噻虫胺胁迫对小白菜中谷胱甘肽和蛋白质含量的影响

目的 寻找较敏感的生物标记物,作为噻虫胺污染蔬菜的早期诊断指标.方法 谷胱甘肽(GSH)含量测定采用Ellman法.可溶性蛋白质含量测定采用考马斯亮蓝.结果 在胁迫初期GSH含量急剧降低,低浓度处理组GSH含量在第5天下降到最低点,高浓度处理组GSH含量在第7天下降到最低点.处理组的蛋白质含量均明显低于对照组,浓度越高...     

慢性心力衰竭患者血浆谷胱甘肽抗氧化系统的变化及意义

目的研究慢性心力衰竭（CHF）患者血浆谷胱甘肽抗氧化系统的改变及其临床意义。方法选择2006年1月至2006年9月收住我院心内科慢性心力衰竭的住院患者53例为观察组，门诊体检健康者25例为对照组。按NYHA心功能分级将CHF组分为心功能Ⅱ级组（n=11例），心功能Ⅲ级组（n=15例），心功能Ⅳ级组（n=27例）。所有患者均于入院后第2天采空腹静脉血，应用酶循环法测定血浆还原型谷胱甘肽（GSH）、氧化型谷胱甘肽（GSSG）浓度，根据Nemst公式计算氧化还原电位（EhGSH/GSSG）。结果①CHF组血浆GSH浓度较对照组明显下降（5．23±0．77）umol／L VS（6．52±1．02）umol]L，P〈0．05）；CHF组血浆GSSG浓度高于对照组（1．51±0．24）umol／L vs（1．16±0．53）umol／L，P〈0．05，CHF组EhGSH/GSSG值较对照组升高（-122．92±4．37）mV vs（-133．67±3．49）mV，P〈0．05。②CHF各亚组患者血浆GSH浓度、GSSG浓度、EhGSH/GSSG值在心功能Ⅱ级组与Ⅲ、Ⅳ级组之间有显著性差异（P〈0．05），Ⅲ、Ⅳ级组之间无差异。结论心衰时存在氧化应激，机体的抗氧化作用减弱；血浆GSH浓度、GSSG浓度及EhGSH/GSSG值均与心功能存在相关性，可作为反映心功能的指标。     

Antioxidative and hepatoprotective effect of CGX, an herbal medicine, against toxic acute injury in mice

Aim

CGX, a modified traditional Chinese herbal drug whose name means “liver cleaning,” is used to treat various liver disorders. This study investigated the protective effects of CGX and its mechanisms.

Material and methods

After pretreating ICR mice twice daily with CGX (po, 50 or 100 mg/kg) or distilled water for three consecutive days, acute liver injury was induced by a single injection of CCl₄ (ip, 10 mL/kg of 0.2% in olive oil) (n = 8 per group).

Results

Pretreatment with CGX significantly attenuated the elevation in biochemical parameters, such as alanine transaminase (ALT), aspartate transaminase (AST), and lactate dehydrogenase (LDH) in serum, and the malondialdehyde concentrations in liver tissue. Pretreatment with CGX significantly restored the reduction of catalase activity and glutathione (GSH) content, but not superoxide dismutase (SOD) activity, and it inhibited the CCl₄-induced high expression of iNOS and TNF-α in hepatic tissue.

Conclusion

This study showed that CGX has hepatoprotective effects against free radical-induced acute injury via primarily antioxidative properties.     

谷胱甘肽及其酶系与黄磷毒作用关系研究

黄磷急性染毒可使肝脏GSH含量降低,染毒60小时后肝GSR明显抑制,肝GST在染毒早期有诱导倾向,24小时后转为抑制。OTC预处理可明显增加肝GSH含量,缓解黄磷所致的肝GSH降低和血清γ-GT的升高。BSO预处理能明显减少肝GSH含量,加剧黄磷所致的肝GSH降低及血清γ-GT的升高。黄磷亚急性染毒对肝GSH及其代谢酶系影响甚微。     

白果活性蛋白的抗生物氧化作用研究

银杏 ( Ginkgo biloba)是我国的古老珍贵树种之一 ,为一科一属一种的特殊植物 ,在我国广泛种植 ,产量占全世界的 70 %。银杏果实的核俗称白果 ,其核仁为可食用部分。由于其营养丰富 ,自古以来被当作养生延年的上品 ,临床用于补虚扶衰 ,止咳平喘 ,涩精固元等 [1]。但国内外对白果中蛋白质的研究还少有报道。本研究采用盐溶法提取白果中的蛋白质并分离出清蛋白和盐溶蛋白两个组分 ,进行抗生物氧化动物实验 ,旨在通过测定血液或组织中 MDA含量和 SOD、GSH- Px活性 ,较系统地研究了白果中蛋白质的抗生物氧化作用。1　材　料　与　方　法1 .…     

The identification of potential alternative biomarkers of nitrofurazone abuse in animal derived food products

Semicarbazide (SEM) was considered to be a characteristic protein-bound side-chain metabolite of the banned veterinary drug nitrofurazone and used as a marker of nitrofurazone abuse. It was recently discovered that SEM can arise in food from sources other than nitrofurazone. This uncertainty over the source of SEM may be overcome if alternative markers specific to tissue-bound nitrofurazone residues can be determined. The structure of nitrofurazone metabolites in vivo and particular proteins to which they are bound are not known. These proteins with altered structure due to the presence of the drug metabolites can be considered as potential alternative biomarkers of nitrofurazone abuse. The proteins implicated in the in vivo binding of nitrofurazone were separated and identified. A crude mixture of proteins extracted from the liver of a rat treated with the drug was separated using a series of different techniques such as preparative isoelectric focusing and size exclusion HPLC. Multiple fractions were assayed by LC-MS/MS to detect the presence of SEM. The proteins containing SEM residues were identified by peptide mass mapping using trypsin digestion and MALDI-TOF. The first protein identified as containing high concentration of SEM was albumin. It was also shown that low molecular weight species within a protein mixture whose main constituent was glutathione S-transferase contained a high concentration of SEM. The chemical composition of these components is under investigation. Preliminary data suggest the SEM forms part of a nitrofurazone metabolite conjugated to glutathione.     

龙葵碱调控还原型谷胱甘肽和活性氧氧化还原体系损伤线粒体超微结构诱导HepG2细胞凋亡

目的 探讨龙葵碱诱导HepG2细胞凋亡与线粒体损伤的关系.方法 倒置显微镜观察细胞形态,Annexin V/PI 双染激光共聚焦扫描显微术检测细胞凋亡,流式细胞仪检测细胞凋亡率.透射电镜观察细胞线粒体超微结构,CDFH-DA染色激光共聚焦扫描显微术检测活性氧(ROS)相对量,比色法检测还原型谷胱甘肽(GSH)量.结果 龙葵碱组HepG2细胞贴壁细胞数量减少,部分出现死亡.Annexin V/PI双染激光共聚焦扫描显微镜下观察发现龙葵碱组细胞Annexin V-FITC高染,细胞膜呈绿色荧光;PI低染,细胞核呈红色荧光,呈现明显的早期凋亡特征.流式细胞术分析0.4、2、10 μmol/L龙葵碱作用HepG2细胞24 h后,早期凋亡率分别为4.0%、8.5%、20.1%.透射电镜观察发现龙葵碱作用HepG2细胞24 h,细胞线粒体超微结构出现肿胀,嵴排列紊乱、嵴消失,重度空泡样变性等变化;细胞内ROS水平升高,GSH的水平降低.结论 龙葵碱通过降低HepG2细胞内GSH量,使ROS不能被及时清除而损伤线粒体结构,导致HepG2细胞凋亡.     

Evaluation of hepatoprotective effect of Zhi-Zi-Da-Huang decoction and its two fractions against acute alcohol-induced liver injury in rats

Aim of the study

To investigate the hepatoprotective effect of Zhi-Zi-Da-Huang decoction (ZZDHD) and its two fractions (one is extracted with diethyl ether as a solvent from the water extract and is called ZD-DE for short, the other is the remained aqueous fraction after extracted with diethyl ether and is abbreviated as ZD-AQ) against acute alcohol-induced liver injury in rats.

Materials and methods

Animals were administered orally with alcohol 6 g/kg at 2 h after the doses of ZZDHD and two fractions everyday for eight consecutive days except rats in normal group. The protective effect was evaluated by biochemical parameters including aspartate transaminase (AST), alanine transferase (ALT), reduced glutathione (GSH), malondialdehyde (MDA) and superoxide dismutase (SOD). The biochemical observations were supplemented by histopathological examination. HPLC-UV was used for phytochemical analysis of the ZZDHD and its two fractions.

Results

The high dose of ZZDHD exhibited a significant protective effect by reversing the biochemical parameters and histopathological changes. ZD-DE and ZD-AQ demonstrated different protective action in biochemical examination. Partly assayed indexes were ameliorated after administrated the media dose of ZZDHD. HPLC analysis indicated that ZZDHD contained flavonoids, anthraquinones and iridoids, which might be the active chemicals.

Conclusions

This study demonstrated the hepatoprotective activity of ZZDHD thus scientifically supported the usage of this formula.     

慢性冷暴露过程中SD大鼠RBC抗氧化系统和膜行为的变化

本研究以SD大鼠为模型,对慢性冷暴露过程中RBC过氧化与抗氧化机制的变化及膜部分行为的改变进行了动态观察。结果表明:(1) 冷适应初期抗氧化机制相对不足,过氧化占主导地位,过氧化物的堆积有可能造成一定的损伤而减弱机体的抗寒能力,而进一步抗氧化能力的增强则可能是冷适应建立的重要机制之一。(2) RBC在冷适应过程中抗氧化系统加强,包括SOD活性的升高与GSHPx活性的增强。(3) 慢性冷暴露过程中,SD大鼠RBC膜发生一定的组成变化和功能调整,而膜流动性变化却不显著。本实验为冷适应过程中脂质过氧化物(LPO)的存在提供了有力依据,为冷适应机理的研究与耐寒能力的探讨,提供了一条新的途径。     

Pathogenic molecular mechanisms in an animal model of fulminant hepatic failure: rabbit hemorrhagic viral disease

In this study we sought to determine whether molecular mechanisms involved in the pathogenesis of fulminant hepatic failure are present in rabbits experimentally infected with rabbit hemorrhagic disease virus (RHDV). The activities of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase, as well as bilirubin concentration, were found to be significantly increased 36 hours after infection. Infected animals also demonstrated significant decreases in factor VII activity, in the Fischer index, and in the deterioration of prothrombin time. The concentration of reduced glutathione was significantly decreased 36 hours after infection, and we noted a marked increase in the ratio of oxidized to reduced glutathione. Infected animals showed progressive decreases in liver activity of the antioxidant enzyme superoxide dismutase. Expression of hepatocyte growth factor and c-met was found to be progressively reduced from 24 hours after infection, during which time we detected no modification in messenger RNA (mRNA) levels of transforming growth factor (TGF)-alpha. TFG-beta 1 was overexpressed 24 and 36 hours after infection, and 36 hours after infection we detected a significant increase in TNF-alpha mRNA levels. Experimental RHDV infection also induced marked activation of nuclear factor-kappaB and a significant increase in inducible nitric oxide synthase mRNA levels from 24 hours after infection. Data obtained from this animal model support its usefulness in the investigation of potential novel therapeutical modalities aimed at neutralizing reactive oxygen species and hepatocyte growth inhibitors or enhancing hepatocyte responsiveness to mitogens.