Dry eye is a prevalent chronic inflammatory disease affecting the ocular surface, causing symptoms such as fatigue, tingling, and burning. It is associated with rheumatic diseases, diabetes, hormone disorders, and contact lens use, which activate inflammatory pathways like mitogen-activated protein kinases (MAPK) and nuclear factor-B (NF-κB), leading to macrophage and T cell activation and the production of inflammatory factors. Clinicians use a combination of anti-inflammatory drugs to manage these symptoms, with some being developed for this purpose. This review discusses the inflammatory mechanisms and factors involved in dry eye, as well as the mechanisms and detection limits of anti-inflammatory drugs. Dry eye, inflammation, mechanism, therapy, review Dry eye is a common ocular surface disease affecting 11.3% of people over 50, impacting visual quality and quality of life. It involves the conjunctival goblet cells, lacrimal glands, and meibomian glands, affecting electrolytes, water, mucin, and lipids in the tear film. Inflammation is crucial in dry eye pathogenesis, activating inflammatory pathways and releasing inflammatory factors, leading to a vicious cycle. Common inflammatory pathways include MAPK, NF-κB, and TGF-β, which regulate cytokine secretion and promote inflammation. Inflammation also affects blood and lymphatic vessels, with increased vascular permeability and fluid accumulation. Common factors contributing to dry eye include diabetes, Sjögren's syndrome, sex hormones, and contact lens use. Anti-inflammatory treatments include cyclosporine, corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, autologous serum, hormone therapy, and other therapies. The choice of treatment depends on the patient's symptoms and underlying conditions.Dry eye is a prevalent chronic inflammatory disease affecting the ocular surface, causing symptoms such as fatigue, tingling, and burning. It is associated with rheumatic diseases, diabetes, hormone disorders, and contact lens use, which activate inflammatory pathways like mitogen-activated protein kinases (MAPK) and nuclear factor-B (NF-κB), leading to macrophage and T cell activation and the production of inflammatory factors. Clinicians use a combination of anti-inflammatory drugs to manage these symptoms, with some being developed for this purpose. This review discusses the inflammatory mechanisms and factors involved in dry eye, as well as the mechanisms and detection limits of anti-inflammatory drugs. Dry eye, inflammation, mechanism, therapy, review Dry eye is a common ocular surface disease affecting 11.3% of people over 50, impacting visual quality and quality of life. It involves the conjunctival goblet cells, lacrimal glands, and meibomian glands, affecting electrolytes, water, mucin, and lipids in the tear film. Inflammation is crucial in dry eye pathogenesis, activating inflammatory pathways and releasing inflammatory factors, leading to a vicious cycle. Common inflammatory pathways include MAPK, NF-κB, and TGF-β, which regulate cytokine secretion and promote inflammation. Inflammation also affects blood and lymphatic vessels, with increased vascular permeability and fluid accumulation. Common factors contributing to dry eye include diabetes, Sjögren's syndrome, sex hormones, and contact lens use. Anti-inflammatory treatments include cyclosporine, corticosteroids, non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, autologous serum, hormone therapy, and other therapies. The choice of treatment depends on the patient's symptoms and underlying conditions.