Abstract：
The pathogenesis of ulcerative colitis (UC), a chronic intestine inflammatory disease primarily affecting adolescents, remains uncertain. Contemporary studies suggest that a confluence of elements, including genetic predispositions, environmental catalysts, dysregulated immune responses, and disturbances in the gut microbiome, are instrumental in the initiation and advancement of UC. Among them, inflammatory activation and mucosal barrier damage caused by abnormal immune regulation are essential links in the development of UC. The impairment of the mucosal barrier is intricately linked to the interplay of various cellular mechanisms, including oxidative stress, autophagy, and programmed cell death. An extensive corpus of research has elucidated that level of cyclic adenosine 3\',5\'-monophosphate (cAMP) undergo modifications in the midst of inflammation and participate in a diverse array of cellular operations that mitigate inflammation and the impairment of the mucosal barrier. Consequently, a plethora of pharmacological agents are currently under development, with some advancing through clinical trials, and are anticipated to garner approval as novel therapeutics. In summary, cAMP exerts a crucial influence on the onset and progression of UC, with fluctuations in its activity being intimately associated with the severity of the disease\'s manifestation. Significantly, this review unveils the paramount role of cAMP in the advancement of UC, offering a tactical approach for the clinical management of individuals afflicted with UC.
摘要：
溃疡性结肠炎（UC）的发病机制，一种主要影响青少年的慢性肠道炎性疾病，仍然不确定。当代研究表明，元素的融合，包括遗传倾向，环境催化剂，失调的免疫反应，和肠道微生物群的紊乱，在UC的启动和发展中发挥了重要作用。其中,炎症激活和免疫调节异常引起的黏膜屏障损伤是UC发生发展的重要环节。粘膜屏障的损伤与各种细胞机制的相互作用密切相关。包括氧化应激,自噬,和程序性细胞死亡。广泛的研究已经阐明了环腺苷3'的水平，5'-单磷酸(cAMP)在炎症中经历修饰,并参与减轻炎症和粘膜屏障损伤的多种细胞操作。因此,目前正在开发大量的药物，随着一些临床试验的进展，并有望获得批准作为新疗法。总之,cAMP对UC的发生和进展有至关重要的影响,其活动的波动与疾病表现的严重程度密切相关。重要的是,这项审查揭示了cAMP在UC发展中的重要作用，为UC患者的临床管理提供了一种战术方法。
