CAJ | 학술논문

目的探讨不同价态水砷暴露及高脂饲料加水砷暴露小鼠肝纤维化模型的建立方法,并进行比较.方法小鼠240只,随机分为正常对照组、亚砷酸钠(iAs3+)组、砷酸钠(iAs5+)组、高脂饲料对照组、高脂饲料+iAs3+组和高脂饲料+iAs5+组6个组,每组40只.正常对照组和高脂饲料对照组(饮用自来水),iAs3+组和高脂饲料+iAs3+组(饮用300 mg/L iAs3+水),iAs5+组和高脂饲料+iAs5+组(饮用300 ms/L iAs5+水).饮水砷暴露3、6、10个月后处死小鼠,检测各组小鼠血清肝功能,HE染色及胶原特殊染色(Masson染色)观察各组小鼠肝组织病理学变化.结果造模3个月时,正常对照组、iAs3+组、iAs5+组、高脂饲料+iAs3+组和高脂饲料+iAs5+组的血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)水平分别为(36.7±5.7)U/L和(110±22)U/L、(55.6±4.6)U/L和(249±41)U/L、(52.6±8.8)U/L和(161±15)U/L、(311.3±19.7)U/L和(484±15)U/L、(515.0±60.8)U/L和(671±24)U/L,各砷组均高于对照组(均P<0.05).各砷组动物肝组织HE染色就显示有不同程度肝损伤,表现肝细胞水样变性、脂肪样变性,点状或灶性坏死及炎性细胞浸润,并有不同程度的肝细胞再生及纤维增生,随着暴露时间的延长,各砷组肝组织病理损伤逐渐加重.10个月Masson染色显示汇管区及中央静脉区纤维条索状增生,正常对照组、iAs3+组、iAs5+组、高脂饲料+iAs3+组和高脂饲料+iAs5+组小鼠肝脏纤维组织面积的均值分别为0.1333、0.5584、0.5250、0.7534、0.7200,各砷组与对照组相比差异有统计学意义(均P<0.05).结论成功建立了不同价态水砷暴露及高脂饲料加水砷暴露小鼠肝损伤、肝纤维化的模型,并进行了评价,为砷致肝损伤、肝纤维的研究提供了较理想的动物模型.
목적 탐토불동개태수신폭로급고지사료가수신폭로소서간섬유화모형적건립방법,병진행비교.방법 소서240지,수궤분위정상대조조、아신산납(iAs3+)조、신산납(iAs5+)조、고지사료대조조、고지사료+iAs3+조화고지사료+iAs5+조6개조,매조40지.정상대조조화고지사료대조조(음용자래수),iAs3+조화고지사료+iAs3+조(음용300 mg/L iAs3+수),iAs5+조화고지사료+iAs5+조(음용300 ms/L iAs5+수).음수신폭로3、6、10개월후처사소서,검측각조소서혈청간공능,HE염색급효원특수염색(Masson염색)관찰각조소서간조직병이학변화.결과 조모3개월시,정상대조조、iAs3+조、iAs5+조、고지사료+iAs3+조화고지사료+iAs5+조적혈청병안산전안매(ALT)화천동안산전안매(AST)수평분별위(36.7±5.7)U/L화(110±22)U/L、(55.6±4.6)U/L화(249±41)U/L、(52.6±8.8)U/L화(161±15)U/L、(311.3±19.7)U/L화(484±15)U/L、(515.0±60.8)U/L화(671±24)U/L,각신조균고우대조조(균P<0.05).각신조동물간조직HE염색취현시유불동정도간손상,표현간세포수양변성、지방양변성,점상혹조성배사급염성세포침윤,병유불동정도적간세포재생급섬유증생,수착폭로시간적연장,각신조간조직병리손상축점가중.10개월Masson염색현시회관구급중앙정맥구섬유조색상증생,정상대조조、iAs3+조、iAs5+조、고지사료+iAs3+조화고지사료+iAs5+조소서간장섬유조직면적적균치분별위0.1333、0.5584、0.5250、0.7534、0.7200,각신조여대조조상비차이유통계학의의(균P<0.05).결론 성공건립료불동개태수신폭로급고지사료가수신폭로소서간손상、간섬유화적모형,병진행료평개,위신치간손상、간섬유적연구제공료교이상적동물모형.
Objective To discuss and compare the model estabhshment of liver fibrosis in oral arsenic solution exposed mice and mice with high-fat feedstuff. Methods A total of 240 mice were divided randomly into 6 groups: control group, sodium arsenite group, sodium arsenate group, high-fat feedstuff group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff with 40 mice esch. Control group and high-fat feedstuff group (drinking tap water), sodium arsenite group and sodium arsenite group with high-fat feedstuff (drinking 300 mg/L iAs3+ water), sodium arsenate group and sodium arsenate group with high-fat feedstuff (drinking 300 mg/L iAs5+ water). The mice were sacrificed after 3, 6, 10 months' arsenic-exposure and examined for liver function. HE dyeing and Masson dyeing were also employed to observe the pathological changes in hepatic tissue in each group. Results After 3 months' modeling, ALT and AST in control group, sodium arsenite group, sodium arsenate group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff were (36.7±5.7 ) U/L and (110±22) U/L, (55.6±4.6) U/L and (249±41) U/L, (52.6±8.8) U/L and (161±15) U/L, (311.3±19.7)U/L and (484±15)U/L and (515.0±60.8)U/L and (671±24)U/L. They were higher in all the arsenic groups than in control group (P<0.05); all the HE dyeing samples in arsenic groups showed liver injury in varying degrees such as hydropic degeneration, fatty degeneration, spotty necrosis, fecal necrosis and inflammatory cell infiltration. There were liver cell regeneration and fibroplasias in varying degrees. The liver injury of the mice in all arsenic groups aggravated as exposure time prolonged. Masson dyeing after 10 months' modeling showed hyperplasia in portal areas and central venous areas; the mean area of fibrosis in control group, sodium arsenite group, sodium arsenate group, sodium arsenite group with high-fat feedstuff and sodium arsenate group with high-fat feedstuff were 0.1333, 0.5584, 0. 5250, 0.7534 and 0.7200 respectively. There was statistical significance between arsenic groups and control group (P<0.05) . Conclusion The liver injury and fibrosis model in oral arsenic solution exposed mice and those with high-fat feedstuff are successfully established and subsequently evaluated. It is a comparatively ideal animal model for studying arsenic liver injury and fibrosis.