Curcumin (diferuloylmethane) derived from the rhizome of Curcuma longa L. has been used for thousands of years in traditional Chinese medicine and Ayurvedic medicine in Asian countries to treat liver diseases, rheumatoid diseases, diabetes, atherosclerosis, infectious diseases and cancer. It exhibits a wide range of pharmacological properties, which include antioxidant, anti-inflammatory, antimutagenic, antimicrobial and anticancer activity. Herein the mechanisms of curcumin impact on oxidative stress, angiogenesis and inflammatory processes are described indicating that curcumin use may inhibit those pathological conditions and restore body homeostasis. Its effectiveness was also proved for major eye diseases. In this review, the influence of curcumin on eye diseases, such as glaucoma, cataract, age-related macular degeneration, diabetic retinopathy, corneal neovascularization, corneal wound healing, dry eye disease, conjunctivitis, pterygium, anterior uveitis are reported. The analysis of a number of clinical and preclinical investigations indicates that curcumin may be used as a therapeutic agent in the treatment of various eye disorders.

The increasing understanding of immune mechanisms changed our perception of the ocular surface, which is now considered a compartment of the common mucosal immune system. It offered the possibility to alter the physiological immune response on the ocular surface and effectively combat inflammation, which impairs stability of the tear film and causes tear hyperosmolarity, causing symptoms of dry eye disease. The paper provides an overview of ocular surface anatomy and physiology, explains the underlying mechanisms of dry eye disease and discusses novel and promising treatment modalities, such as cyclosporine A, biological therapies using autologous serum and various growth factors as well as experimental treatment methods which are currently being investigated.

Introduction : Two human-specific Demodex species have been described: Demodex folliculorum and Demodex brevis. A medical condition caused by the presence of Demodex is called demodicosis. Material and methods: The study material comprised eyelashes collected from 1499 patients....

Co-operation of the endogenous and exogenous defense system maintains redox homeostasis and is essential for health. The endogenous defense system includes enzymatic (e.g. superoxide dismutase, catalase) and non-enzymatic, low molecular-weight scavengers (e.g. glutathione, ascorbic acid). Pathogenesis of many serious diseases (e.g. cancer, ischemic heart disease) includes oxidative stress which can disturb angiogenesis, the process of formation of new blood vessels sprouting from the existing one. Antioxidants, through reduction of oxidative stress and influence on neovascularization, may modulate progress and results of therapy in those diseases where such processes play an important role. Herein the impact of exogenous antioxidants on angiogenesis and factors modulating this process is presented. Most synthetic antioxidants whose activity has been described (namely N-acetylcysteine, pentoxifylline, synthetic analogue of curcumin, synthetic analogue of epigallocatechin-3 gallate [EGCG], tripertenoids) exert an inhibitory effect on neovascularization. A similar effect was also exhibited by several natural origin antioxidants (e.g. resveratrol, EGCG), which suggests that their application in therapy might normalize excessive angiogenesis. Some natural origin antioxidants e.g. purple coneflower and preparations consisting of natural antioxidants such as Padma 28 and Immunal forte increase a too low baseline level of angiogenesis and decreases a too high level. These preparations exert a regulatory effect on and may normalize neovascularization. They can be used in the case of diseases associated with too low or too high angiogenesis.

Dry eye disease (DED) is increasingly recognized as a condition driven by immune dysregulation at the ocular surface (OS). Chronic inflammation, mediated by aberrant activation of both innate and adaptive immune pathways, underlies disease progression and symptom persistence. Neuroimmune interactions further amplify OS inflammation, contributing to epithelial damage and impaired homeostatic regulation. This review summarizes current literature on the immunopathogenesis of DED, highlighting the complex interplay of molecular mechanisms of innate and adaptive immune activation, neuroimmune-mediated inflammation, and emerging molecular and cellular biomarkers. In addition, we examine existing and emerging therapeutic strategies that target these immune-molecular pathways, including precision immunomodulatory approaches, to inform future management of DED. By integrating mechanistic insights with clinical findings, this review aims to provide a comprehensive overview of the molecular mechanisms underlying the dysregulated immune response associated with DED.