诊断超声对人胚胎安全性的研究

目的　探讨诊断级B超对人胚胎发育的安全性。方法　取 12 0名孕 6～ 8周拟行人工流产孕妇 ,随机分成正常对照组 (Ⅰ组 )、辐照 5min(Ⅱ组 )、10min(Ⅲ组 )、2 0min(Ⅳ组 )、30min(Ⅴ组 )于 1h内取绒毛 ,超声辐照 30min(Ⅵ组 )于 7～ 10d后取绒毛。检测绒毛的生物化学变化。结果　诊断剂量超声辐照 2 0min可致人体宫内绒毛发生生物化学变化。丙二醛 (MDA)值随超声剂量增加而升高 (PⅠ -Ⅲ >0 .0 5,PⅠ .Ⅳ <0 .0 1,PⅠ -Ⅴ <0 .0 1) ,而超氧化物歧化酶及谷胱甘肽过氧化物酶活性随超声辐照剂量增加而下降 (PⅠ -Ⅲ >0 .0 5,PⅠ -Ⅳ <0 .0 1,PⅠ -Ⅴ <0 .0 1)。对照组与Ⅵ组比较P >0 .0 5,提示损伤作用是可逆性的。结论　诊断超声辐照时间 2 0min以上时对绒毛可造成潜在危害     

αB-晶状体蛋白在保护过氧化氢所致心肌细胞损伤中的作用

采用热休克对新生大鼠心肌细胞进行预处理 ,以诱导αB 晶状体蛋白的表达 ,并观察其对 1mmol·L- 1 的过氧化氢 (H2 O2 )所致心肌细胞损伤的保护作用。发现 :热休克预处理组心肌细胞中αB 晶状体蛋白表达明显增加 ,H2 O2 所致的细胞死亡率及LDH释放率降低 ,总抗氧化能力增强 ;H2 O2 可引起αB 晶状体蛋白从胞浆向胞核及微丝移位。提示热休克预处理的心肌细胞保护作用与其诱导αB 晶状体蛋白的表达增加有关。αB 晶状体蛋白可能通过细胞内移位 ,保护某些核结构 ,稳定细胞骨架 ,并增强心肌细胞抗氧化能力 ,从而发挥其保护作用     

愈肝汤对慢性乙肝患者脂质过氧化的影响

目的　探讨愈肝汤对慢性乙肝患者的脂质过氧化作用。方法　 43例慢性乙肝患者服愈肝汤治疗 3mo ,观察其治疗前后超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH -Px)活力和过氧化脂质(LPO)水平的变化 ,并与 38例健康对照组比较。结果　慢性乙肝患者SOD、GSH -Px活力降低 (P <0 .0 5 ) ,LPO水平升高 (P <0 .0 5 ) ;愈肝汤可升高SOD和GSH -Px酶活性 (P <0 .0 1) ,降低LPO水平 (P <0 .0 5 )。结论　愈肝汤对慢性乙肝患者有明显的抗脂质过氧化作用 ,这是其治疗慢性乙型肝炎、减轻肝细胞损伤的重要机理之一。     

绞股蓝总皂甙对严重烫伤大鼠胃、肠、肝组织中SOD、GSH-PX、ATPase、MDA含量的影响

观察严重烫伤大鼠胃、小肠、肝组织超氧化物歧化酶（ＳＯＤ）,谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）,丙二醛（ＭＤＡ）、ＡＴＰａｓｅ含量的变化及绞股蓝总皂甙（ＧＰ）的防治效果。方法：选用健康Ｗｉｓｔａｒ大鼠８５只,随机分成①正常对照组 （５只）;②烫伤对照组（４０只）;③烫伤治疗组（４０只）。烫伤后分别于４、８、２４、４８ｈ几个不同时相点（每个时相点１０只）取出胃、小肠、肝组织分别制成匀浆,测定ＳＯＤ、Ｇ     

火器伤合并海水浸泡兔肢体骨骼肌组织脂质过氧化反应

目的：观察兔肢体火器伤合并海水浸泡后,伤道周围骨骼肌过氧化脂质与抗氧化酶活力的 早期救治提供实验依据。方法 用滑膛枪发射２５０ｍｇ钢珠,致伤兔后肢,伤后将致伤兔随机分为两组：一组为海水浸泡组（ＳＩＧ）,将兔浸泡于粗制盐配制的人造海水中３０ｍｉｎ。另一组为单纯致伤组（ＳＷＧ）,伤后不浸泡海水。伤后３、６、１２、２４ｈ手术取距伤道边缘０．５ｃｍ（Ａ区）,１．５ｃｍ（Ｂ区）和２．５ｃｍ（Ｃ区）处肌组织,     

畅脉舒对家兔动脉粥样硬化的防治作用

目的 探讨畅永舒防治动脉粥样化（ＡＳ）的作用机制。方法 采用高胆固醇饲料喂养,建立家兔ＡＳ模型,随机分为对照组、模型组、地奥心血康组（地奥组）和畅脉舒用药组,每组在实验第１４周取血标本因脂、血清一氧化氮（ＮＯ）、血浆内皮素（ＥＴ）、环鸟苷酸（ｃＧＭＰ）、脂质过氧化物（ＬＰＯ）和超氧化物歧化酶（ＳＯＤ）等指标。结果 与模型组比较,畅脉舒及地奥组１３周后均胡提高ＮＯ,ｃＧＭＰ,高密度脂蛋白（ＨＤＬ－Ｃ     

Hydrogen peroxide-induced impairment of reactivity in rat isolated aorta: potentiation by 3-amino-1,2,4-triazole

1. In this study the impairment induced by hydrogen peroxide of vascular reactivity and the role of endogenous catalase in protection against this impairment was assessed in isolated rings of rat aorta.
2. Incubation with hydrogen peroxide at 1 mM, but not at 0.1 mM, for 15, 30 or 60 min followed by washout depressed, in a time-dependent manner, the subsequent ability of endothelium-containing and endothelium-denuded rings to contract to phenylephrine.
3. Incubation with 3-amino-1,2,4-triazole (50 mM, 90 min, followed by washout) to inhibit endogenous catalase had no effect by itself on subsequent phenylephrine-induced contraction. However, pretreatment with 3-amino-1,2,4-triazole did lead to a profound enhancement of the ability of hydrogen peroxide (1 mM, present for the final 30 min of the 90 min incubation, followed by washout) to depress phenylephrine-induced contraction in both endothelium-containing and endothelium-denuded rings.
4. Incubation with hydrogen peroxide at 1 mM, but not at 0.1 mM, for 15, 30 or 60 min followed by washout inhibited, in a time-dependent manner, the subsequent ability of acetylcholine (10 nM–3 μM) to induce endothelium-dependent relaxation. Furthermore, incubation with hydrogen peroxide 1 mM (30 min, followed by washout) also inhibited relaxation induced by glyceryl trinitrate (1–100 nM) or isoprenaline (10 nM–3 μM) in endothelium-denuded rings.
5. Incubation with 3-amino-1,2,4-triazole (50 mM, 90 min, followed by washout) had no effect by itself on relaxation induced by acetylcholine, glyceryl trinitrate or isoprenaline. In contrast, pretreatment with 3-amino-1,2,4-triazole led to profound enhancement of the ability of hydrogen peroxide (1 mM, present for final 30 min of the 90 min incubation) to block relaxation to acetylcholine, glyceryl trinitrate or isoprenaline.
6. On the basis of the actions of 3-amino-1,2,4-triazole, it is likely that endogenous catalase plays an important role in the protection of vascular reactivity of rat aorta against oxidant damage by high (1 mM) but not lower (0.1 mM) concentrations of hydrogen peroxide. The data are consistent with the promotion of non-selective damage to the vascular smooth muscle cells by hydrogen peroxide, but endothelial damage may also be sustained.

     

中老年人脾肾虚证与血脂及抗氧化物关系的探讨

采用前瞻性设计方案,利用现代先进的有针对性的指标,应用单因素及多因素综合分析方法,对７７３例中老年人进行脾肾虚证实质的研究。结果发现：中老年人肾虚证与脂质代谢紊乱、机体经物质减少、过氧化脂质增密切相关。同时发现,脾虚证到肾虚证是一个逐渐发展的病理过程,且有层次性。认为肾虚证脂质代谢紊乱程度高于脾虚证,脾虚证与机体抗氧化物减少无密切关系。     

Reactive oxidant species in piriform cortex extracellular fluid during seizures induced by systemic kainic acid in rats

Kainic acid (KA) administered systemically to rats produces seizures and brain damage. We measured an increase in reactive oxidant species (ROS) during KA-induced seizures in the extracellular fluid (ECF) of the piriform cortex, a brain region known to be subsequently damaged. Intracerebral microdialysis samples were collected and assayed for isoluminol-dependent chemiluminescence before and after injection of KA (16 mg/kg, ip). Hydrogen peroxide (H₂O₂) concentrations were calculated from catalase-sensitive chemiluminescence, the difference between total and catalase-resistant chemiluminescence. During generalized tonic-clonic seizures, both total and catalase-resistant chemiluminescence increased significantly in samples from brain ECF. Catalase-resistant chemiluminescence, most likely produced by ascorbic acid, increased for a full hour during sustained seizure activity. H₂O₂ concentrations showed a trend towards elevation during seizures. Increased ROS suggest that oxidative stress occurs in brain ECF during sustained seizure activity.     

Cytotoxic Effect of Brain Macrophages on Developing

Brain macrophages are transiently present in different regions of the central nervous system during development or in the course of tissue remodelling following various types of injuries. To investigate the influence of these phagocytes on neuronal growth and survival, brain macrophages stemming from the cerebral cortex of rat embryos were added to neuronal primary cultures. A neurotoxic effect of brain macrophages was demonstrated by the reduction of the number of neurons bearing neurites within two days of contact between the two cell types. Neuronal death and phagocytosis were also directly observed in video recordings of living cultures. This toxicity involved the production by brain macrophages of reactive oxygen intermediates, as shown by the protective effect of catalase, a scavenger of H2O2. In addition, the respiratory bursts of brain macrophages were stimulated in the presence of neurons. These results suggest that brain macrophages could favour the appearance of neuroregressive events which occur either during neurogenesis or in neurodegenerative diseases, implying intracerebral recruitment of mononuclear phagocytes.