Inflammatory bowel disease (IBD), mainly consisting of ulcerative colitis and Crohn's disease, represents a multifaceted and chronic inflammatory disorder that has arisen as a critical public health challenge globally. The underlying mechanisms of IBD are not fully elucidated, involving a complex interaction among various elements, such as genetic predispositions, environmental factors, immune system reactions, and changes in gut microbiota. Being a lifelong disorder, IBD currently has no cure. Prostaglandins (PGs), which are derived from arachidonic acid via a series of enzymatic transformations, encompass several forms, including PGE2, PGD2, PGI2, PGF2alpha, and TXA2. These compounds display a diverse array of biological activities and play a key role in regulating numerous physiological and pathological phenomena, including inflammation, immune responses, cancer development, reproductive processes, cardiovascular health, and gastric mucosal defense. Within the gastrointestinal system, PGs perform various essential functions, such as preserving the mucosal barrier and modulating intestinal motility, blood circulation, and immune activities. Research indicates that PGs are crucial in the disease mechanisms related to IBD, with distinct PG types and their receptors displaying both pro-inflammatory and anti-inflammatory properties. Nevertheless, the associated signaling pathways and molecular interactions are still insufficiently investigated. As a result, therapeutic approaches focusing on PGs and the pathways contributing to their synthesis have become a primary objective in IBD treatment research. This paper intends to examine the significance of PG receptors in IBD, providing a fresh viewpoint for understanding the pathogenesis of the disease and establishing a theoretical basis for creating diagnostic tools and treatment strategies centered around PG targets to improve patient outcomes.