神经药理学报
神經藥理學報
신경약이학보
Journal of Hebei North University(Medical Edition)
2011年
4期
33-41
,共9页
肝性脑病%末梢型苯二氮%类受体%葡萄糖转运体-1%水通道蛋白-4%钠/钾-ATPase%微管相关蛋白2%N-甲基-D-天冬氨酸受体%一氧化氮
肝性腦病%末梢型苯二氮%類受體%葡萄糖轉運體-1%水通道蛋白-4%鈉/鉀-ATPase%微管相關蛋白2%N-甲基-D-天鼕氨痠受體%一氧化氮
간성뇌병%말소형분이담%류수체%포도당전운체-1%수통도단백-4%납/갑-ATPase%미관상관단백2%N-갑기-D-천동안산수체%일양화담
hepatic encephalopathy(HE)%peripheral-type benzodiazepine receptor (PTBR)%glucose tranporter-1(GLUT-1)%aquaporin-4(AQP4)%Na+/K+-ATPase%microtubule-asso-ciated protein(MAP-2)%N-methyl-D-aspartate(NMDA)receptor%nitric oxide(NO)
肝性脑病?(hepatic?encephalopathy,HE)?是急、慢性肝衰竭的严重并发症,以星形胶质细胞病变为主要病理变化.肝性脑病的发病可能与多种因素有关,大量研究表明氨在HE发病过程中起关键作用.高血氨诱导星形胶质细胞上末梢型苯二氮类受体?(peripheral-type?benzodiazepine?receptor,PTBR)、葡萄糖转运体-1?(glucose?tranporter-1,GLUT-1)、水通道蛋白-4?(aquaporin-4,AQP4)和Na+/K+-ATPase基因表达上调;影响微管相关蛋-2?(microtubule-associated?protein-2,MAP-2)?磷酸化及N-甲基-D-天冬氨酸?(N-methyl-D-aspartate,NMDA)受体表达;诱导一氧化氮(nitricoxide,NO)合成增加从而改变神经细胞功能.此外,氨能使脑内哇巴因类复合物生成增加,并能够使Na+/K+-ATPase的活性增加.对上述因素的研究将帮助我们理解氨诱导星形胶质细胞功能障碍的基本机制,并进一步制定防治肝性脑病的新策略.
肝性腦病?(hepatic?encephalopathy,HE)?是急、慢性肝衰竭的嚴重併髮癥,以星形膠質細胞病變為主要病理變化.肝性腦病的髮病可能與多種因素有關,大量研究錶明氨在HE髮病過程中起關鍵作用.高血氨誘導星形膠質細胞上末梢型苯二氮類受體?(peripheral-type?benzodiazepine?receptor,PTBR)、葡萄糖轉運體-1?(glucose?tranporter-1,GLUT-1)、水通道蛋白-4?(aquaporin-4,AQP4)和Na+/K+-ATPase基因錶達上調;影響微管相關蛋-2?(microtubule-associated?protein-2,MAP-2)?燐痠化及N-甲基-D-天鼕氨痠?(N-methyl-D-aspartate,NMDA)受體錶達;誘導一氧化氮(nitricoxide,NO)閤成增加從而改變神經細胞功能.此外,氨能使腦內哇巴因類複閤物生成增加,併能夠使Na+/K+-ATPase的活性增加.對上述因素的研究將幫助我們理解氨誘導星形膠質細胞功能障礙的基本機製,併進一步製定防治肝性腦病的新策略.
간성뇌병?(hepatic?encephalopathy,HE)?시급、만성간쇠갈적엄중병발증,이성형효질세포병변위주요병리변화.간성뇌병적발병가능여다충인소유관,대량연구표명안재HE발병과정중기관건작용.고혈안유도성형효질세포상말소형분이담류수체?(peripheral-type?benzodiazepine?receptor,PTBR)、포도당전운체-1?(glucose?tranporter-1,GLUT-1)、수통도단백-4?(aquaporin-4,AQP4)화Na+/K+-ATPase기인표체상조;영향미관상관단-2?(microtubule-associated?protein-2,MAP-2)?린산화급N-갑기-D-천동안산?(N-methyl-D-aspartate,NMDA)수체표체;유도일양화담(nitricoxide,NO)합성증가종이개변신경세포공능.차외,안능사뇌내왜파인류복합물생성증가,병능구사Na+/K+-ATPase적활성증가.대상술인소적연구장방조아문리해안유도성형효질세포공능장애적기본궤제,병진일보제정방치간성뇌병적신책략.
Hepatic encephalopathy(HE)is a serious complication of acute or chronic liver failure,caused by many reasons(i.e. ammonia,multiple neurotoxins,false neurotransmit-ters and benzodiazepine-like compounds). Evidences suggest that ammonia plays a major role in pathogenesis of HE. Hyperammonia up-regulates gene expression of peripheral-type benzodiaz-epine receptor(PTBR),glucose tranporter-1(GLUT-1),aquaporin-4(AQP4),and Na+/K+-ATPase in astrocytes;alters the phosphorylation state of the microtubule-associated protein-2(MAP-2) and the expression of N-methyl-D-aspartate(NMDA)receptor;induces increase of NO,therefore astrocytic disfunction. It was reported previously that ammonia increased production of ouabain-like compounds and Na+/K+-ATPase activity in astrocytes. Research to the relationship of these factors will help us to understand the underlying mechanisms of ammonia-induced astrocytic dis-function and eventually contribute to the new strategies of prevention and therapy of HE.
