程序性坏死在急性胰腺炎发生发展中的作用  

Role of programmed cell necrosis in occurrence and development of acute pancreatitis

作　　者：曲凤智 曹成亮[1] 王刚[1] 孙备[1] 

机构地区：[1]哈尔滨医科大学附属第一医院胰胆外科,150001

出　　处：《中华消化外科杂志》2016年第11期1127-1130,共4页Chinese Journal of Digestive Surgery

基　　金：国家自然科学基金（81100314、81170431、81370565、81372613）;黑龙江省新世纪优秀人才培养计划（1253-NCET-017）;哈尔滨医科大学于维汉院士杰出青年基金

摘　　要：胰腺腺泡细胞死亡方式是急性胰腺炎（AP）早期主要的病理生理学改变，也是决定其病程演进和预后的重要因素。AP时，腺泡细胞同时存在坏死与凋亡两种主要死亡方式。腺泡细胞坏死可导致AP局部和系统强烈的炎症反应，成为其病情发生发展的诱发、加重因素。长期以来，坏死被认为是细胞快速、不可调控、被动性的死亡过程，因无法有效干预而导致其相关机制研究未受到足够重视。程序性坏死是近年来发现的一种新型细胞死亡方式，具有坏死和凋亡的共同特征。程序性坏死在AP领域的前期研究结果证实了腺泡细胞程序性坏死的存在，可能为有效调控AP炎症损伤和改善病情提供潜在的干预途径，但其功能学改变和作用机制仍有待进一步探讨。Pancreatic acinar cell death is the major pathophysiological change in early acute pancreatitis （AP）, which is important factor determining its progression and prognosis. During AP, acinar cell death is composed of necrosis and apoptosis. Acinar cell necrosis can lead to intensely local and systemic inflammatory responses, which both induce and aggravate the lesion. Necrosis has long been considered an unregulated and passive cell death process. Since the effective interventions of necrosis are difficult to perform, its relevant studies have not received adequate attention. Programmed cell necrosis is a newly discovered cell death characterized by both necrosis and apoptosis, it is actively regulated by special genes, while has the typical morphological features of necrosis. Programmed cell necrosis which may be a potential target for the preliminary results in AP have confirmed the existence of acinar cell effectively regulating inflammatory injuries and improving its outcomes, however, the functional changes and mechanisms of programmed cell necrosis still require further investigation. This article reviews the progress of programmed cell necrosis in AP to provide a reference for deeply understanding the pathogenic mechanisms of AP and identifying new therapeutic targets.

关 键 词：急性胰腺炎 程序性坏死 损伤相关分子模式 凋亡 自噬 

分 类 号：R576[医药卫生—消化系统]