CAJ | 학술논문

目的探讨氧应激及脂质过氧化反应在慢性胰腺损伤和胰腺纤维化发病中表达的变化.方法 72只大鼠随机分为6组,每组12只,分别为正常对照组、2、4、6、10和16周高脂饮食组.建立长期高脂饮食诱导的胰腺损伤动物模型,观察胰腺组织形态学变化,检验模型；检测胰腺组织中脂质过氧化产物4-羟基-2,3-反式-丙烯醛(4-HNE)和血栓素A2受体的表达；应用免疫荧光双染色法测定α-平滑肌肌动蛋白(α-SMA)和4-HNE及α-SMA和血栓素A2受体在胰腺组织中的共表达.结果长期高脂饮食诱导大鼠胰腺纤维化,胰腺星状细胞发生增殖和活化,免疫组化染色法测定胰腺组织中脂质过氧化产物4-HNE表达较正常组明显增加,血栓素A2受体在胰腺组织中表达也明显增加.免疫荧光双标染色法显示4-HNE和血栓素A2受体分别与α-SMA在胰腺组织中共表达.结论长期高脂饮食可以诱导胰腺慢性损伤,可能通过促进氧应激及脂质过氧化反应诱导大鼠胰腺星状细胞活化及胰腺纤维化.
목적 탐토양응격급지질과양화반응재만성이선손상화이선섬유화발병중표체적변화.방법 72지대서수궤분위6조,매조12지,분별위정상대조조、2、4、6、10화16주고지음식조.건립장기고지음식유도적이선손상동물모형,관찰이선조직형태학변화,검험모형；검측이선조직중지질과양화산물4-간기-2,3-반식-병희철(4-HNE)화혈전소A2수체적표체；응용면역형광쌍염색법측정α-평활기기동단백(α-SMA)화4-HNE급α-SMA화혈전소A2수체재이선조직중적공표체.결과 장기고지음식유도대서이선섬유화,이선성상세포발생증식화활화,면역조화염색법측정이선조직중지질과양화산물4-HNE표체교정상조명현증가,혈전소A2수체재이선조직중표체야명현증가.면역형광쌍표염색법현시4-HNE화혈전소A2수체분별여α-SMA재이선조직중공표체.결론장기고지음식가이유도이선만성손상,가능통과촉진양응격급지질과양화반응유도대서이선성상세포활화급이선섬유화.
Objective To provide more detailed information on the roles of lipid peroxidation in the pathogenesis of chronic pancreatic injuries in a pre-clinical rat model.Methods Totally 72 rats were divided into 6 groups (12 in each group) Rats in 5 experimental groups (n =12) were fed with a high-fat diet (1％ cholesterol,10％ lard,0.3％ sodium tauroglycocholate,87.3％ standard rodent chow as the control group) for 2,4,6,10 and 16 weeks,respectively.Morphological studies in the pancreas tissue samples from rats were investigated by using various histological methods.Pancreatic stellate cells (PSCs)were identified by immunohistochemical staining for Desmin and α-smooth muscle actin (α-SMA).The expression of the lipid peroxidation was detected by immunostaining for 4-hydroxy-2-nonenal (4-HNE) and thromboxane A2 receptor (TxA2r).The co-localization of α-SMA and 4-HNE or α-SMA and TxA2r in PSCs was also analyzed in this study.Results Pancreatic cells with positive staining for Desmin and α-SMA in HFD rats were distributed in a more extensive way when compared to that in the control group.The levels of pancreatic 4-HNE and TxA2r were increased in rats from HFD groups significantly.The co-localization of 4-HNE and TxA2r were also found within activated PSCs in both of groups.Conclusion The results showed that a chronic HFD feeding may increase the lipid peroxidation process and collagen synthesis through a critical signaling pathway of activated PSCs following pancreatic injuries in rats.