects hypertension-associated oxidative stress, lipid and protein damage, apoptosis in heart and brain tissues and cardiomyocyte contractile function.     

盐酸戊乙奎醚对肺泡Ⅱ型上皮细胞氧化损伤的影响

目的 探讨盐酸戊乙奎醚对肺泡Ⅱ型上皮细胞氧化损伤的保护作用。方法 用过氧化氢（H2O2）加入A549 细胞培养液中制成 A549 细胞氧化损伤模型, 实验分为空白对照组（C 组）、 H2O2处理组（H 组）和盐酸戊乙奎醚-过氧化氢处理组 （P 组）。用 MTT 方法测 A549 细胞存活率, 用 TUNEL 方法测定细胞凋亡指数, 并测定细胞内的丙二醛（MDA）、 超氧化物歧化酶（SOD）、 还原型谷胱甘肽（GSH）、 烟酰胺腺嘌呤二核苷磷酸（NADPH）含量。结果 与 C 组比较, H 组的细胞存活率下降, 凋亡指数增加, MDA 含量上升, SOD、 GSH、 NADPH 的含量下降 （P＜0.05）。与H 组比较, P 组的细胞存活率增加, 凋亡指数下降, MDA 含量下降, SOD、 GSH、 NADPH 的含量增加（P＜0.05）。结论 盐酸戊乙奎醚对A549 细胞过氧化损伤具有保护作用。     

Changes in serum carbonyl and malondialdehyde levels following colchicine and vitamin E treatment in Behcet's disease

Behcet's disease (BD) is an inflammatory disorder of an unknown cause, but growing evidence indicates that the oxidative stress is increased in BD, owing to the overproduction of reactive oxygen species (ROS) and decreased efficiency of antioxidant defenses. ROS affect proteins and lipids and cause their oxidation, therefore, contributing to the formation of oxidation products: carbonyl, a marker of protein oxidation, and malondialdehyde (MDA), a marker of lipid peroxidation. The investigation was undertaken to evaluate protein oxidation (carbonyl group) levels and lipid peroxidation (MDA) levels, and the role of colchicine and vitamin E therapy on protein carbonyl group and MDA levels in serum samples of patients with BD. In this study, subjects were classified as control group, colchicine therapy group alone and colchicine and vitamin E therapy group. Protein carbonyl and MDA levels at the beginning of the study were significantly (p < 0.05) higher in both therapy groups compared with those of the control group. We found that the protein carbonyl and MDA levels at the end of the study showed no significant (p > 0.05) differences between the therapy groups and control group. These results provide some evidence for a potential effect of colchicine and vitamin E therapies on increased protein oxidation and lipid peroxidation in BD.     

Evaluation of oxidative stress markers after vaginal delivery or Caesarean section

BACKGROUND: The effects of vaginal delivery (VD) and of cesarean section (CS) on the markers of oxidative stress were investigated. MATERIALS AND METHODS: Umbilical blood samples were analyzed from 74 full-term neonates, 46 born via VD, 28 via elective CS. The level of lipid peroxidation (LP), protein and DNA damage and the antioxidant status were compared. RESULTS: Differences between CS and VD groups were generally non-significant for oxidative markers, except for the GSH concentrations (VD: 4.18 vs. CS: 2.77 microM/mg protein x 10(-3); p<0.05). LP was significantly higher in the CS group (0.078 vs. 0.042 nM MDA/mg protein; p <0.05). The level of carbonyl proteins was high in the VD group and significantly lower in the elective CS group (9.5 vs. 8.1 mM/mg protein x 10(-4); p<0.05). We found 0.78% more strand breaks in elective CS group than in VD group. CONCLUSION: CS does not have an advantage over VD with respect to oxidative stress.     

藏药三果汤调节Nrf2/HO-1信号通路干预高脂血症大鼠的作用机制研究

目的：基于Nrf2/HO-1信号通路探讨藏药三果汤对高脂血症大鼠保护作用及相关作用机制。方法：雄性SD大鼠48只,随机分为6组,即正常对照组、模型对照组、辛伐他汀组（3.5 mg/kg）,藏药三果汤低、中、高剂量组（0.43 g/kg、0.86 g/kg、1.72 g/kg）,每组8只。正常组给予基础饲料喂养,其余各组给予H00016高脂饲料喂养,制备高脂血症大鼠模型,造模的同时,各给药组每天一次给予相应药物灌胃,正常对照组、模型对照组给予等体积的生理盐水（1次/d）,连续灌胃6周。实验期间每周固定时间称取各组大鼠体重一次,6周后试剂盒检测血清中血脂（TC、TG、LDL与HDL）及氧化指标（MAD、SOD与GSH）的水平。Western Blot法测定肝组织中Nrf2、HO-1、Keap1、NQO1蛋白表达,采用person相关性分析分析血脂与氧化指标之间的相关性。结果：与正常对照组比较,模型对照组的体重明显增加,血清中的TC、TG、LDL、MDA含量明显升高,而血清中HDL含量明显减低,SOD、GSH活力明显减低（P<0.05或P<0.01）;与模型对照组比较,各给药组的体重减轻,血清中的TC、TG、LDL、MDA含量明显减低,血清中的HDL含量明显升高,SOD、GSH活力明显升高（P<0.05或P<0.01）。与空白对照组比较,模型对照组Keap1蛋白水平表达明显上调,Nrf2、HO-1与NQO1蛋白水平表达明显下调（P<0.05或P<0.01）,与模型对照组比较,三果汤低、高剂量肝组织中的Keap1蛋白水平表达明显下调,Nrf2、HO-1与NQO1蛋白水平表达明显上调（P<0.05或P<0.01）。相关性分析可见TG与SOD、HO-1及NQO1呈负相关,与Keap1呈正相关,TC与SOD、HO-1、GSH及Nrf2呈负相关,与Keap1及MDA呈正相关。结论：藏药三果汤可改善高脂血症大鼠体重及血脂水平,其机制可能与调节Nrf2/HO-1信号通路,改善氧化应激有关。     

Protective effects of N-acetylcysteine on triamcinolone acetonide-induced lens damage in rats

Objective: To examine the relationship of cataract forming effect of intravitreal triamcinolone acetonide (IVTA) injection with oxidative status and the effect of N-acetylcysteine (NAC) on these alterations.

Materials and methods: Twenty-six Wistar-Albino rats were included in the study. Rats were assigned into four groups as follows: intravitreal saline injection group (controls); IVTA injection group; IVTA?+?intraperitoneal NAC injection group (IVTA?+?NAC); and intraperitoneal NAC injection group (NAC). Triamcinolone acetonide was intravitreally injected at a dose of 1?mg. NAC was intraperitoneally injected at a dose of 150?µg/g body weight. Animals were sacrificed and lens specimens were analyzed for levels of malondialdehyde (MDA) and protein carbonyl (PC) and activities of glutathione (GSH) and glutathione peroxidase (GSH-Px).

Results: We found that the MDA and PC levels of lenses were increased in the IVTA group (p?p?p?Conclusion: These results indicate that the NAC produces a protective mechanism against IVTA-induced cataract and suggest a role of oxidative stress in pathogenesis.