环维黄杨星D对培养大鼠乳鼠心肌细胞缺氧/复氧损伤的保护作用

目的研究环维黄杨星D对纯化培养大鼠乳鼠心肌细胞缺氧/复氧损伤的保护作用及机制。方法采用纯化培养的心肌细胞建立缺氧/复氧损伤模型,测定细胞凋亡率、caspase-3、超氧化物歧化酶(SOD)、丙二醛(MDA)和乳酸脱氢酶(LDH)含量。结果与正常组比较,模型组LDH、MDA含量、caspase-3活性及细胞凋亡率明显增高(P<0.01),SOD活性明显降低(P<0.01);CVB-D(1×10-5mol.L-1)组降低LDH、MDA含量、caspase-3活性和细胞凋亡率,提高SOD活性,与缺氧/复氧组比较各实验指标均差异具有显著性(P<0.05)。结论CVB-D对缺氧/复氧造成的心肌细胞损伤具有保护作用,作用机制与清除氧自由基,抗脂质过氧化及降低细胞凋亡率有关。     

黄芪多糖对乳鼠心肌细胞缺氧/复氧损伤的保护作用

目的探讨黄芪多糖(APS)对乳大鼠培养心肌细胞缺氧/复氧损伤的保护作用及其机制。方法取体外培养的乳大鼠心肌细胞建立缺氧/复氧心肌细胞损伤模型,实验分为5组:空白对照组;模型组(A/R组);3个APS给药组,于缺氧及复氧开始时分别加入终浓度为10、30、100mg·mL-1的APS,观察APS对细胞上清液中缺氧/复氧后LDH、CK、AST漏出量、MDA含量、SOD活性。用MTT法检测APS对缺氧/复氧损伤心肌细胞存活率的影响。用流式细胞仪测定APS对缺氧/复氧损伤心肌细胞凋亡的影响。结果 APS可明显减少缺氧/复氧后LDH、CK、AST漏出量(P<0.05或P<0.01);降低MDA含量,提高SOD活性(P<0.05或P<0.01);明显提高缺氧/复氧损伤心肌细胞的存活率,并能明显抑制缺氧/复氧损伤心肌细胞凋亡。结论 APS对培养心肌细胞的缺氧/复氧损伤具有保护作用,作用机制与其增强细胞抗氧化作用,减少自由基及脂质过氧化物导致的细胞膜损伤和抑制细胞凋亡有关。     

新型褪黑素受体激动剂Neu-P11激活AMPK减轻心肌细胞缺氧/复氧损伤

目的研究新型褪黑素受体激动剂Neu-P11对心肌细胞缺氧/复氧损伤的作用及分子机制。方法实验分为对照组、缺氧/复氧模型组(H/R组)、H/R+Neu-P11组、H/R+Compound C组、H/R+Neu-P11+Compound C组。构建H9c2心肌细胞缺氧/复氧模型,检测各组心肌细胞凋亡情况,细胞培养液中乳酸脱氢酶(LDH)、肌酸激酶(CK)、SOD活性及MDA含量及心肌细胞AMPK的活性。结果与缺氧/复氧组细胞相比,Neu-P11预处理组细胞凋亡率明显减少,CK、LDH、MDA含量明显下降,SOD活性增加,心肌细胞AMPK活性明显增高,而AMPK特异性抑制剂Compound C可以阻断Neu-P11的保护作用。结论 Neu-P11能够减轻心肌细胞缺氧/复氧损伤,这一保护作用与激活AMPK有关。     

茜草双酯对缺氧/复氧心肌细胞的保护作用研究

目的探讨茜草双酯对缺氧复氧的乳鼠心肌细胞是否具有保护作用。方法原代培养乳鼠心肌细胞,建立缺氧复氧模型,分别测各组细胞乳酸脱氢酶(LDH)活性、丙二醛(MDA)含量及细胞的凋亡与坏死。结果与缺氧/复氧模型组比较发现,缺氧/复氧模型预先加茜草组较缺氧/复氧模型组LDH活性和MDA含量降低有统计学意义(P<0.05),细胞凋亡和坏死有所减少。结论茜草双酯对体外培养的缺氧/复氧心肌细胞具有保护和抗凋亡作用。     

蒺藜皂苷预适应对大鼠心肌缺血/再灌注损伤的保护作用

目的探讨蒺藜皂苷(GSTT)预适应对大鼠心肌缺血/再灌注损伤的保护作用。方法 56只大鼠随机分假手术组(Sham)、缺血/再灌注(I/R)组、缺血预适应组(IP)、阳性药(尼可地尔1.0mg·kg-1)组、GSTT100、30、10mg·kg-1组。采用分光光度法测定血清乳酸脱氢酶(LDH),二氨基二苯甲烷(MDA),超氧化物歧化酶(SOD)水平。ELISA法测定血清TNF-α与IL-6的含量。光学显微镜下观察受损心肌病理组织学改变,采用TUNEL法检测心肌细胞凋亡,Western blot检测心肌组织内caspase-3表达。结果与模型组比较,GSTT100、30mg·kg-1组LDH、MDA含量明显降低,SOD活性明显升高(P<0.01),TNF-α及IL-6含量也明显降低,凋亡细胞数明显减少(P<0.01),caspase-3表达下降,心肌组织形态明显改善。结论蒺藜皂苷预先给药对大鼠心肌缺血/再灌注损伤具有保护作用,能减少自由基生成,抑制细胞凋亡。     

蒺藜皂苷对阿霉素损伤心肌细胞的保护作用

 观察蒺藜皂苷 (gross saponins of Tribulus terrestris, GSTT) 对阿霉素 (adriamycin, ADR) 诱导大鼠乳鼠心肌细胞损伤的保护作用, 并初步探讨其作用机制。分离出生1～3 d大鼠心肌细胞, 培养72 h后随机分为正常对照组、ADR (终浓度为2.0 mg·L⁻¹) 模型组和GSTT (100、30及10 mg·L⁻¹) 组, 继续培养24 h后, 应用MTT比色法检测细胞存活率, 测定培养基中肌酸激酶 (CK)、乳酸脱氢酶 (LDH)、天门冬氨酸氨基转移酶 (AST) 释放量, 超氧化物歧化酶 (SOD) 活性, 丙二醛 (MDA)、一氧化氮 (NO) 含量, 并采用流式细胞仪检测细胞凋亡及应用Western blotting检测GSTT对凋亡相关蛋白caspase-3的作用。结果表明, 与正常对照组比较, ADR模型组心肌细胞存活数明显减少, 心肌细胞培养液中CK、LDH、AST释放量增加 (P < 0.01, P < 0.001), 同时SOD活力下降 (P < 0.01) 而MDA、NO含量升高 (P < 0.001); 与ADR模型组比较, GSTT (100和30 mg·L⁻¹) 组存活心肌细胞数增多 (P < 0.05, P < 0.001), 心肌细胞培养液中CK、LDH、AST含量明显降低, SOD活力增加、MDA和NO含量降低 (P < 0.05, P < 0.01, P < 0.001)。流式细胞仪检测GSTT (100和30 mg·L⁻¹) 组心肌细胞凋亡数明显减少 (P < 0.05, P < 0.01), caspase-3含量下降 (P < 0.05, P < 0.001)。GSTT对ADR损伤的心肌细胞具有保护作用, 可减轻心肌细胞损伤, 抑制心肌细胞凋亡, 其机制与抗自由基作用有关。     

去葡萄糖竹节参皂苷Ⅳa对缺氧复氧心肌细胞损伤的保护作用

目的研究去葡萄糖竹节参皂苷Ⅳa(DCⅣa)是否为龙牙木匆心木总皂苷抗心肌缺血的有效成分之一。方法取体外培养的新生大鼠心肌细胞建立缺氧6 h复氧3 h心肌细胞损伤模型,并于缺氧及复氧开始时分别加入终浓度为2.5,1.0和0.1 mg.L-1的DCⅣa。检测细胞培养上清液中乳酸脱氢酶(LDH)和肌酸激酶(CK)漏出量,丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。MTT法检测心肌细胞存活率。结果DCⅣa(2.5,1.0 mg.L-1)显著减少缺氧及复氧后LDH和CK漏出量,降低MDA含量,提高SOD活性,提高心肌细胞存活率。结论DCⅣa为龙牙木匆心木总皂苷抗心肌缺血的有效成分之一,可减轻缺氧复氧对心肌细胞的损伤,对心肌细胞具有直接的保护作用。     

竹叶提取物对缺氧／复氧心肌细胞的保护作用

目的本研究旨在探讨竹叶提取物(BLE)对缺氧/复氧心肌细胞的保护作用及其分子机制。方法采用原代培养的新生大鼠心肌细胞建立缺氧/复氧损伤模型,实验分为正常细胞培养组、缺氧/复氧损伤模型组、缺氧/复氧损伤 BLE(10-1,10-2,10-3,10-4,10-5g.L-1)组、缺氧/复氧损伤 X iangdan(2.5×10-3g.L-1)组。检测培养基质乳酸脱氢酶(LDH)的活性,细胞线粒体脱氢酶活性,超氧化物歧化酶活性(SOD),NO的含量,心肌细胞Ca2 和丙二醛(MDA)浓度。结果BLE可显著提高缺氧/复氧心肌细胞SOD的活性及细胞线粒体脱氢酶活性,并能显著抑制LDH的活性、MDA的生成,提高NO的含量,降低Ca2 的含量。结论BLE对缺氧/复氧心肌细胞损伤具有一定的保护作用。     

二氢石蒜碱对大鼠乳鼠培养心肌细胞缺氧/复氧损伤的保护作用

目的观察二氢石蒜碱(dihydrolycorine,DL)对Wistar大鼠的乳鼠培养心肌细胞缺氧/复氧损伤(H/R)的保护作用。方法采用培养的Wistar乳鼠的心肌细胞,建立H/R损伤模型,检测指标包括:①心肌细胞存活率;②超氧化物歧化酶(SOD)活性;③丙二醛(MDA)含量;④乳酸脱氢酶(LDH)活性。结果模型组缺氧后心肌细胞存活率降低,复氧后进一步下降,各个时间点细胞内SOD活性下降,MDA含量升高,乳酸脱氢酶(LDH)活性升高,与正常组比较差异具有显著性(P<0.01);在DL1、10、100μmol·L-1组,随着给药浓度的增加,细胞存活率升高,LDH活性变低,MDA含量逐渐趋于恢复正常,SOD活性逐渐回升,表明经DL干预之后,心肌细胞抗损伤能力加强,发生损伤的程度减轻。结论DL对培养的乳鼠心肌细胞H/R损伤具有保护作用,其作用在一定范围内呈剂量依赖关系,机制可能与其阻断α、β受体、抑制心肌细胞脂质过氧化反应有关。     

竹叶提取物对缺氧/复氧心肌细胞的保护作用

目的本研究旨在探讨竹叶提取物(BLE)对缺氧/复氧心肌细胞的保护作用及其分子机制.方法采用原代培养的新生大鼠心肌细胞建立缺氧/复氧损伤模型,实验分为正常细胞培养组、缺氧/复氧损伤模型组、缺氧/复氧损伤+ BLE(10-1, 10-2, 10-3, 10-4, 10-5 g·L-1)组、缺氧/复氧损伤+ Xiangdan(2.5×10-3g·L-1)组.检测培养基质乳酸脱氢酶(LDH)的活性,细胞线粒体脱氢酶活性,超氧化物歧化酶活性(SOD),NO的含量,心肌细胞Ca2+和丙二醛(MDA)浓度.结果 BLE可显著提高缺氧/复氧心肌细胞SOD的活性及细胞线粒体脱氢酶活性,并能显著抑制LDH的活性、MDA的生成,提高NO的含量,降低Ca2+的含量.结论 BLE对缺氧/复氧心肌细胞损伤具有一定的保护作用.     

金丝桃苷对新生大鼠神经细胞缺氧/再给氧损伤的保护作用及其机制

目的探讨金丝桃苷(hyperin,Hyp)对新生大鼠脑细胞缺氧/再给氧损伤的保护作用及其机制。方法将分离的新生大鼠脑细胞缺氧30min或缺氧30min后再给氧40min造成细胞缺氧或再给氧损伤模型,测定细胞培养上清液中乳酸脱氢酶(LDH)、丙二醛(MDA)和一氧化氮(NO)水平的变化,用Fura2-AM方法测定脑细胞内游离钙离子浓度([Ca2+]i)的变化。结果脑细胞缺氧时,细胞培养上清液中LDH从(62.0±13.0)U·L-1(Sham组)增高到(116.0±16.6)U·L-1(Control组,P<0.01),再给氧时,LDH和MDA分别从(45.6±9.2)U·L-1和(9.1±0.9)μmol·L-1(Sham组)增高到(106.0±17.4)U·L-1和(16.4±2.7)μmol·L-1(Control组,P<0.01)。Hyp在1.0～16.0μmol·L-1范围内,明显地抑制缺氧及再给氧损伤诱导的上述LDH和NO增高,并呈一定的浓度依赖性。1.0～16.0μmol·L-1的Hyp不仅可明显地抑制缺氧诱导的细胞培养上清液中NO和脑细胞内[Ca2+]i的增高(P<0.05或P<0.01),也可明显地抑制再给氧时NO和脑细胞内[Ca2+]i的升高(P<0.05或P<0.01),16.0μmol·L-1的Hyp可将再给氧时NO和[Ca2+]i分别从(34.4±6.3)μmol·L-1和(640±94)nmol·L-1(Control组)降至(25.0±5.1)μmol·L-1(P<0.05)和(331±56)nmol·L-1(P<0.01)。结论Hyp对神经细胞缺氧/再给氧损伤保护作用可能与抑制NO的释放、钙超载及自由基脂质过氧化有关。     

Improving effect and mechanism of fisetin on cell model of diabetic cerebral microangiopathy

OBJECTIVE To explore the effect and mechanism of fisetin on prevention and treatment of diabetic cerebral microangiopathy at the cellular and molecular level. METHODS In vitro experiments, high glucose(HG, 25 mmol·L~(-1)) and palmitic acid(PA, 200 μmol·L~(-1))were used to intervene in the mouse brain microvascular endothelial cells to establish the model of diabetic brain microangiopathy. Groups are divided into control, model(25 mmol·L~(-1) HG+200 μmol·L~(-1) PA, HG+PA) and fisetin(1, 5, 10 and 20 μmol·L~(-1)) groups. The effect of fisetin on hyperglycemic and hyperlipid-induced cell damage was detected by cell counting kit-(CCK-) 8 assay, cytotoxicity was detected by LDH assay. After treatment, the changes of oxidative stress related factors(ROS, NO, i NOS, MMP-2, MMP-9, TIMP-1, MDA, SOD, CAT) were detected by ELISA. RESULTS Compared with the control group, the cell viability of model group was significantly reduced(P<0.01), indicating that the model was successful y prepared.LDH content, the expression levels of ROS, NO, i NOS,MMP-2, MMP-9, TIMP-1 and MDA in the model group significantly increased(P< 0.01), while the expression of SOD and CAT in the model group decreased significantly(P<0.01). Compared with the model group, the activity of the cells, in the fisetin group was significantly increased(P<0.01). LDH content, the expression levels of ROS,NO, i NOS, MMP-2, MMP-9, TIMP-1 and MDA were decreased in the fisetin group(P<0.01), the expression of SOD and CAT, were significantly increased(P<0.01).The expression levels of antioxidant proteins HO-1 and NQO1 were significantly increased in the fisetin group(P<0.05). CONCLUSION Fisetin can improve the cell injury induced by HG and PA, which mimic the diabetic cerebral microvascular lesions, and its mechanism might be related to inhibiting the production of endogenous ROS in cells, activating the expression of antioxidant proteins and inhibiting the production of related oxidative factors.     

Neocryptotanshinone protects cardiomyocyte hypoxia/reoxygenation-induced H9C2 cell injury through targeting RxRα

OBJECTIVE Neocryptotanshinone(NCTS) is a natural product extracted from traditional Chinese herb Salvia miltiorrhiza Bunge. Previous studies have demonstrated the anti-inflammatory of NCTS in lipopolysaccharide(LPS)-stimulated mouse macrophage(RAW 264.7). However, the protective effect and mechanism of NCTS in cardiomyocytes are still undefined. This study is to investigate whether NCTS exerts its cardioprotective effect against hypoxia/reoxygenation(H/R)-induced H9 C2 cell injury. METHODS The model of H/R injury was established through hypoxia for 8 h and reoxygenation for 12 h in H9 C2 cardiomyocytes of rats. Cultured cardiomyocytes were randomly divided into four groups, control group, H/R group, H/R+NCTS pretreated group(1, 2, 5 and 10 μmol·L~(-1)), and H/R+NCTS+HX531(an RXRα antagonist, 2 μmol·L~(-1)) co-treated group. The cell viability was measured by Cell Counting Kit-8, Hoechst33258 staining was used to observe the morphology of apoptotic changes. Mitochondrial membrane potential was detected by JC-1 fluorescent probe, and protein expressions of RXRα, Bcl-2, Bax, caspase-3 and cleaved caspase-3 with Western blotting. RESULTS Compared with control group, the cell viability in model group was decreased(P<0.05). After treated with NCTS in different concentrations, the CCK8 results showed that NCTS in 2 μmol·L~(-1) had protective effects. Result of Hoechst33258 staining suggested that the apoptosis was notably increased in model group(P<0.05), Meanwhile, the JC-1 results showed that the mitochondrial membrane potential of the model group decreased which was consistent with previous study. impressively, NCTS could restore the mitochondrial membrane potential as well as apoptosis. Further western blot experiments showed that NCTS treat could upregulate Bcl-2 protein, and downregulate the levels of Bax and cleaved caspase-3/caspase-3 ratio. Since RXRα is a critical upstreaming proteins which can directly mediate the apoptosis, we then determined the effect of NCTS on it. Intriguingly, RXRα was notably activated by NCTS, while the HX531, the antagonist of RXRα, could abolished NCTS' effect when co-treated with NCTS. CONCLUSION NCTS in 2 μmol·L~(-1) was effective to protect H9 C2 cell from H/R-induced cell injury through RXRα-mediated mitochondria apoptosis. Current results provide possible drugs for the treatment of ischemic cardiomyopathy.     

δ阿片受体激活对过氧化氢损伤的心肌细胞的保护作用

目的研究δ阿片受体激活剂D-丙(2)-D-亮-(5)-脑啡肽(DADLE)对过氧化氢(H2O2)损伤的心肌细胞的保护作用及其机制。方法分离乳大鼠心肌细胞,培养48h后分为正常对照、H2O2(200μmol.L-1)、H2O2+DADLE(1μmol.L-1)、H2O2+DADLE+纳曲吲哚(10μmol.L-1)和H2O2+DADLE+U0126(10nmol.L-1)组,继续培养48h。用[3H]TdR掺入法检测心肌细胞增殖反应,流式细胞仪检测心肌细胞凋亡百分率,乳酸脱氢酶(LDH)活性测定试剂盒测定培养上清LDH活性,硫代巴比妥酸显色法测定细胞内丙二醛(MDA)含量,黄嘌呤氧化酶法测定细胞内超氧化物歧化酶(SOD)活性,Western蛋白印迹法检测细胞外信号调节激酶磷酸化(p-ERK)水平。结果①与正常对照组比较,H2O2组心肌细胞[3H]TdR掺入值明显降低,细胞凋亡率升高;培养上清LDH活性和MDA含量明显增加,SOD活性和Ap-ERK/AERK的比值降低。②与H2O2组比较,DADLE可使心肌细胞[3H]TdR掺入值升高,细胞凋亡率下降;培养上清LDH活性和MDA含量降低,SOD活性和Ap-ERK/AERK的比值升高。③分别加入δ阿片受体拮抗剂纳曲吲哚和ERK拮抗剂U0126,DADLE对上述指标的逆转作用被抑制。结论δ阿片受体激活对H2O2损伤的心肌细胞具有保护作用,其机制可能与其增强心肌细胞的抗氧化功能及促进ERK磷酸化有关。     

果糖二磷酸钠对脑出血患者的心肌酶谱的影响

目的 探讨脑出血患者应用果糖二磷酸钠(FDP)对心肌酶谱的影响.方法 选取脑出血患者64例,根据是否应用FDP分为对照组和治疗组,各32例,两组均给予常规治疗.其中治疗组在常规治疗的基础上给予果糖二磷酸钠(用法用量:5.0克/次,静脉滴注,2次/天,疗程7天),比较入院时第1天、第3天、第7天心肌酶谱乳酸脱氢酶(LDH)、磷酸肌酸激酶(CK)、门冬氨酸氨基转移酶(AST)及磷酸肌酸激酶同工酶(CKMB)水平.结果 心肌酶AST、LDH、CK及CKMB入院第3天治疗组的检测结果为:(46.41±27.53)IU·L-1、(285.94±42.84)IU·L-1、(352.81±148.69)IU·L-1、(37.47±12.05)IU·L-1;心肌酶AST、LDH、CK及CKMB入院第7天治疗组的检测结果为:(35.59±13.44)IU·L-1、(249.28±50.37)IU·L-1、(260.81±98.12)IU·L-1、(23.13±8.35)IU·L-1.入院第1天AST、LDH、CK及CKMB治疗组与对照组差异无统计学意义(P分别为0.504、0.935、0.672、0.588),第3、7天对照组AST、LDH、CK及CKMB均较治疗组升高,差异有统计学意义(第3天P分别为0.003、0.001、0.025、0.009;第7天P值分别为:0.001、0.013、0.013、0.001).治疗组和对照组的AST、LDH、CK及CKMB第3天均较第1天时升高,差异有统计学意义(P<0.01),治疗组AST、LDH、CK及CKMB第7天与第1天相比较差异无统计学意义(P>0.05),对照组AST、LDH、CK、及CKMB第7天高于第1天,差异有统计学意义(P<0.01).结论 果糖二磷酸钠应用于脑出血患者可以降低急性期心肌酶谱,对心脏有保护作用.     

Tribulosin protects rat hearts from ischemia/ reperfusion injury

Aim:

To investigate the protective effect of tribulosin, a monomer of the gross saponins from Tribulus terrestris, against cardiac ischemia/reperfusion injury and the underlying mechanism in rats.

Methods:

Isolated rat hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion using Langendorff''s technique. The hearts were assigned to seven groups: control, ischemia/reperfusion (I/R), treatment with gross saponins from Tribulus terrestris (GSTT) 100 mg/L, treatment with tribulosin (100, 10, and 1 nmol/L) and treatment with a PKC inhibitor (chelerythrine) (1 μmol/L). Infarct size was assessed by triphenyltetrazolium chloride staining. Malondialdehyde (MDA), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) contents as well as superoxide dismutase (SOD) and creatine kinase (CK) activities were determined after the treatment. Histopathological changes in the myocardium were observed using hematoxylin-eosin (H&E) staining. Apoptosis was detected with terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) assay. Bcl-2, Bax, caspase-3, and PKCɛ protein expression were examined using Western blotting.

Results:

Tribulosin treatment significantly reduced MDA, AST, CK and LDH contents, and increased the activity of SOD. The infarct size of I/R group was 40.21% of the total area. GSTT and various concentrations of tribulosin treatment decreased the infarct size to 24.33%, 20.24%, 23.19%, and 30.32% (P<0.01). Tribulosin treatment reduced the myocardial apoptosis rate in a concentration-dependent manner. Bcl-2 and PKCɛ protein expression was increased after tribulosin preconditioning, whereas Bax and caspase-3 expression was decreased. In the chelerythrine group, Bcl-2 and PKCɛ expression was decreased, whereas Bax and caspase-3 expression was increased.

Conclusion:

Tribulosin protects myocardium against ischemia/reperfusion injury through PKCɛ activation.     

Anti-aging effect of aqueous extract from Astragalus membranaceus on Drosophila melanogaster

OBJECTIVE To study the anti-aging effect of aqueous extract from Astragalus membranaceus on Drosophila melanogaster. METHODS Drosophila(male and female) were collected within 3 d in adult stage.Drosophila were randomly divided into control group and aqueous extract from Astragalus groups(0.625, 1.25,2.5, 5 and 10 g·L~(-1)). The pharmacodynamics experiment of aqueous extract from Astragalus was investigated by using lifespan experiment, crawling assay, hydrogen peroxide stress assay, paraquat stress assay. To evaluate the antioxidant effect of aqueous extract from Astragalus,the enzyme activity of superoxide dismutase(SOD), catalase(CAT) were conducted. RESULTS The results of lifespan showed that 1.25 g·L~(-1) of aqueous extract from Astragalus could significantly prolong the life span of both male and female Drosophila(P<0.05). The 0.625 g·L~(-1) of aqueous extract from Astragalus could significantly extend the life span of female Drosophila(P<0.01). The1.25 g·L~(-1) of aqueous extract from Astragalus could significantly improve the crawling ability of male Drosophila at 25 d age(P<0.05). The 1.25 g·L~(-1) of aqueous extract from Astragalus significantly extended the life span of male Drosophila after hydrogen peroxide exposure(P<0.01). The 0.625 g·L~(-1) of aqueous extract from Astragalus could significantly prolong the life span of female Drosophila after hydrogen peroxide exposure(P<0.05). The 1.25 g·L~(-1) of aqueous extract from Astragalus could significantly prolong the life span of male and female Drosophila after paraquat exposure(P<0.01). The 1.25 g·L~(-1) of aqueous extract from Astragalus significantly increased SOD and CAT activity in fruit flies at 25 d age(P<0.01). CONCLUSION The aqueous extract from Astragalus prolongs the life span of Drosophila by improving the activity of SOD,CAT and alleviating the damage of free radicals caused by aging.     

大豆异黄酮活性组分对阿尔茨海默病小鼠抗氧化作用的研究

目的:探讨大豆异黄酮活性组分对阿尔茨海默病(Alzheimer’sdisease,AD)小鼠的抗氧化作用。方法:取10月龄的小鼠,以D-半乳糖和三氯化铝复制AD模型小鼠,用本实验室制备的大豆异黄酮活性组分灌胃15d后,眼球取血,测定血清中超氧化物歧化酶(SOD)、乳酸脱氢酶(LDH)和丙二醛(MDA)的含量,观察脑内海马组织切片神经元细胞的形态改变。结果:与模型组小鼠相比,实验组小鼠血清SOD活力显著提高(P<0.01)、血清LDH含量显著升高(P<0.05)、血清MDA含量明显降低(P<0.01),海马区神经元细胞数量也显著增多,形态改善。结论:异黄酮活性组分能有效地改善衰老AD小鼠的抗氧化系统的功能。