神经干细胞衰老与核因子E2相关因子2/抗氧化反应元件信号通路的关系

目的 建立D-半乳糖（D-gal）诱导小鼠神经干细胞（NSCs）体外衰老模型,探讨NSCs衰老与细胞核因子E2相关因子2（Nrf2）/抗氧化反应元件（ARE）信号通路的关系。方法 取新生C57BL/6J小鼠全脑,分离、鉴定NSCs,培养至第3代,随机分为对照组和衰老组。对照组细胞在NSCs培养基中常规培养48 h,衰老组细胞在对照组基础上加入D-gal（终浓度为10 g/L）。细胞计数试剂盒8（CCK-8）法检测NSCs增殖活力;衰老相关β-半乳糖苷酶（SA-β-gal）染色检测衰老阳性神经球百分率;锥虫蓝染色检测细胞存活率;酶标比色法检测细胞培养上清液中超氧化物歧化酶（SOD）与过氧化氢酶（CAT）活性和丙二醛（MDA）含量;Western boltting检测NSCs中Nrf2和血红素加氧酶 1（HO-1）蛋白表达水平;Real-time PCR检测GCLC和GCLM基因表达水平。结果 与对照组相比,衰老组NSCs增殖活力明显下降,锥虫蓝染色显示,NSCs存活率下降明显,S-β-gal染色阳性神经球百分率显著上升,SOD活性与CAT活性均显著降低,MDA含量显著升高,NSCs中Nrf2/ARE信号通路相关蛋白Nrf2和HO-1表达水平显著下调,通路相关GCLC和GCLM基因表达下调。结论 采用D-gal可以构建NSCs体外衰老模型,其氧化损伤机制可能与抑制Nrf2/ARE抗氧化信号通路有关。     

人参茎叶总皂苷对衰老小鼠的作用研究

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D 半乳糖 ( 1 0 0 0mg/kg)造成衰老模型 ,同时灌胃 5 0mg/kg .d 1和 1 0 0mg/kg .d 1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 (GSH Px)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 :1 0 0mg/kg .d 1人参茎叶总皂甙使衰老小鼠全血中CAT和GSH Px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 ;5 0mg/kg .d 1和 1 0 0mg/kg .d 1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 ,且与衰老模型组比较有显著性差异。结论 :人参茎叶总皂甙口服对D 半乳糖致诱导的小鼠皮肤衰老具有抗衰老作用     

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。     

D-半乳糖致小鼠胰腺损伤

目的探讨D-半乳糖(D-gal)对小鼠胰腺的损伤及其机制。方法 C57BL/6J小鼠随机分为对照组和D-gal组(D-gal 120 mg/kg,qd×42 d)。注射完成第2天,采外周血测定空腹血糖(FBG)与空腹胰岛素(FINS)水平;称小鼠体质量(g)与胰腺湿重(mg)计算胰腺脏器指数;HE染色观察胰腺组织形态学;透射电镜观察胰腺细胞超微结构;制备冷冻切片,衰老相关β-半乳糖苷酶(SA-β-gal)染色检测胰岛内染色阳性细胞的相对吸光度(RA)值;免疫组织化学法观察胰腺组织晚期糖基化终产物(AGEs)的RA值;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)含量。结果 D-gal组小鼠FBG显著升高(P0.05),FINS水平降低;胰腺湿重和胰腺脏器指数明显升高(P0.01);胰腺光镜结构无显著损伤,但胰岛内单个有核细胞所占面积增加(P0.05);胰腺内外分泌部显示细胞超微结构损伤,脂褐素明显沉积;胰腺SA-β-gal染色阳性细胞的RA值增加(P0.05);AGEs阳性表达区域RA值升高(P0.01);SOD与T-AOC含量降低(P0.05),MDA含量升高(P0.01)。结论 D-gal复制衰老小鼠模型可致胰腺损伤,发生机制可能与D-gal致胰腺细胞氧化应激损伤有关。     

褪黑激素对中老年大鼠大脑皮质MDA含量和GSH-px、Ca~(2+)-ATPase活性的影响

目的 观察褪黑激素对中老年大鼠大脑皮质脂质过氧化产物含量和氧自由基、游离钙离子清除剂活性的影响,探讨其抗氧化、抗衰老作用机理.方法 连续30天给中、老年大鼠补充褪黑激素,用生化比色法,测定大脑皮质丙二醛(MDA)含量和谷胱甘肽过氧化物酶(GSH-px)、钙离子-三磷酸腺苷酶(Ca~(2+)-ATPase)活性.结果 与对照组比较,实验组大鼠大脑皮质MDA含量下降了26.8%,GSH-px和Ca~(2+)-ATPase活性增加了27.5%和12.5%.结论 褪黑激素能增强大脑皮质对氧自由基和细胞内钙离子的清除能力,对抗神经细胞过氧化和延缓神经组织衰老具有一定的作用.     

β-淀粉样蛋白对D-半乳糖致衰大鼠行为及海马SOD活性和MDA含量的影响

目的: 探讨β-淀粉样蛋白(β-AP)和D-半乳糖(D-gal)对大鼠学习记忆及海马SOD活性和MDA含量的影响。方法: 检测各组大鼠学习记忆行为,包括开场行为、Y-迷宫分辨学习和一次被动回避反应,并测定海马中SOD活性和MDA含量。结果: D 组、D+A组大鼠在新异环境中自发活动和探究行为减少,学习记忆减退;同时海马SOD活性降低、MDA含量明显增加,与N组比较有显著性差异(P＜0.05,P＜0.01)。结论: β-AP和D-gal两者联合可导致大鼠海马内自由基损伤效应加重,学习记忆能力显著减弱。     

Treatment of D-Galactose Induced Mouse Aging with Lycium Barbarum Polysaccharides and Its Mechanism Study

We evaluated the effects of Lycium barbarum polysaccharides LBP) on D-galactose aging model mouse, and explored its possible mechanism. Kunming mice were randomly divided into the control group, the model group, the high-dose LBP group, and the low-dose LBP group. Except the control group, D-galactose was used for modelling. The drug was administrated when modelling. Mouse behavioural, learning and memory changes were observed, and the contents of lipid peroxidation (LPO), lipofuscin (LF) and monoamine oxidase B (MAO-B) in mouse brain tissue and the weight of immune organs were measured after 6 weeks. Compared with the control group, mouse weight gain in the model group reduced significantly. Compared with model group, after mice drank LBP, the times of electric shock was less than aging mice (in which, the high-dose LBP group, P<0.05), and electric shock incubation period was longer (P<0.01). On Day 45 after modelling and drug administration, the contents of LPO, LF and MAO-B in mouse brain tissue in the model group increased significantly, while those in the drug administration groups decreased significantly. The thymus index in the aging model group decreased significantly; the thymus index and the spleen index in the high-dose LBP group and the low-dose LBP group rebounded significantly (P<0.01). We concluded that LBP has an anti-aging effect on D-galactose induced aging model mouse, and its mechanism may be related with the alleviation of glucose metabolism disorder and the resistance of the generation of lipid peroxide and other substances, which damage cell membrane lipid.     

改构型酸性成纤维细胞生长因子对衰老模型大鼠自由基与脂质过氧化物的影响

背景：有研究表明改构型酸性成纤维细胞生长因子是多功能生长因子,但其抗衰老作用至今尚未见报道。 目的：观察改构型酸性成纤维细胞生长因子对D-半乳糖致衰老大鼠脑组织、肝组织及血清中超氧化物歧化酶活力、丙二醛含量和抑制羟自由基能力的影响。 方法：选择成年Wistar大鼠皮下注射D-半乳糖建立衰老模型,建模成功后随机分为模型组、生理盐水对照组和改构型酸性成纤维细胞生长因子治疗组,另设正常对照组。改构型酸性成纤维细胞生长因子组按12 µg/kg剂量肌肉注射改构型酸性成纤维细胞生长因子,生理盐水对照组肌肉注射等量的生理盐水,模型组不作干预。 结果与结论：与模型组和生理盐水对照组相比,改构型酸性成纤维细胞生长因子治疗组脑组织、肝组织及血清中超氧化物歧化酶活力和抑制羟自由基能力均显著升高(P < 0.01或P < 0.05),丙二醛含量均显著降低(P < 0.01或P < 0.05)。结果证实,改构型酸性成纤维细胞生长因子可通过降低自由基,提高机体的抗氧化能力来发挥延缓衰老的作用。     

铜,锌对培养心肌细胞缺氧／再给氧损伤的影响

本文观察了不同浓度的铜、锌对培养乳鼠心肌细胞缺氧/再给氧损伤后超氧歧化酶(superoxid dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-px)活性和脂质过氧化(lipid peroxidation,LPO)代谢产物丙二醛(malondialodehyde,MDA)含量改变,以及乳酸脱氢酶(lactate dehydrogenase,LDH)释放的影响。结果表明:缺氧/再给氧后,心肌细胞SOD活性降低,GSH-px活性和MDA含量增高,LDH释放增加。铜、锌均能不同程度地提高SOD活性,但铜的作用强于锌。锌、铜均可降低LDH的释放,但锌的作用强于铜,锌、铜浓度过高反而增加LDH的释放。此外,铜使GSH-px活性明显升高,并显著降低MDA含量。     

红景天总黄酮对自然衰老大鼠抗氧化和免疫功能的影响

目的探讨红景天总黄酮对自然衰老大鼠抗氧化和免疫功能的影响。方法Wistar雄性大鼠40只,分成4组:正常组(健康青年大鼠),自然衰老模型组,和低、高剂量红景天总黄酮组。分别灌胃相应剂量的红景天总黄酮或生理盐水;6周后,Elisa法测定血清SOD、MDA、GSH-Px、IL-2和IL-6,胸腺、脾指数,MTT法检测淋巴细胞转化刺激指数的变化。数据分析采用SPSS软件统计学处理。结果模型组比较正常组,血清SOD、GSH-Px、IL-2含量以及胸腺、脾指数和T、B淋巴细胞增殖能力明显降低,而血清MDA、IL-6含量明显升高;红景天总黄酮可明显提高衰老大鼠血清SOD、GSH-Px、IL-2含量,并使MDA、IL-6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。结论红景天总黄酮可增强衰老大鼠抗氧化和免疫功能,具有延缓衰老功效。     

Protective effects of Cu/Zn-SOD and Mn-SOD on UVC radiation-induced damage in NIH/3T3 cells and murine skin

Superoxide dismutase (SOD) is an antioxidant enzyme with multiple metal cofactors that can specifically clear reactive oxygen species (ROS), which plays an important role in a variety of ultraviolet-induced lesions. Therefore, SOD has the anti-ultraviolet radiation effect. The objective of this study was to compare the differences in the anti-ultraviolet radiation effect of SOD with distinct metal cofactors: Cu/Zn-SOD and Mn-SOD. SOD was first purified using hydrophobic interaction chromatography and ion-exchange chromatography. Second, the Methylthiazolyldiphenyl-tetrazolium bromide method and cell senescence kits were used to study the protective effect of SOD on ultraviolet-induced cell damage. Finally, the protective effect of SOD on ultraviolet -induced skin damage was histopathologically evaluated, and the expression levels of malondialdehyde (MDA) and matrix metalloproteinases (MMPs) in tissues were detected. The results showed that Cu/Zn-SOD was superior to Mn-SOD in promoting cell proliferation, alleviating cell damage, protecting skin structure, and regulating the expression levels of MDA and MMPs, and it has no side effects. In conclusion, Cu/Zn-SOD had a better anti-ultraviolet radiation effect than Mn-SOD, and it can be used in anti-aging and anti-ultraviolet skin-care products.     

Amelioration of cisplatin-induced nephrotoxicity by pravastatin in mice

This study investigated the protective effects of pravastatin against cisplatin-induced nephrotoxicity and the possible mechanisms in mice. Pravastatin showed significant protection as evidenced by the decrease of elevated serum creatinine (CRE) and blood urea nitrogen (BUN), and improvement of histopathological injury induced by cisplatin. The formation of kidney malondialdehyde (MDA) with a concomitant reduction of reduced glutathione (GSH) were inhibited by pravastatin, while the activities of kidney superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-px) were increased. The over expressions of kidney induced nitric oxide synthase (iNOS) and nitrotyrosine (3-NT) were suppressed by pravastatin. Pravastatin suppressed cisplatin-induced p38 mitogen-activated protein kinase (MAPK) activation in the kidney of mice. These results suggest that pravastatin pre-administration can prevent the nephrotoxicity induced by cisplatin. Pravastatin may exert the protective effect via inhibiting oxidative and nitrosative stress.     

力竭游泳后大鼠大脑微循环超微结构与自由基代谢动态变化的同步研究

观察力竭游泳后即刻、24h和48h大鼠大脑微循环超微结构的动态变化，并测定大鼠大脑组织MDA含量、SOD和GSH—px的活性。实验结果表明，力竭游泳后即刻大鼠大脑微循环结构发生明显的变化，24h后较力竭游泳后即刻有所好转，48h后大鼠大脑微循环形态结构恢复接近正常。力竭游泳后观察各时段MDA含量无显著性改变，而SOD的活性在力竭游泳后即刻显著升高，24h后显著下降，48h后又显著上升；GSH—px活性动态变化呈下降趋势，且24h下降具统计学意义，特别是在24h与SOD同步明显下降，表明此时SOD和GSH—px消耗量最大，以及时清除自由基，减轻自由基对脑组织造成的损伤，有利于大脑微循环形态结构的修复。     

rhEPO affects apoptosis in hippocampus of aging rats by upregulating SIRT1

The aim of this study was to elucidate the signaling pathway involved in the anti-aging effect of erythropoietin (EPO) and to clarify whether recombinant human EPO (rhEPO) affects apoptosis in the aging rat hippocampus by upregulating Sirtuin 1 (SIRT1). In this study, a rat model of aging was established using D-galactose. Behavioral changes were monitored by the Morris water maze test. Using immunohistochemistry, we studied the expression of SIRT1, B-cell lymphoma/leukemia-2 gene (Bcl-2), and Bcl-2 associated X protein (Bax) expression, and apoptotic cells in the hippocampus of a rat model of aging in which rhEPO was intraperitoneally injected. The escape latency in rats from the EPO group shortened significantly; however, the number of platform passes increased significantly from that in the D-gal group (P < 0.05). Compared to the D-gal group, in the EPO group, the number of SIRT1 and Bcl-2-positive cells increased (P < 0.05), but the number of Bax-positive cells and apoptotic cells decreased in the hippocampus of aging rats (P < 0.05). These results suggest that rhEPO regulates apoptosis-related genes and affects apoptosis in the hippocampus of aging rats by upregulating SIRT. This may be one of the important pathways underlying the anti-aging property of EPO.     

Status of lipid peroxidation and antioxidant enzymes in goats naturally infected with Babesia ovis

This study aimed to assess lipid peroxidation and antioxidant enzymes in goats naturally infected with Babesia ovis. Red blood cell count (RBC), hemoglobin (Hb) concentration, packed cell volume (PCV), malondialdehyde (MDA) concentration, erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) activities and total antioxidant capacity (TAC) were determined in 15 goats naturally infected with B. ovis as well as same number of healthy goats. The parasitological diagnosis was confirmed using polymerase chain reaction (PCR) analysis by amplifying a partial 18S rRNA gene sequence of B. ovis. Percentage of parasitemia varied from 0.01 to 1%. The activities of erythrocyte GSH-Px, SOD, CAT and TAC were significantly lower (p<0.05) in the infected goats than in healthy ones. MDA concentration in erythrocytes of infected goats was significantly higher in infected goats than in healthy ones (p?0.05). Severity of parasitemia showed a positive correlation with the MDA and negative correlation with PCV, SOD, CAT, GSH-Px and TAC. Also, MDA was negatively correlated with PCV, SOD, CAT, GSH-Px and TAC. The results of this study suggested that oxidative damage to RBCs may contribute to the pathogenesis of anemia in caprine babesiosis.     

氧自由基对严重烧伤后红细胞免疫粘附功能的影响

目的探讨氧自由基对烧伤后红细胞免疫粘附功能的影响。方法于伤后1d、3d、5d、7d、14d、21d、28d和35d,观察RBC-C3b受体花环形成率(RC3bRR)和RBC-IC花环形成率(RICR),以及SOD、Lpo-MDA、CAT、GSH-px和GSH水平的变化,并进行相关性分析。结果①伤后RC3bRR显著下降,RICR显著升高(P＜0.05～0.001),但4wk后逐渐恢复至正常。②伤后SOD、CAT、GSH-px和GSH的水平显著下降,Lpo-MDA的水平则显著上升(P＜0.05～0.001),至少伤后3wk才恢复到正常水平。③RC3bRR与SOD、CAT、GSH-px和GSH的水平呈显著的正相关(r值依次分别为0.601,0.799,0.715和0.597),与Lpo-MDA的水平呈显著的负相关(r=-0.564);RICR与SOD、CAT、GSH-px和GSH的水平也呈显著的负相关(r值依次分别为-0.359、-0.577、-0.420和-0.427),与Lpo-MDA的水平则呈显著的正相关(r=0.433)。结论红细胞膜极易产生脂质过氧化作用,烧伤后自由基损伤的程度,可直接影响红细胞膜的功能,特别是红细胞免疫粘附功能。在烧伤治疗过程中,提示减少机体自由基的产生,提高患者红细胞免疫粘附功能是十分必要的。     

蛇菰多糖降低实验性肝损伤大鼠肝脏BDNF和TrkB的表达

目的蛇菰多糖(BPS)对D-半乳糖(D-gal)所致实验性肝损伤大鼠的肝功能及肝组织内BDNF、TrkB蛋白和凋亡相关蛋白表达的影响。方法将大鼠随机分为对照组(control),D-gal组(皮下注射D-半乳糖200 mg/kg),BPS低(D-gal+BPS-L)、中(D-gal+BPS-M)、高(D-gal+BPS-H)剂量组,分别每天灌胃50、100和200 mg/kg BPS,共6周。心脏取血检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST)水平;HE染色法观察肝组织形态;免疫组织化学染色检测BDNF和TrkB的定位;Western blot检测BDNF、TrkB、Bcl-2、caspase-3和Bax蛋白表达;ELISA测定肝组织内丙醛(MDA)含量和超氧化物歧化酶(SOD)活性。结果与对照组相比,D-gal组肝细胞水肿、点状坏死;血清ALT和AST水平升高(P<0.05),SOD活性降低、MDA含量升高(P<0.05);Bax、caspase-3、BDNF、TrkB表达增加(P<0.05),Bcl-2表达降低(P<0.05);与D-gal组相比,BP...     

Reference values of oxidative stress parameters (MDA, SOD, CAT) in dogs and cats

The present study was performed on 56 clinically healthy dogs and 52 clinically healthy cats, age and sex matched. The reference values of principal parameters of oxidative stress—malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT)—were determined in blood samples of dogs and cats. It was found that MDA plasma concentrations in male dogs were higher than those in females. The same difference was found in cats but the sex difference was much higher. SOD activity did not show any sex differences in dogs or cats. The CAT values were lower in males compared to females in only cats .     

X射线对仔鼠大脑枕叶皮层结构及大脑超氧化物歧化酶、过氧化氢酶活性及丙二醛含量的影响

目的观察X射线辐射后仔鼠大脑枕叶皮层结构、大脑重量及大脑中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量的动态变化,探讨X射线辐射对仔鼠大脑发育的影响。方法对160只仔鼠(出生6～7d)用不同吸收剂量(0Gy、1Gy、3Gy、5Gy和7Gy)X射线进行全身辐射,分别于辐射后1d、5d、10d和20d,用比色法检测仔鼠大脑中SOD、CAT活性及MDA含量的变化,称量检测各期仔鼠大脑重量的变化,用显微技术观察仔鼠大脑枕叶皮层结构的变化。结果 X射线辐射影响仔鼠大脑的生长发育,辐射后1～20d,除1Gy辐射组在1～10d时仔鼠大脑重量高于对照组,其他辐射组仔鼠大脑重量均低于对照组,差异显著或极显著(P0.05或P0.01);1Gy辐射组在5～20d时,仔鼠大脑中SOD和CAT活性高于对照组,差异显著(P0.05),MDA含量低于对照组,差异显著或极显著(P0.05或P0.01);3Gy辐射组仔鼠大脑中SOD、CAT活性先降低后又逐渐升高,但仍低于对照组,MDA含量先升高后降低,但仍高于对照组;5Gy、7Gy辐射组仔鼠大脑中SOD、CAT活性明显低于对照组,差异极显著(P0.01),MDA含量明显高于对照组,差异极显著(P0.01);辐射组仔鼠大脑枕叶皮层厚度减小,皮层结构不清,除1Gy辐射组在1d时仔鼠大脑枕叶皮层第II、III、VI层的细胞面密度值高于对照组及在20d时第III、V、VI层的细胞面密度值高于对照组,其他辐射组仔鼠大脑枕叶皮层各层细胞密度值均低于对照组。结论 X射线辐射影响仔鼠大脑的重量和皮层组织结构,这可能与大脑中抗氧化酶活性降低和MDA含量升高有一定的关系。     

当归多糖对D-半乳糖致小鼠胰腺损伤的保护作用

目的 探讨当归多糖（ASP）对D-半乳糖（D-gal）致小鼠胰腺损伤的保护作用。 方法 雄性C57BL/6 J 小鼠随机分为3组,每组10只。D-gal组: 小鼠皮下注射- gal (120 mg/kg, qd×42 d）; ASP+D-gal组: D-gal注射时间与剂量同D-gal模型组,从模型复制第16天起,腹腔注射ASP(40 mg/kg,qd×27 d）;正常对照组: 小鼠皮下注射等量与等时的生理盐水。各组给药完成后第2天检测相关指标,取外周血检测空腹血糖含量并行口服葡萄糖耐量测定（OGTT）;取胰腺称湿重计算脏器指数;制备石蜡切片,HE染色观察胰腺组织病理结构,图像分析法计数胰岛内有核细胞数和相关面积;制备胰腺组织匀浆,检测丙二醛(MDA)含量和总抗氧化能力（T-AOC）。 结果 从注射D-gal第16天开始,腹腔注射ASP共27 d（ASP+D-gal组）,小鼠胰腺湿重与脏器指数明显降低,组织病理损伤减轻;空腹血糖显著下降;在30 min和120 min的OGTT水平差别不明显;OGTT曲线下面积（AUC）降低;胰岛内有核细胞数减少,单个细胞面积减小;T-AOC活性上升,MDA含量下降。 结论 D-gal可致胰腺结构损伤和功能衰退,ASP能拮抗D-gal从而减轻对胰腺的损伤,其机制可能与减轻氧化损伤有关。