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Effect of acupuncture on free radicals after spinal cord injury was observed in rats with experimental spinal cord injury (SCI). Results indicated that within 24 hours after SCI malondialdehyde (MDA) increased progressively, 2 hours after SCI it reached the peak; and the superoxide dismutase (SOD) activity decreased significantly at the same hours, the decrease being the most marked 2-6 hours after SCI. The MDA content in the acupuncture group was significantly lower (P<0.05) and the SOD activity higher (P<0.01) than that of the control group respectively. It is suggested that acupuncture inhibits production of MDA and increases the SOD activity.
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终末期肾病的DNA氧化损伤
大量研究表明,在终末期肾病(End-Stage Renal Disease,ESRD)存在氧化损伤增强及抗氧化能力减弱,其结果是肾功能进一步恶化和各种并发症(包括心血管疾病、贫血、淀粉样变性、肿瘤等)出现.氧自由基(Oxygen Free Radicals,OFR)可引起细胞内任何结构及分子的氧化损伤,其中DNA是一个重要的靶物质.DNA氧化损伤的方式包括嘌呤、嘧啶、核苷酸的修饰和DNA 单/双链的断裂及链内交联等.其中碱基修饰是DNA氧化损伤的主要形式,而绝大部分的碱基损伤部位位于鸟嘌呤脱氧核苷酸的C-8位置,形成8-羟基脱氧鸟苷(8-OHdG).迄今为止,在已发现了20余种的DNA氧化损伤产物中[1],8-OHdG因其形成的量大,影响的因素少,检测相对简单和相对敏感,已被公认为能反映体内DNA氧化损伤程度的理想生物标志物.
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门奇静脉断流术对门脉高压症一氧化氮及氧自由基的影响
目的:探讨NO系统、OFR系统对门脉高压症(PHT)的影响及门奇静脉断流术的作用.方法:门脉高压症患者19例,肝功能A级9例,B级10例;正常对照组15例.术前、术后d3晨空腹抽静脉血应用硝酸盐还原酶法测定NO,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD),比色法测定一氧化氮和酶(NOS),硫代巴比妥酸(TBA)法测定丙二醛(MDA)结果:肝硬化PHT患者术前血清NO(μmol.L-1)含量、NOS活性(kU.L-1)A级分别为63.8±10.7,26.3±7.9,B级分别为79.2±14.8,36.7±9.0,较正常对照组32.7±6.2,12.5±4.1显著升高(P<0.01);术前肝功能B级No、NOS较A级显著升高(P<0.01);门奇静脉断流术后3d NO、NOS A级分别为40.2±9.4,16.9±5.3,B级分别为58.7±12,26.6±6.5与术前比均有显著降低(P<0.05,P<0.01),但仍高于正常对照组(P<0.05,P<0.01);且门奇静脉断流术后肝功能A级的NO、NOS的下降幅度分别为37.0%,35.8%较B级的25.8%,26.3%明显.肝硬化PHT患者术前血清SOD活性(kNU.L-1)A、B级分别为70 5±16.7,53.3±1.1均较正常对照组119 1±20.1显著降低(P<0.01);而PHT患者术前血清MDA含量(μmol L-1)A、B级分别为21.4±4.8,32 6±6.3则显著高于对照组6.7±2 0(P<0.01);术前肝功能B级SOD、MDA与A级比也有显著性差异(P<0.01,P<0 05);门奇静脉断流术后3d,A、B级MDA分别为10.3±30,20.4与术前比均有显著降低(P<0.05);而SOD术后3d A、B级分别为101.0±21 1,72.7±17.3显著高于术前(P<0.01,P<0.05);但MDA仍高于正常对照组(P<0.01),SOD仍低于正常对照组(P<0 01,P<0.05);且门奇静脉断流术后肝功能A级SOD、MDA的改变幅度(分别为43.4%和51.79%)较B级(分别为36.3%和37.7%)明显.结论:NO、NOS、OFR、SOD的变化在肝硬化门脉高压症的形成过程中起重要作用;且随肝功能的恶化上述各参数的变化越明显;门奇静脉断流术能逆转上述各参数的变化,且肝功能A级者术后的变化率高于肝功能B级.
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In addition to its lipid-lowering effect, atorvastatin exerts anti-inflammatory and antioxidant effects as well. In this study, we hypothesized that atorvastatin could protect against cerebral isch-emia/reperfusion injury. The middle cerebral artery ischemia/reperfusion model was established, and atorvastatin, 6.5 mg/kg, was administered by gavage. We found that, after cerebral ischemia/reperfusion injury, levels of the inflammation-related factors E-selectin and myeloperoxidase were upregulated, the oxidative stress-related marker malondialdehyde was increased, and super-oxide dismutase activity was decreased in the ischemic cerebral cortex. Atorvastatin pretreatment signiifcantly inhibited these changes. Our ifndings indicate that atorvastatin protects against ce-rebral ischemia/reperfusion injury through anti-inlfammatory and antioxidant effects.
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Previous experimental studies have shown that cerebral infarction can be effectively reduced following treatment with scutellaria baicalensis stem-leaf total lfavonoid (SSTF). However, the mechanism of action of SSTF as a preventive drug to treat cerebral infarction remains unclear. In this study, Sprague-Dawley rats were pretreated with 50, 100, 200 mg/kg SSTF via intragastric ad-ministration for 1 week prior to the establishment of focal cerebral ischemia/reperfusion injury. The results showed that pretreatment with SSTF effectively improved neurological function, re-duced brain water content and the permeability of blood vessels, ameliorated ischemia-induced morphology changes in hippocampal microvessels, down-regulated Fas and FasL protein expres-sion, elevated the activity of superoxide dismutase and glutathione peroxidase, and decreased malondialdehyde content. In contrast to low-dose SSTF pretreatment, the above changes were most obvious after pretreatment with moderate-and high-doses of SSTF. Experimental ifndings indicate that SSTF pretreatment can exert protective effects on the brain against cerebral isch-emia/reperfusion injury. The underlying mechanisms may involve reducing brain water content, increasing microvascular recanalization, inhibiting the apoptosis of hippocampal neurons, and attenuating free radical damage.
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噪声暴露引起耳蜗损伤机制的研究
噪声是常见的职业性伤害和听力致残因素,预防噪声性耳聋的发生及降低其听觉损害的程度一直是我们研究的重要课题。近年的研究发现噪声暴露可引起耳蜗内活性氧、活性氮自由基及金属蛋白酶增加,毛细胞内DNA损伤,Caspase-3激活,AIF及EndoG的转移等一系列变化,终导致毛细胞死亡,以凋亡为主。噪声损伤机制的研究为预防和治疗噪声性耳聋开辟了新的思路。
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氧自由基与心血管系统疾病的关系
氧自由基(oxygen free radicals,OFR)与心血管系统疾病的关系密切,现综述如下.1病毒性心肌炎
关键词: 氧自由基 心血管系统疾病 free radicals 病毒性心肌炎 -
内源性一氧化氮对肝缺血/再灌注损伤保护作用的实验研究
近年来,肝移植的开展及肝门阻断术的临床应用越来越广泛,但在肝移植或肝门阻断再开放过程中始终存在着缺血/再灌注损伤,而且是导致术后肝功能不全的一个重要因素.以往实验证实,氧自由基(oxygen free radicals, OFR )在肝缺血/再灌注损伤(hepatic ischemia/reperfusion injury, HIRI)中起重要的介导作用.而一氧化氮(nitric oxide, NO)在HIRI中起何作用,目前国外尚无一致的意见:国内未见详细报道.
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早期肠道营养对烧伤大鼠模型内脏缺血损害的效应
AIM:To compare the effects of early enteral nutrition and early parenteral nutrition on ameliorating visceral ischemia and relieving free radical damage.METHODS:66 Wistar rats were divided into 3 groups: control group(C),parenteral nutrition group( PN) and enteral nutrition group( EN), PN and EN groups made up of 30% TBSAⅢ degree burn model.We delivered nutrient solution with same calorie and calorie- nitrogen ratio via vein or enteral tract respectively.Blood flow of liver,kidney and change of SOD of heart,liver and kidney at 6,12,24,48,72 h after burn were tested.RESULTS:Tissue blood flow and SOD of EN group were higher than those of PN group in many phase( P< 0.05-0.01) .CONCLUSION: Early enternal nutrition can relieve the increase of visceral vascular permeability and damage of oxygen free radical.
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自由基损害与红细胞免疫功能状态对急性脑血管病预后的影响
Background: Recent studies show free radicals play an important role in pathogenesis of brain infarction. Over formation of free radicals damage neurons primarily and secondly. A series of free radical reaction accounts from the most part during generation and necrosis due to brain ischemia and reperfusion. Changes in free radicals and immunological state of red cells will affect prognosis in patients with cerebral infarction.
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支气管哮喘患者红细胞膜流动性与氧自由基关系的研究
膜流动性是生物膜结构的基本特征.氧自由基(oxygen free radicals,OFR)诱发脂质过氧化及其代谢产物如丙二醛(malony dialdehyde,MDA)作用于红细胞后,使红细胞膜流动性降低,寿命缩短[1].本研究的目的在于探讨支气管哮喘(简称哮喘)患者血红细胞膜流动性与氧自由基之间的关系.
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氧自由基在家兔低血容量性休克-再灌注损伤中的作用及地塞米松干预
目的:探讨地塞米松对低血容量性休克-再灌注氧自由基(oxygen free radicals ,OFR) 导致脏器损伤的治疗作用.方法:制备家兔低血容量性休克模型,随机分为地塞米松保护组 (II组)和未用地塞米松的非保护组(I组),检测血浆和组织丙二醛(MDA)含量及平均动脉压(MAP)值.结果:休克前2组动物MDA及MAP均无统计学差异.休克90 min时2组动物M DA明显升高(II组为5.31±0.17 kPa, I组为5.27±0.14 kPa, , P<0.01),休克-再灌注后,I I组MDA均逐渐下降,休克-再灌流3小时后接近休克前水平(5.79±0.72 μmol/L, P< 0.05), 明显低于休克90 min(8.14±0.91 μmol/L, P<0.01)和I组同时相水平(9.30±0 .96 μmol/L, P< 0.01), II组为8.14±0.91 μmol/L, I组为8.06±0.88 μmol/L, P<0.01, MAP均显著下降(I I组为II组MAP逐渐上升,休克-再灌注3小时后接近休克前水平(11.96±1.63 kPa, P >0.05) ,明显高于休克90 min(5.31±0.17 kPa, P<0.01)和I组同时相水平(8.22±1 .30 k Pa, P<0.01).此外,II组心、肺、肝、肾、肠道组织MDA含量均明显低于I组(P <0.05, P< 0.01).结论:地塞米松可降低OFR水平,减轻脂质过氧化反应,对休克-再灌注损伤起良好的防护作用 .