首页|基于环氧合酶-2/p53轴防治溃疡性结肠炎异型增生的研究进展

基于环氧合酶-2/p53轴防治溃疡性结肠炎异型增生的研究进展

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溃疡性结肠炎(UC)是一种慢性炎症性肠病,非特异性、持续的肠道炎症为其主要特征,这种慢性炎症往往会增加罹患结直肠癌等严重并发症的风险.异型增生作为推动癌症发展的后备军,对慢性肠道炎症与结直肠癌的发生发展起到衔接作用.而细胞增殖/凋亡失衡则是异型增生发展的驱动因素.其中,肠黏膜上皮细胞增殖/凋亡异常可能受环氧合酶-2(COX-2)、抑癌基因p53及二者串扰关系的影响,对COX-2/p53轴的合理调控可能是实现肠黏膜增殖/凋亡平衡的关键.本文从肠黏膜上皮增殖/凋亡失衡入手,思考COX-2、p53在UC异型增生发生发展中的影响及其具体作用机制,以期为UC异型增生疾病机制及靶向治疗药物的开发提供参考.
Progress in Prevention and Treatment of Dysplasia in Ulcerative Colitis Based on Cyclooxygenase-2/p53 Axis
Ulcerative colitis(UC)is a chronic inflammatory bowel disease characterized by non-spe-cific,persistent inflammation in the intestines.This chronic inflammation often increases the risk of serious com-plications such as colorectal cancer.Dysplasia acts as a driver of cancer development and plays a connecting role in the occurrence and development of chronic intestinal inflammation and colorectal cancer.Cell proliferation/ap-optosis imbalance is the driving factor for dysplasia development.The abnormal proliferation/apoptosis of intestinal mucosal epithelial cells may be affected by cyclooxygenase-2(COX-2),tumor suppressor gene p53,or both.Therefore,reasonable regulation of COX-2/p53 axis may be a key to achieving intestinal mucosal prolifera-tion/apoptosis balance.This article discusses the effects and mechanism of COX-2 and p53 in regulating the oc-currence and development of dysplasia in UC from the proliferation/apoptosis imbalance of intestinal mucosal epi-thelial cells,aiming to provide a reference for understanding the mechanism of dysplasia in UC and developing targeted therapeutic drugs.

ulcerative colitisdysplasiacyclooxygenase-2p53 gene

张仪霖、杨树森、刘禹杉、闫曙光

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陕西中医药大学基础医学院,陕西咸阳 712046

陕西省胃肠病证方药重点研究室,陕西咸阳 712046

溃疡性结肠炎 异型增生 环氧合酶-2 p53

2024

中国医学科学院学报
中国医学科学院,北京协和医学院

中国医学科学院学报

CSTPCD北大核心
影响因子:1.496
ISSN:1000-503X
年,卷(期):2024.46(6)