阿折地平降压效果评价及其抑制动脉粥样硬化的作用

目的： 探讨长效二氢吡啶类（DHPS）降压药物阿折地平对高血压病患者的降压效果及对血浆超敏C反应蛋白（hs-CRP）、超氧化物歧化酶（SOD）、6-酮前列腺素F1α（6-keto-PGF1α）水平的影响,阐明阿折地平的降压效果及其抑制动脉粥样硬化（As）的作用。方法：48例高血压病患者随机分为阿折地平组(24例) 和氨氯地平组(24例),2 组患者经过2 周药物洗脱期后,分别给予8 周的阿折地平（8～16 mg/d）或苯磺酸氨氯地平（安内真,5～10 mg/d）治疗,治疗前后检测患者血压、血液生化指标及血浆hs-CRP、SOD、6-keto-PGF1α水平并进行比较。结果：2组患者治疗后收缩压（SBP）和舒张压（DBP）均显著下降,阿折地平组血压降低总有效率为87.5%,氨氯地平组为91.7%,2组比较差异无统计学意义（P>0.05）。2组患者治疗前后血液生化指标比较差异无统计学意义（P>0.05）。2组患者治疗前血浆hs-CRP、SOD和6-keto-PGF1α水平比较差异无统计学意义（P>0.05）;与治疗前比较,2组患者治疗后hs-CRP显著下降（P<0.05）,SOD显著升高（P<0.05）;阿折地平组患者6-keto-PGF1α在治疗后有升高趋势（P<0.05）,而氨氯地平组患者则无明显变化（P>0.05）。结论： 阿折地平具有显著的降压疗效,同时对As有抑制作用。     

微波辐射对人宫颈癌HeLa细胞的增殖抑制作用及其机制

目的 : 探讨不同强度微波辐射对人宫颈癌HeLa细胞的增殖抑制作用及对氧化应激水平的影响,阐明微波辐射对人宫颈癌HeLa细胞的增殖抑制作用机制。方法：分别以强度为2.5、5.0、10.0、15.0和20.0 mW/cm的微波处理HeLa细胞20 min作为不同剂量辐射组,同时设立假辐射组（0 mW/cm）作为对照组,采用倒置显微镜观察细胞形态改变;MTT法检测微波辐射对细胞增殖的抑制情况;试剂盒测定辐射后细胞超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量;Western blotting法检测细胞内核转录因子-κB(NF-κB)和热休克蛋白70(HSP 70)表达水平。结果：各剂量微波辐射组HeLa细胞数量明显减少,细胞皱缩变形,体积缩小,随着辐射强度的增加变化愈明显; 2.5、5.0、10.0、15.0和20.0 mW/cm强度的微波作用细胞24 h,HeLa细胞的增殖抑制率均明显高于对照组（P<0.05）; 微波辐射后细胞内MDA含量随着辐射强度的增加,与对照组细胞比较呈上升趋势,各剂量辐射组HeLa细胞SOD活性较对照组显著下降（P<0.05）。Western blotting检测,微波辐射后细胞内HSP 70表达水平呈增加趋势,而NF-κB蛋白的表达水平呈明显的下降趋势。结论: 微波辐射对人宫颈癌HeLa细胞增殖具有抑制作用,其可能机制是改变细胞内氧化及抗氧化平衡。     

自拟活血通脉灵对心肌缺血大鼠SOD活性和MDA含量的影响

目的探讨活血通脉灵(HXTML)对异丙肾上腺素(ISO)所致心肌缺血大鼠心肌超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量的影响。方法将50只Wistar雄性大鼠随机分为空白对照组、模型组、阿司匹林组及活血通脉灵大剂量治疗组(HXTMLmax)和小剂量治疗组(HXTMLmin),采用ISO复制心肌缺血模型,观察心肌组织中SOD活性和MDA含量的变化。结果与空白对照组比较,模型组SOD活性明显下降,MDA含量增加(P<0.01);与模型组比较,阿司匹林组、HXTMLmax组和HXTMLmin组SOD活性增高、MDA含量降低(P<0.05或P<0.01);与阿司匹林组比较,HXTMLmax组和HXTMLmin组SOD活性升高、MDA含量下降(P<0.05,P<0.01);而HXTMLmax组与HXTMLmin组比较,差异无统计学意义(P>0.05)。结论活血通脉灵能提高心肌缺血损伤大鼠心肌组织中SOD活性,降低MDA含量,具有一定抗心肌氧化损伤作用。     

褪黑素对脊髓损伤早期大鼠神经生长因子表达的影响

目的:通过观察褪黑素(MT)对脊髓损伤(SCI)早期大鼠体内神经生长因子(NGF)表达的影响,探讨MT治疗SCI的机制。方法:60只成年SD大鼠随机分为3组:模型组、MT组和假手术组,每组20只。前2组以改良的Allen’sWD法建立脊髓T12水平损伤模型,假手术组仅行椎板切除不损伤脊髓。MT组于术后10min腹腔注射MT100mg/kg,模型组则腹腔注射等体积无水乙醇。术后12h对3组大鼠进行BBB运动功能评分后处死,取血液检测NGF水平;取脊髓标本进行病理观察,RT-PCR法检测NGFmRNA,免疫组化SP法检测NGF蛋白。结果:模型组和MT组大鼠于术后均出现了严重的下肢神经功能障碍,2组的BBB运动功能评分差异无统计学意义(P>0.05)。MT组脊髓组织病理变化较模型组减轻。3组大鼠脊髓内NGFmRNA、NGF蛋白表达水平和血清NGF水平差异均有统计学意义(F=336.819,321.762和122.707,P均<0.001),3者均在MT组中最高,SCI组次之,假手术组最低(P<0.01)。结论:MT可通过提高SCI大鼠体内NGF的表达减轻SCI。     

参姜锁阳益气片抗疲劳作用机制的研究

目的探索参姜锁阳益气片抗疲劳的作用机制。方法选择在-30℃以下的某地区驻训部队官兵210例,按随机数字表法分为两组:参姜锁阳益气片组130例和对照组80例,参姜锁阳益气片组口服参姜锁阳益气片,对照组口服安慰剂,服药前、服药2周后野外长跑3 000 m后观察各项客观指标的变化。结果①参姜锁阳益气片组血乳酸水平服药后为(3.03±1.95)mol/L,与服药前相比明显降低(P<0.05);②参姜锁阳益气片组血清乳酸脱氢酶、磷酸肌酸激酶水平服药后与服药前相比差异有统计学意义(P<0.05);③参姜锁阳益气片组运动后超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量服药后与服药前相比显著降低(P<0.05)。结论参姜锁阳益气片可增强人体的运动适应能力,具有抗疲劳作用,该作用可能与其增强机体的抗氧化能力有关。     

阿托伐他汀对动脉粥样硬化兔氧化应激/炎症反应的影响

目的通过研究氧化应激和炎症反应探讨阿托伐他汀治疗动脉粥样硬化的非调脂作用机制。方法以高脂饲料和免疫刺激方法制备动脉粥样硬化家兔模型,给予0.435 mg/(kg.d)阿托伐他汀混悬液治疗1个月,观察家兔血清超氧化物歧化酶活性、丙二醛和氧化型低密度脂蛋白含量以及血凝素样氧化型低密度脂蛋白受体1、主动脉血管细胞黏附分子1、细胞间黏附分子1、单核细胞趋化蛋白1基因和蛋白表达的变化。结果与正常对照组比较,动脉粥样硬化模型组家兔血清超氧化物歧化酶活性显著下降(P<0.01),血清丙二醛、氧化型低密度脂蛋白含量明显升高(P<0.01);主动脉血凝素样氧化型低密度脂蛋白受体1、血管细胞黏附分子1、细胞间黏附分子1、单核细胞趋化蛋白1的mRNA和蛋白表达明显升高(P<0.05或P<0.01)。与模型组比较,阿托伐他汀组家兔血清超氧化物歧化酶活性显著升高(P<0.01),血清丙二醛、氧化型低密度脂蛋白含量均显著下降(P<0.01),主动脉血凝素样氧化型低密度脂蛋白受体1、血管细胞黏附分子1、细胞间黏附分子1、单核细胞趋化蛋白1的mRNA和蛋白表达明显下调(P<0.05或P<0.01)。结论阿托伐他汀具有抗氧化应激和炎症反应的作...     

丹参粉针剂对高血压病患者氧自由基、纤溶活性、一氧化氮的干预作用

目的：探讨丹参粉针剂对原发性高血压病（EH）患者氧自由基、纤溶活性、一氧化氮的干预作用。方法：测定80例EH患者血浆丙二醛（MDA）、超氧化物歧化酶（SOD）、组织型纤维酶原激活物（t-PA）,t-PA抑制剂（PAI）及一氧化氮（NO）,随机分为常规治疗对照组（40例,予左旋氨氯地平75 mg/d降压治疗）;观察组（40例,在常规治疗对照组的基础上加用丹参粉针剂400mg加入250ml 5%葡萄糖注射液中静脉滴注,1次/d）,治疗2周后测定并比较两组治疗前后MDA、SOD、t-PA、PAI及NO水平的变化。结果：治疗前两组MDA、SOD、t-PA、PAI及NO水平比较无显著性差异（P〉0.05）。常规治疗对照组治疗前后上述指标无显著性差异（P〉0.05）。与治疗前比较,观察组治疗后MDA[（5.66±1.30）μmol/L∶（3.86±0.88）μmol/L]、PAI[（5.67±2.15）AU/ml∶（2.65±1.10）AU/ml]水平明显下降（P〈0.01）,且明显低于常规治疗对照组治疗后水平（P均〈0.01）,而SOD[（87.4±21.6）U/L∶（138.2±18.9）U/L],t-PA[（0.67±0.3）IU/ml∶（1.23±0.46）IU/ml],NO[（7.58±2.66）μmol/L∶（12.86±3.61）μmol/L]水平则明显升高（P〈0.01）,且明显高于常规治疗对照组治疗后水平（P均〈0.01）。结论：丹参粉针剂能提高患者的超氧化物歧化酶活力,降低丙二醛含量,促进纤溶活性及增加一氧化氮合成、释放。     

Single‐nucleotide polymorphisms within the antioxidant defence system and associations with aggressive prostate cancer

What’s known on the subject? and What does the study add? Prior studies have identified potential interaction effects between antioxidant nutrients and germline gene variants with regards to prostate cancer risk. In particular, the rs4880 gene variant in SOD2 (or MnSOD) has been linked to several cancers, including prostate, and appears to interact with antioxidant status and cancer risk. We identified additional variants in SOD2 and SOD1 that may affect risk of prostate cancer, or interact with selenium status to affect prostate cancer risk.

OBJECTIVE

To study the effects of oxidative stress on prostate cancer development as the exact biological mechanisms behind the relationship remain uncertain. We previously reported a statistically significant interaction between circulating selenium levels, variants in the superoxide dismutase 2 gene (SOD2; rs4880), and risk of developing prostate cancer and presenting with aggressive prostate cancer.

PATIENTS AND METHODS

We genotyped men with localized/regional prostate cancer for 26 loci across eight genes that are central to cellular antioxidant defence: glutathione peroxidase (GPX1, GPX4), peroxisome proliferator‐activated receptor γ coactivator (PPARGC1A, PPARGC1B), SOD1, SOD2, and SOD3, and ‘X‐ray repair complementing defective repair in Chinese hamster cell 1’ (XRCC1). Among 489 men, we examined the relationships between genotypes, circulating selenium levels, and risk of presenting with aggressive prostate cancer at diagnosis, as defined by stage, grade and prostate‐specific antigen (PSA) level (213 aggressive cases).

RESULTS

Two variants in SOD2 were significantly associated with the risk of aggressive prostate cancer (rs17884057, odds ratio 0.83, 95% confidence interval 0.70–0.99; and rs4816407, 1.27, 1.02–1.57); men with A alleles at rs2842958 in SOD2 had lower plasma selenium levels (median 116 vs 121.8 µg/L, P= 0.03); and the association between plasma selenium levels and risk of aggressive prostate cancer was modified by SOD1 (rs10432782) and SOD2 (rs2758330).

CONCLUSION

While this study was cross‐sectional and these associations might be due to chance, further research is warranted on the potential important role of antioxidant defence in prostate cancer.     

Sodium selenite protects against diabetes-induced alterations in the antioxidant defense system of the liver

BACKGROUND: Free radical genesis of disorder is one of the major subjects of discussion in the explanation of pathological conditions. In this study, the effects of micro molar quantities of sodium selenite treatment on diabetes-induced alterations in the antioxidant defense system were investigated. METHODS: Diabetes was induced by administration of streptozotocin (STZ, 50 mg/kg body weight) and both diabetic and control animals were treated with sodium selenite (5 micromol/kg/day) for 4 weeks. RESULTS: Our results have shown that induction of diabetes in the liver tissue of animals for 5 weeks resulted in decreased superoxide dismutase (SOD), glutathione reductase (GR) and glutathione peroxidase (GSHPx) activities and concomitantly increased lipid peroxidation (LPO). CONCLUSION: Sodium selenite treatment of the diabetic rats resulted in almost full restoration of all the parameters mentioned above. Metallothionein, which is known to be one of the major antioxidants and a central protein in heavy metal regulation, is altered by diabetes, and sodium selenite treatment restored this alteration as well.     

Chronic schisandrin B treatment improves mitochondrial antioxidant status and tissue heat shock protein production in various tissues of young adult and middle-aged rats

The effects of chronic schisandrin B (Sch B) treatment (10 mg/kg/day×15) on mitochondrial antioxidant status and sensitivity to Ca²⁺-induced permeability transition, as well as tissue heat shock protein (Hsp)25/70 production were examined in various tissues (brain, heart, liver, skeletal muscle) of young adult and middle-aged female rats. Age-dependent impairment in mitochondrial antioxidant status, as assessed by levels/activities of antioxidant components (reduced glutathione, α-tocopherol, Se-glutathione peroxidase and Mn-superoxide dismutase) and the extent of reactive oxygen species generation in vitro, was observed in brain, heart, liver and skeletal muscle tissues. While tissue Hsp25 levels remained relatively unchanged with aging, the Hsp70 level was increased in both brain and heart tissues of middle-aged rats. Chronic Sch B treatment was able to enhance mitochondrial antioxidant status and the resistance to Ca²⁺-induced mitochondrial permeability transition in an age-independent manner in various tissues of rats. However, Hsp25 and Hsp70 levels were only increased in young adult rats. The Sch B-induced enhancement of mitochondrial protective parameters in the heart was associated with the protection against myocardial ischemia-reperfusion injury in both young adult and middle-aged rats. The results suggest that chronic Sch B treatment may be beneficial for reversing the mitochondrial changes with aging and enhancing the heat shock response.