癌变·畸变·突变
癌變·畸變·突變
암변·기변·돌변
CARCINOGENSES,TERATOGENSIS AND MUTAGENESIS
2014年
1期
52-55
,共4页
何宁%张静姝%张静%姜淑卿%刘英华%管彤%李新
何寧%張靜姝%張靜%薑淑卿%劉英華%管彤%李新
하저%장정주%장정%강숙경%류영화%관동%리신
NF-κB%乙醇%肝细胞%损伤
NF-κB%乙醇%肝細胞%損傷
NF-κB%을순%간세포%손상
NF-κB%alcohol%hepatocytes%injury
目的:研究核因子NF-κB在乙醇诱导小鼠急性肝细胞损伤中的表达及意义。方法:40只小鼠随机分成对照组和3个乙醇(250、500、1000 mmol/kg)染毒组,每组10只。一次性灌胃染毒,16 h后检测小鼠血清中天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)的活力;染毒24 h后采用HE及油红O染色进行病理学观察;采用免疫组织化学法观察小鼠肝细胞中NF-κB蛋白的表达。结果:3个乙醇染毒组小鼠血清中的转氨酶AST和ALT活力均高于对照组(P均<0.05);HE染色发现小鼠肝组织中出现肝细胞内空泡变性。油红O染色显示损伤的肝细胞内出现大量脂滴。免疫组织化学检测发现500和1000 mmol/kg乙醇染毒组小鼠肝细胞胞质及胞核内NF-κB蛋白表达的积分光密度明显高于对照组(P<0.05)。结论:成功复制了急性小鼠酒精性肝损伤的模型,NF-κB升高是小鼠急性酒精性肝细胞损伤的一个重要分子事件。
目的:研究覈因子NF-κB在乙醇誘導小鼠急性肝細胞損傷中的錶達及意義。方法:40隻小鼠隨機分成對照組和3箇乙醇(250、500、1000 mmol/kg)染毒組,每組10隻。一次性灌胃染毒,16 h後檢測小鼠血清中天鼕氨痠轉氨酶(AST)、丙氨痠轉氨酶(ALT)的活力;染毒24 h後採用HE及油紅O染色進行病理學觀察;採用免疫組織化學法觀察小鼠肝細胞中NF-κB蛋白的錶達。結果:3箇乙醇染毒組小鼠血清中的轉氨酶AST和ALT活力均高于對照組(P均<0.05);HE染色髮現小鼠肝組織中齣現肝細胞內空泡變性。油紅O染色顯示損傷的肝細胞內齣現大量脂滴。免疫組織化學檢測髮現500和1000 mmol/kg乙醇染毒組小鼠肝細胞胞質及胞覈內NF-κB蛋白錶達的積分光密度明顯高于對照組(P<0.05)。結論:成功複製瞭急性小鼠酒精性肝損傷的模型,NF-κB升高是小鼠急性酒精性肝細胞損傷的一箇重要分子事件。
목적:연구핵인자NF-κB재을순유도소서급성간세포손상중적표체급의의。방법:40지소서수궤분성대조조화3개을순(250、500、1000 mmol/kg)염독조,매조10지。일차성관위염독,16 h후검측소서혈청중천동안산전안매(AST)、병안산전안매(ALT)적활력;염독24 h후채용HE급유홍O염색진행병이학관찰;채용면역조직화학법관찰소서간세포중NF-κB단백적표체。결과:3개을순염독조소서혈청중적전안매AST화ALT활력균고우대조조(P균<0.05);HE염색발현소서간조직중출현간세포내공포변성。유홍O염색현시손상적간세포내출현대량지적。면역조직화학검측발현500화1000 mmol/kg을순염독조소서간세포포질급포핵내NF-κB단백표체적적분광밀도명현고우대조조(P<0.05)。결론:성공복제료급성소서주정성간손상적모형,NF-κB승고시소서급성주정성간세포손상적일개중요분자사건。
OBJECTIVE:To investigate the expression and significance of nuclear factor-κappa B in alcohol-induced acute hepatocyte injury. METHODS:Forty mice were randomly divided into a control group and three alcohol treated groups (250,500,1 000 mmol/kg). Each group included ten mice. 16 h after gavage,serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured. After 24 h,the liver was examined by HE staining and oil Red O staining. The expression of NF-κB protein in hepatocytes was assessed by immunohistochemistry. RESULTS:Serum AST and ALT levels in three alcohol-treated groups were significantly increased compared with that in the control group (P<0.05). There was vacuolar degeneration in hepatocytes by HE staining. There were large amounts of Oil Red O staining droplets in the hepatocytes. In alcohol-treated groups (500, 1 000 mmol/kg),the integrated optical density expression of NF-κB protein in hepatocytes cytoplasm and nucleus were significantly higher (P<0.05). CONCLUSION:This study successfully set up an alcohol-induced acute hepatocyte injury mouse model,and illustrated the role of NF-κB in the development and progression of acute alcoholic-induced hepatocyte injury.