共被期刊论文引用了3次
您的检索式：您选中1篇文献正在查看引证文献汇总
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Antioxidant role of heme oxygenase-1 in prehepatic portal hypertensive rats显示文摘瞄准:在氧化的肝地位和这项活动和表示上学习胆红素的效果他我在老鼠肝损伤的 oxygenase-1 (HO-1 ) 由 prehepatic 门静脉高血压导致了。方法:Wistar 雄的老鼠,称 200-250 g,在随机被划分成二个组:有调整 prehepatic 门静脉结扎(PPVL ) 导致的 prehepatic 门静脉高血压(PH ) 的一个组和另外的组对应于假冒的操作老鼠。门压力,氧化压力参数,抗氧化剂酶, HO-1 活动和表示和肝的正弦曲线血管舒张被测量。结果:在 PPVL 老鼠,氧化应力被在减少的谷胱甘肽(GSH ) 的反应物质(TBARS ) 内容和减少铺平的 thiobarbituric 酸的显著增加证实。当 HO-1 的活动和表示被提高时,肝抗氧化剂酶,超级氧化物歧化酶(草皮) ,过氧化氢酶(猫) 和谷胱甘肽过氧化物酶(GSH-Px ) 的活动也被减少。胆红素(5 mumol/kg 体重) 的管理在实验的结束前的 24 h 完全阻止了所有这些效果。有 Sn-protoporphyrin IX (Sn-PPIX ) 的预告的处理(100 mug/kg 体重, i.p ) ,一个有势力禁止者惊讶,完全废除了氧化压力并且每氧化象类脂化合物的增加一样在肝 GSH 层次挑起了细微减少。而且,一氧化碳,另一他我分解代谢的产品,在在 PPVL 的肝的区域组织的正弦曲线导致了重要增加。有 Sn-PPIX 的 PPVL 老鼠的预告的处理完全阻止了这效果。结论:这些结果在 prehepatic 门 hypertensive 老鼠在表示上建议 HO-1 的一个有益的角色。 | Soledad Gonzales María Julia Pérez Juan C Perazzo María Luján Tomaro | 2006 | World Journal of Gastroenterology2006，12，26： | 6 |
| 2 | 肝性脑病发病机制研究新进展显示文摘肝性脑病(hepatic eneephalopathy,HE)是以严重肝脏疾病和(或)门体分流所致的代谢紊乱为基础的中枢神经系统功能失调综合征,以神经精神症状为主。HE是重症或晚期肝病、某些肝胆疾病术后常见的并发症,是肝脏解毒功能不全和衰竭的表现,其发病机制目前尚未完全阐明, | 段志军 张鸣 | 2011 | 中华内科杂志2011，50，5： | 5 |
| 3 | Glutamine synthetase activity and glutamate uptake in hippocampus and frontal cortex in portal hypertensive rats显示文摘AIM: To study glutamine synthetase (GS) activity and glutamate uptake in the hippocampus and frontal cortex (FC) from rats with prehepatic portal vein hypertension. METHODS: Male Wistar rats were divided into shamoperated group and a portal hypertension (PH) group with a regulated stricture of the portal vein. Animals were sacrificed by decapitation 14 d after portal vein stricture. GS activity was determined in the hippocampus and FC. Specific uptake of radiolabeled L-glutamate was studied using synaptosome-enriched fractions that were freshly prepared from both brain areas. RESULTS: We observed that the activity of GS increased in the hippocampus of PH rats, as compared to control animals, and decreased in the FC. A significant decrease in glutamate uptake was found in both brain areas, and was more marked in the hippocampus. The decrease in glutamate uptake might have been caused by a deficient transport function, signif icantly and persistent increase in this excitatory neurotransmitter activity. CONCLUSION: The presence of moderate ammonia blood levels may add to the toxicity of excitotoxic glutamate in the brain, which causes alterations in brain function. Portal vein stricture that causes portal hypertension modif ies the normal function in some brain regions. | Gabriela Beatriz Acosta María Alejandra Fernández Diego Martín Roselló María Luján Tomaro Karina Balestrasse Abraham Lemberg | 2009 | World Journal of Gastroenterology2009，15，23： | 1 |
您所在的机构暂未开通此部分的功能，请联系管理员