长期乙醇摄入导致胰腺腺泡细胞退行性改变  

Retrogression of pancreatic acinar cells induced by prolonged alcohol intake in rats

作　　者：周旭春[1] 唐承薇[2] 刘纯伦[1] 

机构地区：[1]重庆医科大学附属第一医院消化内科,400016 [2]四川大学华西医院消化内科,成都610041

出　　处：《中华消化杂志》2005年第5期284-286,共3页Chinese Journal of Digestion

基　　金：国家杰出青年科学基金(39725012)

摘　　要：目的探讨长期摄入乙醇对胰腺腺泡细胞结构和外分泌功能的影响。方法将12只Wistar大鼠平均分为乙醇组和对照组,乙醇组饲以25%乙醇6个月,在光镜和电镜下观察胰腺腺泡细胞结构变化,用比色法检测胰腺组织匀浆淀粉酶和脂肪酶,用TUNEL法检测细胞凋亡,用免疫组化检测COX2的变化。结果与对照组相比,乙醇组腺泡细胞中出现较多空泡,腺泡细胞内脂滴增加,酶原颗粒减少,髓样结构形成。乙醇组胰腺组织匀浆淀粉酶、脂肪酶分别为(2807.26±50.10)U/G组织、(3650.00±80.18)U/G组织,与对照组相比有显著降低(P<0.05)。乙醇组胰腺组织细胞凋亡指数、COX2的表达与对照组比较差异无统计学意义。结论长期乙醇摄入可导致大鼠胰腺腺泡细胞退行性改变及外分泌功能减低。Objective To investigate the effect of prolonged ethanol intake on the cellular structure and exocrine function of the rat pancreatic acinar cells. Methods Twelve Wistar rats were divided to ethanol-fed group and control group. Rats in ethanol-fed group were fed diet containing 25% concentration of ethanol for 6 months.Histological studies were conducted by light microscopy and electron microscopy.Lipase and amylase were assayed in pancreatic tissue homogenate by colorimetry.Apoptosis and the expression of cyclooxygenase-2(COX-2) in acinar cell were detected by TdT-mediated dUTP nick end-labeling assay(TUNEL)and immunohistochemical staining,respectively. Results Compared with control group,the acinar cells with vacuolization,lipid droplets,myelin figure and decreased number of zymogen granules were observed in ethanol-fed group.Lipase and amylase were (2807.26±50.10) U/G tissue and (3650.00±80.18) U/G tissue in ethanol-fed group,respectively.Compared with control group,lipase and amylase were significantly decreased (P<0.05).The expression of COX-2 and apoptosis indices were not statistically different between the two groups.Conclusions Long-term alcohol consumption could induce acinar cell retrogression and decrease pancreatic exocrine function.

关 键 词：胰腺腺泡细胞 退行性改变 乙醇 摄入 Wistar大鼠 外分泌功能 COX-2 细胞结构变化 TUNEL法 免疫组化检测 细胞凋亡指数 组织匀浆 对照组 镜下观察 酶原颗粒 胰腺组织 脂肪酶 淀粉酶 比色法 细胞内 统计学 相比 

分 类 号：R576[医药卫生—消化系统] R681.5[医药卫生—内科学]