Galectin-1 overexpression protects damaged optic nerve and visual function in mice by inhibiting the p38/ MAPK-NF-κB signaling pathway.

The role of galectin-1 (Gal-1) in traumatic optic neuropathy (TON) remains unclear. Therefore, we investigated the role and action mechanism of Gal-1 in TON induced by optic nerve crush (ONC). Forty male C57BL/6J mice were randomly divided into five groups: control (Con), ONC, phosphate-buffered saline (PBS) intravitreal injection, PBS intravitreal injection combined with ONC (PBS + ONC), and Gal-1 overexpression combined with ONC (Gal-1+ONC) groups. The PBS + ONC group was intravitreally injected with PBS and the Gal-1+ONC group was intravitreally injected with a recombinant adeno-associated virus carrying the Gal-1 target gene (TON was induced 23 days later). Subsequent experiments were performed 5 days post-ONC induction. Gal-1 expression was detected using western blotting (WB) and immunohistochemistry. Retinal ganglion cell (RGC) survival was examined using retinal flat mount immunofluorescence. Flash electroretinography and optomotor response analysis were used to determine retinal and visual functions. Furthermore, WB was performed to evaluate Gal-1-associated molecular mechanisms during TON. RGC survival rate and retinal and visual functions of mice decreased post-TON. However, Gal-1 overexpression inhibited ONC-induced RGC death, flash electroretinogram a-wave and b-wave amplitude decrease, and visual function decline. Moreover, p38/mitogen-activated protein kinase and nuclear factor-κB expression reduced with Gal-1 upregulation. Gal-1 exerts a protective effect against TON in mice by inhibiting the inflammatory response.