CAJ | 학술논문

目的探讨高脂高果糖饮食诱导的非酒精性脂肪性肝病(NAFLD)小鼠枯否细胞(KCs)活化及其信号通路蛋白的变化,了解KCs在非酒精性脂肪性肝病(NAFLD)致病机制中的意义.方法将20只6～8周龄SPF级C3H小鼠随机分为4组(正常组、果糖组、高脂组、高脂果糖组)饲养,每组5只.16周后处死小鼠,做肝脏病理检查,同时使用蛋白免疫印迹(Western Blot)方法检测肝组织中F4/80、NF-κB、p-AKT、AKT的表达情况.结果与正常组比较,果糖组、高脂组、高脂果糖组肝组织脂质沉积明显,肝脏HE染色存在明显的炎症及肝细胞脂肪变,高脂高果糖组最为严重.与正常组比较,3组模型组小鼠肝组织中F4/80、NF-κB显著升高,果糖组p-AKT(P＜0.01)、高脂高果糖组AKT(P ＜0.05)明显降低.结论高脂高糖饮食可使C3H/HeN小鼠出现典型的非酒精性脂肪肝表现,NAFLD形成涉及肝组织中KCs活化及其相关信号通路的激活.
목적 탐토고지고과당음식유도적비주정성지방성간병(NAFLD)소서고부세포(KCs)활화급기신호통로단백적변화,료해KCs재비주정성지방성간병(NAFLD)치병궤제중적의의.방법 장20지6～8주령SPF급C3H소서수궤분위4조(정상조、과당조、고지조、고지과당조)사양,매조5지.16주후처사소서,주간장병리검사,동시사용단백면역인적(Western Blot)방법검측간조직중F4/80、NF-κB、p-AKT、AKT적표체정황.결과 여정상조비교,과당조、고지조、고지과당조간조직지질침적명현,간장HE염색존재명현적염증급간세포지방변,고지고과당조최위엄중.여정상조비교,3조모형조소서간조직중F4/80、NF-κB현저승고,과당조p-AKT(P＜0.01)、고지고과당조AKT(P ＜0.05)명현강저.결론 고지고당음식가사C3H/HeN소서출현전형적비주정성지방간표현,NAFLD형성섭급간조직중KCs활화급기상관신호통로적격활.
Objective To investigate the expression of F4/80,NF-κB,p-AKT,AKT in the liver of nonalcoholic fatty liver disease (NAFLD) mice.To determine the role of Kupffer cells (KCs) in the development of NASH (non-alcoholic steatohepatitis),and understand the pathogenic mechanism of NASH.Methods Five C3H/HeN mice fed with normal diet were served as controls,while fifteen fed with high fat,high fructose,high fat combined fructose diet respectively for 16 weeks were as NAFLD mice models.The liver inflammation and hepatic damage were examined,and the expression of F4/80,NF-Kb,p-AKT,AKT and the content of lipid in the liver were also detected.Results Chronic intake of high fat and 30％ fructose solution caused a significant increase in hepatic steatosis in animals in comparison to water controls.Liver F4/80 and NF-κB were significantly higher in high fat and high fat combined fructose diet fed mice than that in controls(P ＜ 0.01,P ＜0.01),F4/80 protein were higher in high fat diet treated mice than those in fructose and high fat combined fructose groups(P ＜0.01,P ＜0.01).Markers of insulin resistance (e.g,hepatic phospho-AKT,AKT) were only altered in fructose-fed or high fat combined fructose animals (P ＜0.01,P ＜ 0.01).Conclusion High fat and fructose diet may induce NAFLD in C3H/HeN mice.Kupffer cells and signal pathway proteins were activated,and they may play key roles in the initiation and progression of NASH.