人参茎叶总皂甙抗皮肤抗衰老作用的研究

目的:观察人参茎叶总皂甙口服对皮肤的抗衰老作用。方法:小鼠颈背部皮下每日注射D2半乳糖(1000mg/kg)造成衰老模型,同时灌胃50mg/kg·d21和100mg/kg·d21的人参茎叶总皂甙,42天后,测定全血中的过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH2Px)活力;测定皮肤组织匀浆中的羟脯氨酸、超氧化物歧化酶(SOD)和丙二醛(MDA)含量。结果:100mg/kg·d21人参茎叶总皂甙使衰老小鼠全血中CAT和GSH2Px活力显著升高,皮肤组织匀浆中SOD活力显著升高,MDA含量降低;50mg/kg·d21和100mg/kg·d21人参茎叶总皂甙均使衰老小鼠皮肤组织中羟脯氨酸含量升高,且…     

褪黑素对衰老小鼠脑组织NO和氧自由基生成的作用

观察褪黑素对D 半乳糖衰老模型小鼠NO生成和氧自由基的作用以探讨其抗衰老机制。D 半乳糖诱导昆明小鼠衰老同时每日腹腔注射外源性褪黑素 (5mg kg)连续 8周 ,测定小鼠不同脑区NO、NOS、SOD、MDA、脂褐素的变化。模型组NO、NOS、MDA 脂褐素水平明显升高 (P <0 0 1;P <0 0 1;P <0 0 1;P <0 0 5 ) ,SOD活性明显减弱 (P <0 0 1) ,给药 (D +MT)组则上述变化逆转。褪黑素抑制NO的过度生成及减轻脂质过氧化损伤是其抗衰老机制之一     

人参皂苷对衰老小鼠皮肤和人角质形成细胞的抗衰老研究

目的:观察人参皂苷在体内和体外抗皮肤衰老的作用。在体外实验中,观察HaCaT细胞在不同剂量的中波紫外线(UVB)照射下的存活率、损伤情况,并探讨人参皂苷Rg1Rb1对人角质形成细胞(HaCaT)的保护作用;在体内实验中,观察人参茎叶总皂甙口服对小鼠皮肤的抗衰老作用。方法:采用MTT法分析剂量为30,60,90,120mJ.cm2的UVB照射后细胞存活率的变化,用Hoechst33258核染色法和单个细胞凝胶电泳(彗星电泳)技术观察细胞核的损伤情况以及20μg.ml-1人参皂苷Rg1、Rb的保护作用。小鼠被随机分为四组:正常对照组;D-半乳糖衰老模型组;人参茎叶总皂甙低剂…     

人参茎叶总皂苷对衰老皮肤胶原纤维和弹力纤维的保护作用

目的:观察人参茎叶总皂苷口服对衰老皮肤弹力纤维和胶原纤维的作用。方法:小鼠颈背部皮下每日注射D-半乳糖(1000 mg.kg-1)造成衰老模型,同时灌胃50 mg.kg-1和100 mg.kg-1的人参茎叶总皂苷,42天后处死,10%甲醛固定。观察衰老皮肤胶原纤维和弹力纤维的改变。结果:50 mg.kg-1和100 mg.kg-1人参茎叶总皂苷使衰老小鼠皮肤中胶原纤维和弹力纤维的含量增加,100 mg.kg-1人参茎叶总皂苷作用更显著。结论:50 mg.kg-1和100 mg.kg-1人参茎叶总皂苷均对衰老皮肤的胶原纤维和弹力纤维有保护作用。     

白藜芦醇对D-半乳糖诱导的亚急性衰老小鼠海马神经元的保护作用

目的 探讨白藜芦醇对亚急性衰老小鼠海马神经细胞的保护作用.方法 D-半乳糖颈背部皮下注射制备亚急性衰老小鼠模型,设正常对照组、对照组、高低剂量处理组和阳性对照组.第3周始,处理组分别给予白藜芦醇15、45mg/kg(低、高剂量)灌胃,对照组给予生理盐水或DMSO溶液灌胃.8周后,检测小鼠血清、脑组织中超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量.制作石蜡切片,尼氏染色观察小鼠海马CA1区形态结构,免疫组化检测P53蛋白表达,TUNEL法检测细胞凋亡.结果 各组小鼠海马组织形态结构无明显变化;与对照组相比,白藜芦醇45 mg/kg体重组小鼠血清和脑组织中SOD活性明显升高,MDA含量明显下降;白藜芦醇45 mg/kg体重组小鼠海马CA1区P53蛋白表达阳性细胞较对照组小鼠减少,但各组均无明显的凋亡细胞.结论 白藜芦醇能增强亚急性衰老小鼠的抗氧化功能,降低亚急性衰老小鼠海马CA1区神经元P53蛋白的表达.     

衰老模型小鼠胰腺结构与功能的变化

目的探讨D-半乳糖(D-gal)致衰小鼠胰腺结构与功能变化。方法 2月龄雄性C57BL/6J小鼠随机分为两组,每组10只。衰老组:小鼠皮下注射D-gal(120mg/kg),每天1次,共42 d;对照组:小鼠皮下注射等时与等量生理盐水。衰老模型建立完成第2天,采外周血测定空腹血糖(FBG)与空腹胰岛素(FINS)水平;称小鼠体重(g)与胰腺湿重(mg)计算胰腺脏器指数;石蜡切片,HE染色观察胰腺光学显微镜下形态;制备胰腺冷冻切片,检测衰老相关β-半乳糖苷酶(SA-β-Gal)染色阳性胰腺细胞的相对吸光度(RA);免疫组织化学法观察胰腺组织晚期糖基化终产物(AGEs)的RA;制备胰腺组织匀浆检测超氧化物歧化酶(SOD)、总抗氧化能力(T-AOC)和丙二醛(MDA)的含量。结果衰老组小鼠FBG显著升高,FINS水平降低;胰腺湿重和胰腺脏器指数明显升高;胰腺光学显微镜下结构未见显著改变,但胰岛内单个有核细胞所占面积增加;胰腺SA-β-Gal染色阳性细胞数显著增加;AGEs阳性表达区域RA值明显升高;SOD与T-AOC含量显著降低,MDA含量显著升高。结论 D-gal复制衰老小鼠可致其胰腺损伤,其机制与D-gal致胰腺组织细胞的氧化应激损伤有密切关系。     

墨旱莲对D-半乳糖所致衰老模型小鼠体内自由基和免疫功能影响的实验研究

目的 观察旱莲草对衰老模型小鼠体内自由基和免疫功能的影响.方法 小鼠颈背部皮下注射D-半乳糖建立亚急性衰老模型,同时旱莲草高、中、低剂量保护组灌服旱莲草口服液.检测各组小鼠全血超氧化物歧化酶(SOD)、丙二醛(MDA)、血清白细胞介素-2(IL-2)水平和脾脏指数.并取脾脏光镜切片,H-E染色,现察组织学变化对照.结果 模型小鼠全血SOD、血清IL-2水平以及脾脏指数均显著性降低,而血清MDA水平显著性升高(均P＜0.05);旱莲草高、中、低剂量组均可不同程度地升高SOD、IL-2水平及脾脏指数,降低MDA水平(P＜0.05或P＜0.01).结论 墨旱莲口服液能明显减轻衰老模型小鼠免疫器官的萎缩,可能与其能清除自由基、提高机体免疫功能有关.     

当归多糖对D-半乳糖致衰老小鼠睾丸的保护作用

目的探讨当归多糖(ASP)对D-半乳糖(D-Gal)所致衰老小鼠睾丸的保护作用与机制。方法C57BL/6 J雄性小鼠40只,随机分为对照组、ASP对照组、衰老模型组ASP衰老模型组,每组10只。衰老模型组:小鼠颈背部皮下注射D-Gal(120 mg/kg,qd×42);对照组小鼠皮下注射等时与等量生理盐水; ASP对照组小鼠皮下注射等量生理盐水15 d,第16天开始腹腔注射ASP(140 mg/kg,qd×27); ASP衰老模型组小鼠建立方法同衰老模型组小鼠,第16天开始腹腔注射ASP(同ASP对照组)。模型复制完成第2天,采集各组小鼠内眦静脉血测定血清睾酮水平;取睾丸测定脏器指数;石蜡切片,HE染色观察睾丸组织学形态;做冷冻睾丸组织切片,衰老相关β-半乳糖苷酶(SA-β-Gal)染色观察睾丸组织细胞衰老情况;制备睾丸组织匀浆上清液,酶学法检测超氧化物歧化酶(SOD)活性,2,2’-连氮基-双-(3-乙基苯并二氢噻唑啉-6-磺酸)二铵盐(ABTS)法检测总抗氧化能力(T-AOC),硫代巴比妥酸法检测丙二醛(MDA)含量; Western blotting检测衰老相关蛋白P53、P21表达水平。结果各组间睾丸湿重及睾丸器官指数无明显差异,但衰老模型组小鼠睾丸组织结构损伤明显,生精小管的细胞层数减少,生精细胞出现退变,睾丸间质细胞明显减少;血清睾酮水平显著降低; SA-β-Gal染色阳性细胞密度显著增加;睾丸组织匀浆中SOD活性及T-AOC显著降低,MDA含量显著升高; P53、P21蛋白表达显著升高。与衰老模型组比较,注射ASP干预衰老过程,睾丸组织学结构损伤明显减轻,生精细胞退变与睾丸间质细胞减少均不明显;血清睾酮水平降低不明显; SA-β-Gal染色阳性细胞密度减少; SOD活性和T-AOC增高,MDA含量降低; P53、P21蛋白表达显著降低。结论 ASP具有拮抗致衰剂Dgal对睾丸的损伤作用,其机制可能与ASP抑制氧化应激损伤及抑制衰老相关基因表达有关。     

油橄榄叶提取物干预海洛因依赖小鼠认知和氧化损伤及细胞凋亡的变化（英文）

目的探讨油橄榄叶提取物(OLE)对海洛因依赖小鼠认知和氧化损伤及细胞凋亡的影响。方法 150只小鼠皮下注射海洛因(10 mg/kg)40 d,再分别给予不同剂量的(0、50、100、200 mg/kg)的OLE进行皮下注射治疗,用Morris水迷宫观察空间学习记忆能力的变化,用透射电子显微镜观察海马细胞结构的改变,用比色法检测小鼠海马超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化酶(GPx)、还原型谷胱甘肽(GSH)的活性及丙二醛(MDA)的含量,免疫组织化学和Western blotting检测海马Bax蛋白和Caspase-3的表达。结果模型组小鼠海马神经元核膜不规则,细胞器结构异常或空泡化,小鼠逃避潜伏期和逃避的距离高于正常组,在目标象限探索的时间及游泳距离占总距离的百分比低于正常组(P0.01),海马组织SOD、CAT、GPx、GSH活性低于正常组,MDA含量高于正常组(P0.01),海马组织Bax蛋白和caspase-3的表达高于正常组(P0.01)。OLE治疗组小鼠海马神经元损害程度减轻,小鼠逃避潜伏期和逃避的距离缩短,在目标象限探索的时间及游泳距离占总距离的百分比延长,海马组织SOD、CAT、GPx、GSH活性又升高,MDA含量及Bax蛋白和Caspase-3的表达又显著降低(P0.05或P0.01)。结论 OLE对海洛因诱导的脑损伤的神经保护与其具有抗氧化能力。抑制细胞凋亡的特性有一定的关系。     

木材锯末与谷壳烟雾致豚鼠肺部炎性反应和氧化-抗氧化失衡

目的 探讨木材锯末和谷壳烟雾致豚鼠肺部的异常炎性反应及氧化损伤作用.方法 20只白化豚鼠随机分为两组,每组10只.实验组每天暴露于木材锯末和谷壳燃烧所产生的烟雾中两次,每次30 min,共21 d;对照组暴露于新鲜空气.3周后进行肺组织病理检测,并检测肺组织匀浆中的谷胱甘肽过氧化物酶(GSH-PX)、还原型谷胱甘肽(GSH)、丙二醛(MDA)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、总抗氧化能力及肺泡灌洗液(BALF)中的MDA、SOD、总抗氧化能力、白细胞介素8(IL-8)、IL-6、细胞问黏附分子1(ICAM-1)的活力或含量.结果 与对照组豚鼠比较,实验组肺实质、小动脉及支气管炎性细胞浸润明显增多;肺泡面积比例及平均肺泡面积明显增大;单位而积肺泡数明显减少[(134.11±18.22)个/视野比(178.76±21.72)个/视野,P<0.01];肺小动脉及支气管平滑肌层显著增厚.肺组织匀浆中SOD、GSH-PX、GSH、CAT、总抗氧化能力的活力或含量降低[(225.55±12.52)U/mg比(296.57±13.46)U/mg,(23.60±1.85)mg/g比(34.38±1.85)mg/g,(119.67±9.61)mg/g比(134.73±8.07)mg/g,(7.10±0.21)U/mg比(9.20±0.24)U/mg,(0.89±0.10)U/mg比(1.27±0.15)U/mg,P均<0.01];MDA的含苗显著升高[(3.05±0.38)U/mg比(2.09±0.17)U/mg,P<0.01].BALF中,SOD、总抗氧化能力的活力显著降低;MDA的含量显著升高;BALF中IL-6、IL-8、ICAM-1浓度增高.结论 木材锯末与谷壳烟雾可导敛豚鼠肺组织及气道氧化-抗氧化失衡,引起氧化损伤.     

A Study of Lycium Barbarum Polysaccharides (LBP) Extraction Technology and Its Anti-Aging Effect

The objective of the study was to optimise the LBP extraction technology and to study the anti-aging effect of LBP by establishing D-gal aging mouse model. Orthogonal design was used to study the extraction technology. The experimental aging mouse model was formed by continuous injection of D-gal, and the anti-aging capacity of LBP was tested using measuring MDA, CAT and GSH-px contents and SOD activity in blood and SOD, MDA and Hyp levels in skin. The results showed that the optimum LBP extraction option determined by the orthogonal design is as follows: solid-liquid ratio of 1:30, extraction for 2 times, 90 min each time, and power is 100 kHz. Thus, LBP can increase SOD, CAT and GSH-px levels in blood and reduce MDA level. It can also improve skin SOD activity, reduce skin MDA content, and increase Hyp content. We concluded that the extraction method established in this experiment is easy and feasible, and the yield of LBP is high, apparently showing that LBP has the potential of delaying senility in D-gal induced mice.     

Antihyperglycemic, antihyperlipidemic and antioxidant activities of traditional aqueous extract of Zygophyllum album in streptozotocin diabetic mice

Objective: The aim of this work was to investigate the antihyperglycemic, antioxidant and antihyperlipidemic effects of the aqueous extract of Zygophyllum album on streptozotocin (STZ)-induced diabetic mice. Methods: Diabetes was induced in Swiss albino mice by the administration of STZ (45mg/kg b.w.) intraperitoneally. Aqueous extract of Z. album (100 and 300mg/kg b.w.) was administered by oral gavage once a day for a period of 15days. The effect of the extract on blood glucose, lipids, cholesterol levels in plasma, and also on enzymatic and non enzymatic antioxidants of defence systems such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) enzyme activities, and vitamin C, vitamin E and glutathione reductase (GSH) levels in liver and pancreas were studied. Results: Our results showed that Z. album extract reduced the blood glucose, total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) levels in STZ-diabetic mice. It also significantly abolished the increase in MDA level, and GPx, SOD and CAT activities in both liver and pancreas. The levels of GSH, vitamin C and high-density lipoprotein (HDL) were significantly augmented in Z. album treated diabetic mice in comparison with control group. Our findings suggest that Z. album aqueous extract prevented the diabetic induced MDA levels via the enhancement of the tissue GSH and blood vitamin C levels. Conclusions: These results suggest that Z. album extract exerts the anti-diabetic and antihypercholesterolemic activities through its antioxidant properties.     

对氧磷酶3基因过表达对急性中毒小鼠肝损伤的保护作用及机制

目的 探讨对氧磷酶3（PON3）对急性中毒肝损伤的保护作用及作用机制。 方法 将40只Balb/c小鼠随机分为4组,正常对照（NC）组、敌敌畏（DDVT）对照组、绿色荧光蛋白慢病毒（Lv-GFP）组和重组PON3慢病毒（Lv-PON3）组,每组10只。LV-GFP组和Lv-PON3组小鼠经尾静脉分别注射2×10⁷ TU的Lv-GFP、Lv-PON3慢病毒,3 d后腹腔注射敌敌畏（DDVT）溶液9 mg/kg,DDVT组只需腹腔注射同等剂量DDVT,NC组注射同等剂量生理盐水。各组于DDVT染毒后12 h麻醉处死10只小鼠取肝组织,ELISA法检测各组血清乙酰胆碱酯酶（AChE）、肝功能指标谷丙转氨酶（ALT）和谷草转氨酶（AST）和肝组织氧化应激指标丙二醛（MDA）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和谷胱甘肽（GSH）,HE染色法观察肝组织形态学改变,Real-time PCR检测肝组织Kelch样环氧氯丙烷相关蛋白-1（Keap1）、血红蛋白加氧酶（HO-1）和转录因子NF-E2相关因子2（Nrf2） mRNA的表达。 结果 与NC组比较,DDVT组和Lv-GFP组肝组织MDA、ALT、AST水平,HO-1和Nrf2 mRNA表达量明显升高,AChE、CAT、SOD、GSH水平和Keap1 mRNA表达量均明显降低（P<0.05）。与DDVT组比较,Lv-PON3组肝组织MDA、ALT、AST水平,Keap1 mRNA表达量降低,AChE、CAT、SOD和GSH水平均明显著升高,HO-1和Nrf2 mRNA表达量显著上升（P<0.05）。正常对照组肝细胞结构清晰,未出现肝细胞坏死和脂肪病变的情况,DDVT组和Lv-GFP组出现肝细胞坏死和脂肪变性等病理改变,Lv-PON3组肝脏病变组织肝细胞坏死和脂肪变性细胞数有一定的减少。 结论 PON3可通过Keap1-Nrf2/HO-1途径缓解氧化应激反应,改善肝功能,对敌敌畏急性中毒小鼠肝损伤有一定的保护作用。     

高压氧与环孢素A对皮肤移植小鼠脾活性氧及一氧化氮含量的影响

目的:探讨高压氧与环孢素A对皮肤移植小鼠脾中活性氧、一氧化氮含量的影响。方法:供鼠BALB/C,受鼠C⁵⁷BL/6,皮肤移植,环孢素A组每日腹腔注射CsA5mg/kg,高压氧(HBO)组每日用99.2%氧气0.25MPa作用1.5h,14d后,取脾称重,测脾中丙二醛(MDA)的含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)、过氧化氢酶(CAT)的活性和一氧化氮(NO)的含量,一氧化氮合酶(NOS)的活性。结果:(1)移植组、高压氧组和环孢素A组的MDA含量,GSH-PX、CAT的活性均高于对照组;环孢素A组GSH-PX、CAT活性低于、SOD的活性高于移植组;高压氧组GSH-PX活性低于、CAT和SOD活性高于移植组(P<0.01)。(2)移植组的NOS活性及NO含量高于对照组;高压氧组的NO含量低于、NOS活性高于移植组(P<0.01);环孢素A组的NO含量、NOS活性变化无显著意义。结论:皮肤移植小鼠脾细胞过氧化增强,NO含量及NOS活性增高;高压氧与环孢素A对上述二个系统具有一定作用,这可能与其抑制排斥反应有关。     

Efficacy of melatonin as protectant against oxidative stress and structural changes in liver tissue in pinealectomized rats

Previous observations demonstrated that physiological levels of melatonin, the pineal secretory product, are important in protecting against oxidative stress-induced tissue damage. We investigated the effects of pinealectomy and administration of exogenous melatonin on liver tissue in rats. Pinealectomized (Px) and sham-operated (non-Px) rats were used. We evaluated structural changes, reduced glutathione (GSH) levels and malondialdehyde (MDA) levels. Rats were divided into three groups (10 rats in each group): control (non-Px), Px+vehicle and Px+melatonin (4 mg/kg given daily intraperitoneally for 10 days). Liver GSH levels were significantly lower in Px rats than in the control group. Melatonin administration significantly increased GSH levels (p < 0.05). Px caused a significant increase in MDA levels as compared with the control group and melatonin administration to Px rats significantly reduced MDA levels in the liver (p < 0.05). Sinusoidal dilatation to a varying degree developed in all Px rats. Severity of mononuclear cell infiltration and sinusoidal congestion were lower in Px+melatonin group than in the Px group. These findings suggest that a significant increase in oxidative and structural changes occur in rat livers after pinealectomy, which can be diminished by melatonin treatment.     

配比油对家兔体内抗氧化酶类活性的影响

观察不同配比n-3,n-6系脂肪酸的配比油对家兔体内几种抗氧化酶活性的影响，实验用家兔，共50只随机分为5组。对照组喂饲基础饲料，高脂组喂饲富含猪油和胆固醇（Ch)的饲料，配比油组（配比1组。配比2组，配比3组）喂饲的饲料中除了猪油和胆固醇外，还有不同配比n-3,n-6系脂肪酸的配比油，实验三个月中每间隔一个月耳缘静脉取血一次，检测各组家兔红细胞中超氧化物歧化酶（SOD）。过氧化氢酶（CAT），谷胱甘肽过氧化物酶9GSH-Px)。活性的变化，结果表明配比油使SOD，CAT活性均明显增强，但不同油脂对GSH-Px活性的影响较复杂，说明不同配比n-3,n-6系脂肪酸的混合油均可增强抗氧化系统酶活性，其增强作用与不同配比剂量密切相关。     

Effect of Methylsulfonylmethane on Paraquat-Induced Acute Lung and Liver Injury in Mice

Methylsulfonylmethane (MSM) is a natural organosulfur compound that exhibits antioxidative and anti-inflammatory effects. This study was carried out to investigate the effect of MSM on paraquat (PQ)-induced acute lung and liver injury in mice. A single dose of PQ (50 mg/kg, i.p.) induced acute lung and liver toxicity. Mice were treated with MSM (500 mg/kg/day, i.p.) for 5 days. At the end of the experiment, animals were euthanized, and lung and liver tissues were collected for histological and biochemical analysis. Tissue samples were used to determine malondialdehyde (MDA), myeloperoxidase (MPO), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH), and tumor necrosis factor-α (TNF-α) levels. Blood samples were used to measure plasma alanine transaminase (ALT), γ-glutamyl transferase (GGT), and alkaline phosphatase (ALP). Histological examination indicated that MSM decreased lung and liver damage caused by PQ. Biochemical results showed that MSM treatment significantly reduced tissue levels of MDA, MPO, and TNF-α, while increased the levels of SOD, CAT, and GSH compared with PQ group. MSM treatment also significantly reduced plasma levels of ALT, GGT, and ALP. These findings suggest that MSM as a natural product attenuates PQ-induced pulmonary and hepatic oxidative injury.     

D-半乳糖致衰老小鼠胸腺T细胞重要膜型分子的改变及其意义

目的:建立D-半乳糖亚急性衰老小鼠模型,并探讨其胸腺T细胞重要膜型分子的改变及其意义。方法:8周龄雌性昆明种小鼠,12.5 mL/(kg.d)颈后部皮下注射100 g/LD-半乳糖溶液,连续注射42 d;逐日观察小鼠的生存状态和行为变化,并通过对小鼠血清中SOD活力和MDA含量的检测,对此衰老模型进行生物学鉴定;在D-半乳糖亚急性衰老小鼠模型成功建立的基础上,采用免疫荧光标记技术和流式细胞仪检测技术对胸腺T细胞重要膜型分子进行检测分析。结果:造模过程中小鼠逐渐表现出脊椎隆起,体形消瘦,皮肤松弛等衰老体征;血清中SOD活力下降[模型组:(2.16±0.43)mKat/L,对照组:(5.52±1.55)mKat/L,P<0.01],MDA含量上升[模型组:(4.14±0.82)μmol/L,对照组:(1.24±0.21)μmol/L,P<0.01];小鼠胸腺初始T细胞相关分子CD45RA表达下降[模型组:(2.16±0.47)%,对照组:(2.98±0.53)%,P<0.05];小鼠胸腺T细胞活化相关分子CD28[模型组:(91.52±1.68)%,对照组:(95.12±1.21)%,P<0.05]和CD25[模型组:(7.42±0.75)%,对照组:(8.84±0.58)%,P<0.05]表达下降;小鼠胸腺T细胞活化负性调控分子PD-1表达上升[模型组:(21.25±1.95)%,对照组:(12.92±3.28)%,P<0.01];小鼠胸腺记忆T细胞相关分子CD196表达上升,但与对照组相比没有显著性差异[模型组:(21.13±1.44)%,对照组:(19.73±2.02)%]。结论:成功建立了D-半乳糖亚急性衰老小鼠模型,机体衰老时胸腺中初始和活化T细胞减少,记忆T细胞有增加的趋势。     

Antioxidant Status and Oxidative Stress in Patients with Chronic ITP

The aim of this study was to establish the antioxidant status and oxidative stress in adult patients with chronic idiopathic thrombocytopenic purpura (ITP). Eighty‐four patients diagnosed with chronic ITP were studied. Fifty‐eight age‐matched healthy subjects were selected as controls. Serum nitrogen monoxide ( NO), oxidized glutathione (GSSG), malondialdehyde (MDA), total antioxidant status (TAS), total oxidant status (TOS), superoxide dismutase(SOD), hydrogen peroxide enzyme (CAT), glutathione peroxidase (GSH‐Px), glutathione (GSH) were evaluated by enzyme‐linked immunosorbent assay (ELISA). It was found that serum SOD, CAT, GSH‐Px, GSH, TAS levels were significantly lower in patients with chronic ITP than controls (all P < 0.05), while serum NO, GSSG, MDA, TOS values were significantly higher (P < 0.05). The number of platelet showed a negative correlation with NO, GSSG, MDA, TOS, respectively,while platelet number showed a positive correlation with SOD, CAT, GSH‐Px, GSH, TAS. These findings suggested that oxidants were increased and antioxidants were decreased in patients with chronic ITP, these may be prominent factors in destructing the platelet membrane. The scavenging of oxygen radical provides a theoretical basis for the treatment of ITP patients.