Protective effect of Tisochrysis lutea on dry eye syndrome via NF-κB inhibition

Abstract

Dry eye syndrome (DES) affects the cornea, causes pain and hypersensitivity to light. Although inflammation and endoplasmic reticulum stress are known to be involved, the detailed mechanisms remain unknown. DES is characterized by a decrease in corneal thickness, tear volume, and lacrimal gland size, and damage to corneal cells. Tisochrysis lutea is a microalga that has been shown to reduce immune factors. Therefore, we hypothesized that T. lutea could ameliorate DES. We investigated the role of T. lutea in scopolamine-induced DES in BALB/c mice. Oral administration of T. lutea increased corneal thickness, tear volume, and size of the corneal cells, and reduced damage to the corneal cells. Furthermore, treatment of ARPE-19 human retinal pigmented epithelial cells with T. lutea reduced expression of the inflammatory factor, NF-κB, MAPK, and AKT. T. lutea may be used therapeutically to reduce the symptoms of DES.

Enhancing Ocular Surface in Dry Eye Disease Patients: A Clinical Evaluation of a Topical Formulation Containing Sesquiterpene Lactone Helenalin

“…The short-term nature of the clinical follow-up, especially in the efficacy study, restricts our ability to assess the long-term effects of the helenalin-based formulation. On the other hand, the rapid and multi-targeted efficacy of the studied formulation aligns with previous outcomes of similar studies that blocked NF-κB/TNF-α pathways [ 65 , 74 , 75 ]. It is important to recognize that the rapid improvement observed in this study may not be representative of the standard response across all DED therapies.…”

“…The exact mechanisms behind NF-κB activation in DED are not fully understood. Still, oxidative stress and continuous tear film hyperosmotic stress are believed to contribute to its dysregulation, leading to persistent inflammation in the cornea and conjunctiva of DED patients [ 64 , 65 ]. NF-κB activation pathways release pro-inflammatory cytokines (such as IL-1b, IL-2, IL-6, IL-8, IL-12, and TNF-α) and chemokines (MCP-1, IL-18, and CXCL 10), which can not only trigger an inflammatory response but also lead to goblet cell loss.…”

APX‑115A, a pan‑NADPH oxidase inhibitor, reduces the degree and incidence rate of dry eye in the STZ‑induced diabetic rat model

“…Furthermore, pathological alterations were detected in the cornea and lacrimal glands of the diabetic rat models. The relationship between changes in cornea thickness and diabetic dry eye remains unclear, but studies have demonstrated that reduced corneal epithelial thickness is a diabetic complication (65,66). However, in the present study, the change in corneal thickness in diabetic rats was not reversed, although the intracellular vacuoles and acinar atrophy were ameliorated by APX-115A treatment in the diabetic rats.…”

Lacrimal gland Alterations and the Effect of artesunate on experimental induced diabetes rat models and related mechanisms

“…However, the DM + ART (50 mg/kg) and DM + INS intervention groups displayed normal lobular patterns and no acinar atrophy and fibrosis. The relationship between changes in cornea thickness and diabetic dry eye remains unclear, but studies have demonstrated that reduced corneal epithelial thickness is a diabetic complication [29][30][31] We have observed corneal epithelial staining was improved significantly with ART treatment. ART has also been shown to alleviate inflammatory cell infiltration in the lacrimal gland, increased cell nuclei, and fewer vacuoles were seen in the cortical region of the lens.…”