Sleep deprivation exacerbates lens‑induced myopia in association with ERK/NF‑κB pathway activation

The objective of the present study was to examine the molecular mechanisms by which sleep deprivation (SD) exacerbates lens‑induced myopia (LIM). Guinea pig models were established for the LIM and LIM + SD groups, with 15 animals per group. Guinea pigs in the LIM + SD group underwent 20 h of daily SD in addition to wearing concave lenses on the right eye. Additional guinea pig models were established for the LIM + SD and LIM + SD + BVD‑523 groups, each containing 15 animals. The LIM + SD + BVD‑523 group received oral administration of BVD‑523, an inhibitor of the ERK1/2. Biological parameters, including diopter and axial length, were measured. Retinal dopamine (DA) levels were evaluated with high‑performance liquid chromatography-electrochemistry, tyrosine hydroxylase (TH) expression by immunofluorescence staining, retinal ERK/NF‑κB signaling pathway expression by western blotting and retinal inflammatory cytokine levels by ELISA. Relative to the LIM group, the LIM + SD group demonstrated increased diopter and axial length, decreased retinal DA and TH levels, elevated inflammatory cytokine expression and activation of the ERK/NF‑κB signaling pathway, which were associated with myopia progression. However, administration of BVD‑523 inhibited increases in diopter and axial length, restored retinal DA and TH levels and downregulated inflammatory cytokine expression, which was associated with alleviation of myopia. In conclusion, SD may exacerbate LIM in association with ERK/NF‑κB pathway activation, representing a potential therapeutic target for myopia, as the ERK1/2 inhibitor BVD‑523 can suppress SD‑induced myopia.