Abstract
An important mechanism involved in dry eye (DE) is the association between tear hyperosmolarity and inflammation severity. Inflammation in DE might be mediated by the NLRP3 inflammasome, which activated by exposure to reactive oxygen species (ROS). A combination of carboxymethylcellulose (CMC) and α-melanocyte stimulating hormone (α-MSH) may influence DE through this mechanism, thus avoiding defects of signal drug. In this study, we assessed whether treatment comprising CMC combined with α-MSH could ameliorate ocular surface function; we found that it promoted tear secretion, reduced the density of fluorescein sodium staining, enhanced the number of conjunctival goblet cells, and reduced the number of corneal apoptotic cells. Investigation of the underlying mechanism suggested that the synergistic effect of combined treatment alleviated DE inflammation through reduction of ROS level and inhibition of the NLRP3 inflammasome in human corneal epithelial cells. These findings indicate that combined CMC + α-MSH treatment could ameliorate lesions and restore ocular surface function in patients with DE through reduction of ROS level and inhibition of NLRP3 signalling.
Highlights
The prevalence of dry eye (DE) is reportedly between 5 and 34% worldwide; it is higher among women and elderly individuals[1]
Α-Melanocyte stimulating hormone (α-MSH) is an immunoregulatory neuropeptide derived from melanin precursors; it is mainly produced by the pituitary gland, hypothalamus, and various peripheral tissue cells
Corneal fluorescence staining scores were significantly lower in the CMC, α-Melanocyte stimulating hormone (α-MSH), and CMC + α-MSH groups than in the NaCl group; the lowest score was observed in the CMC + α-MSH group
Summary
The prevalence of dry eye (DE) is reportedly between 5 and 34% worldwide; it is higher among women and elderly individuals[1]. Therapeutic agents include artificial tears, anti-inflammatory drugs, immunosuppressive drugs, and autologous serum. Artificial tears only provide temporary alleviation of symptoms and are ineffective in patients with severe disease. Ns α-Melanocyte stimulating hormone (α-MSH) is an immunoregulatory neuropeptide derived from melanin precursors; it is mainly produced by the pituitary gland, hypothalamus, and various peripheral tissue cells. It was the first immunoregulatory neuropeptide identified in the e yes. Α-MSH contributes to numerous key processes in the eyes, including growth and development, anti-inflammatory function, and immune regulation[6,7,8,9]. To investigate the underlying mechanisms of the combined effects, we performed in vitro examination of reactive oxygen species (ROS) level, as well as the levels of NLRP3 inflammasome and caspase-1 expression
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