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慢性胰腺炎大鼠肝细胞IR、IRS-1 mRNA的表达及罗格列酮的干预作用

论文标题:慢性胰腺炎大鼠肝细胞IR、IRS-1 mRNA的表达及罗格列酮的干预作用
The Expression of IR、IRS-1 mRNA of Hepatic Cell of Chronic Pancreatitis Rats and the Intervention of Rosiglitazone
论文作者 赵战朝
论文导师 薛承锐;胡文全,论文学位 硕士,论文专业 中西医结合临床
论文单位 天津医科大学,点击次数 373,论文页数 99页File Size9381k
2004-05-01论文网 http://www.lw23.com/lunwen_1006312/ 胰源性糖尿病;慢性胰腺炎;模型;病理;超微结构
Pancreatogenic Diabetes, Chronic Pancreatitis, Model,Pathology,Ultrastructure,
目的:建立油酸诱导的慢性胰腺炎大鼠模型,观察其病理及超微结构改变规律,为探讨慢性胰腺炎继发胰源性糖尿病的可能机制,药物防治胰源性糖尿病的研究奠定基础。方法:选用健康雄性Wistar大鼠经肠壁逆行胰胆管插管,经插管向胰腺内逆行灌注油酸的方法制作慢性胰腺炎大鼠模型,动态观察大鼠术后1h、24h、72h、1周、3周、6周的胰腺形态改变。对照大鼠经插管灌注等量的生理盐水。结果:胰腺病理显示:模型组油酸灌注24h内即出现胰管周围腺泡实质坏死,腺泡腔隙变宽和细胞囊泡形成。1周后出现腺泡退化,组织间水肿、炎性细胞浸润和导管样小管复合物形成。6周后腺泡萎缩,伴不规则纤维化,并被脂肪和临近组织取代;胰岛游离,结构松散。超微结构显示:术后24h出现胰腺腺泡细胞退变,毛细血管闭合,炎性细胞浸润和纤维组织增生,并进行性加重。结论:油酸诱导的慢性胰腺炎大鼠模型表现为外分泌腺体广泛退化,内分泌腺体继发损伤,适合进行胰源性糖尿病的研究。
Objective: To establish model of chronic pancreatitis and to observe its pathological and ultrastructural changes, so as to discuss mechanism of overt pancreatogenic diabetes developed by chronic pancreatitis, as well as to provide foundation for the medical research of pancreatogenic diabetes. Methods: An experimental model of chronic pancreatitis was induced by a retrograde injection of oleic acid into the rat pancreatic duct. Pathological and ultrastructural changes were investigated over a period of 6 weeks after induction of this model. Results: Histologically, the widening of acinar lumen and cellular vacuolization occurred within 24 h at the parenchyma neighboring the small ducts filled with the injected solution. Degenerative parenchyma, interstitial edema, and inflammatory cell infiltration were pronounced 1 week later. Thereafter, duct-like tubular complex formation progressed, and the exocrine tissue exhibited marked atrophy of the gland with irregular fibrosis and fat replacement after 6 weeks. Meanwhile, endocrine tissue showed overt damage. Ultrasrucrure of pancreas demonstrated progressive degenerative parenchyma, closed capillary vessel, inflammatory infiltration and fiber proliferation. Conclusion: The model of chronic pancreatitis induced by oleic acid demonstrated extensive acinar degeneration and overt damage of islet. So, it is suitable for research work of pancreatogenic diabetes.

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