五丹胃福汤对慢性萎缩性胃炎模型大鼠自由基水平的影响

目的 :研究五丹胃福汤对慢性萎缩性胃炎的作用机制。方法 :用 Wistar大鼠 75只随机分为 5组 ,即正常对照组、造模组、自然恢复组、小剂量治疗组和大剂量治疗组 ,治疗组给予五丹胃福汤进行干预 ,采用单一试剂法检测大鼠胃粘膜及血清超氧化物歧化酶 (SOD)与丙二醛 (MDA)。结果 :五丹胃福汤能够增强萎缩性胃炎大鼠胃粘膜及血清 SOD水平而降低 MDA水平 ,从而减轻自由基对胃粘膜的损害。结论 :五丹胃福汤可有效调节血清及胃粘膜的自由基水平 ,是本方有效治疗萎缩性胃炎的作用机制之一。     

血清TSH测定与纸片TSH测定的对比观察

观察了６３例正常成人血清ＴＳＨ与纸片ＴＳＨ关系，并与１０４例新生儿纸片ＴＳＨ进行对比分析。结果表明，成人血清ＴＳＨ与纸片ＴＳＨ无显著性差异；成人纸片ＴＳＨ与新生儿纸片ＴＳＨ也无显著性差异。提示纸片ＴＳＨ测定可代替血清ＴＳＨ测定用于碘缺乏病的人群监测。     

慢性肺源性心脏病红细胞超氧化物歧化酶脂质过氧化物的变化及意义

目的：观察慢性肺源性心脏病（肺心病）急性加重期及临床缓解期、阻塞性肺气肿急性加重期患者红细胞超氧化物歧化酶（SOD）、脂质过氧化物（LPO）的变化及其与动脉血气分析的关系。方法测定健康对照者及慢性肺心病急性加重期及临床缓解期、肺气肿急性加重期患者的血SOD、LPO和动脉血气分析。结果慢性肺心病及肺气肿急性加重期的红细胞SOD含量均明显低于健康对照组（P<0.01,P<0.01）,慢性肺心病临床缓解期红细胞SOD含量高于急性加重期（P<0.05）。慢性肺心病及肺气肿急性加期的红细胞LPO含量均明显高于健康对照组（P<0.01,P<0.01）,慢性肺心病临床缓解期红细胞LPO含量低于急性加重期（P<0.01）。慢性肺心病红细胞SOD与血pH、氧饱和度（SaO2）呈负相关,与二氧化碳分压（PaCO2）呈正相关。结论阻塞性肺气肿和肺心病患者存在自由基代谢紊乱,在一定范围内,血PaCO2升高、血pH和PaO2的降低可影响红细胞SOD含量。     

Patient-Physician Agreement Using Summary Outcome Determination Scores

Objective

To determine whether the Summary Outcome Determination (SOD) score had exhibited a high level of physician-patient agreement in surgical patients.

蒙成药阿那日一4对大鼠幽门结扎性胃溃疡的影响

目的：探讨蒙成药阿那日-4对大鼠幽门结扎性胃溃疡的影响。方法：通过幽门结扎性胃溃疡大鼠模型,并测定血清丙二醛（MDA）、超氧化物歧化酶（SOD）含量、胃液量、胃酸浓度、胃蛋白酶活性来考察蒙成药阿那日-4对该模型胃溃疡的影响结果：各给药组与模型组比较SOD含量均有明显增高（分别为P〈0．05、P〈0．01、P〈0．01）;MDA含量均明显降低（分别为P〈0．05、P〈0．05、P〈0．01）;比较胃液量及蛋白酶活性均有明显降低（分别P〈0．01、P〈0．05）;对胃酸的影响从数据来看具有降低的趋势但没有显著影响。结论：通过数据来看初步判断蒙成药阿那日-4-对幽门结扎性胃溃疡大鼠具有胃黏膜保护作用。     

复合刺激对亚健康大鼠模型耐疲劳能力及血清SOD、MDA的影响

目的:观察复合刺激对亚健康大鼠模型耐疲劳能力及其血清SOD、MDA的影响.方法:采用游泳运动、睡眠剥夺和夹尾刺激等复合因素制造亚健康大鼠模型,检测动物体重、进食量、耐疲劳能力及血清SOD、MDA等指标的变化.结果:模型组动物体重低于正常组,饮水量、进食量均明显少于正常组,5 min内不动时间明显多于正常组,血清SOD活性明显低于正常组,MDA明显高于正常组.结论:复合因素造模法兼顾了亚健康的成因和表现,模型动物的宏观表现和微观指标均具备亚健康的基本特征,该造模方式具有一定的科学性和合理性.     

超声靶向微泡破坏对支持细胞的生物学效应研究

目的:探讨超声靶向微泡破坏对体外培养大鼠支持细胞的影响.方法:分离与培养大鼠支持细胞,制作细胞悬液,添加0.01ml微泡造影剂后即行超声辐照,超声辐照时间为60s,输出声强为0.5W/cm~2,频率为1MHz,分别取照射后5min,2、6、12、24h作为分组时间点,在各时间点及进行波形蛋白免疫组化染色、测定细胞超氧化物歧化酶(Superoxide dismutase,SOD)、丙二醛(Malondialdehyde,MDA)以及细胞计数.结果:超声联合微泡可以降低支持细胞内波形蛋白的表达,引起细胞内早期MDA含量可逆性升高,SOD活性下降,后期(24h)MDA含量恢复正常,SOD活性升高,而支持细胞的存活不受影响.结论:超声靶向微泡破坏支持细胞的结构和功能引起可逆性损伤,通过降低支持细胞紧密连接蛋白的表达从而开放血睾丸屏障,继而影响生精细胞功能,为男性避孕的研究提供新的思路.     

明目地黄丸对白内障大鼠晶状体内SOD、MDA影响的实验研究

[目的] 研究明目地黄丸对白内障大鼠晶状体中超氧化物歧化酶(SOD) 活性和丙二醛(MDA)含量的影响。[方法] 建立大鼠白内障模型, 采用黄嘌呤氧化酶法和硫代巴比妥酸(TBA)法对模型组、治疗组及对照组大鼠晶状体中SOD活性和MDA含量进行检测。[结果] 明目地黄丸高、中剂量组大鼠晶状体中MDA含量明显低于模型组, 高、中剂量组大鼠晶状体中SOD活性明显高于模型组, 差异具有显着性(P<0.05).[结论] 明目地黄丸能明显降低白内障大鼠晶状体中MDA含量, 且能明显升高白内障大鼠晶状体中SOD活性。     

Nrf2/ARE is the potential pathway to protect Sprague–Dawley rats against oxidative stress induced by quinocetone

3-methyl-2-quinoxalin benzenevinylketo-1, 4-dioxide (Quinocetone, QCT) is a newly used veterinary drug which has been proven to promote feed efficiency and growth of animals; however, its potential toxicity can’t be ignored. Therefore, the present study was aimed to investigate the nephrotoxicity of QCT and the oxidative stress induced by it. Sprague–Dawley rats (SD rats) were randomly divided into four groups with doses of 2400, 800, 50 and 0 mg/kg/day with administration of QCT for 4 weeks. Results proved that QCT could induce nephrotoxicity and this phenomenon had dose dependent manner. Simultaneously, this phenomenon was accompanied by intracellular reactive oxygen species (ROS) accumulation, enhanced lipid peroxidation and inhibited antioxidant system, i.e. glutathione S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GSH). Additionally, the higher expression of Nrf2 in QCT treated groups illustrated that QCT-induced oxidative stress would be partly mitigated by the induction of phase II detoxifying enzymes via increasing Nrf2 expression.     

Impairment of autophagy: From hereditary disorder to drug intoxication

At first, the molecular mechanism of autophagy was unveiled in a unicellular organism Saccharomyces cerevisiae (budding yeast), followed by the discovery that the basic mechanism of autophagy is conserved in multicellular organisms including mammals. Although autophagy was considered to be a non-selective bulk protein degradation system to recycle amino acids during periods of nutrient starvation, it is also believed to be an essential mechanism for the selective elimination of proteins/organelles that are damaged under pathological conditions. Research advances made using autophagy-deficient animals have revealed that impairments of autophagy often underlie the pathogenesis of hereditary disorders such as Danon, Parkinson's, Alzheimer's, and Huntington's diseases, and amyotrophic lateral sclerosis. On the other hand, there are many reports that drugs and toxicants, including arsenic, cadmium, paraquat, methamphetamine, and ethanol, induce autophagy during the development of their toxicity on many organs including heart, brain, lung, kidney, and liver. Although the question as to whether autophagic machinery is involved in the execution of cell death or not remains controversial, the current view of the role of autophagy during cell/tissue injury is that it is an important, often essential, cytoprotective reaction; disturbances in cytoprotective autophagy aggravate cell/tissue injuries. The purpose of this review is to provide (1) a gross summarization of autophagy processes, which are becoming more important in the field of toxicology, and (2) examples of important studies reporting the involvement of perturbations in autophagy in cell/tissue injuries caused by acute as well as chronic intoxication.