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Updated: Jan 15, 2026
An Optic Nerve Crush Injury Murine Model to Study Retinal Ganglion Cell Survival
Published on: April 25, 2011
Galectin-1 overexpression protects damaged optic nerve and visual function in mice by inhibiting the p38/ MAPK-NF-κB
Xuejun He1, Ning Yang1, Ningzhi Zhang1
1Eye Center, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei Province, China.
Abstract:
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.
Insights
Galectin-1 (Gal-1) overexpression protects against traumatic optic neuropathy (TON) by reducing inflammation and preserving retinal ganglion cell survival and visual function in mice.
Area of Science:
- Ophthalmology
- Neuroscience
- Immunology
Background:
- Traumatic optic neuropathy (TON) is a severe condition with unclear therapeutic targets.
- The specific role of galectin-1 (Gal-1) in the pathogenesis of TON requires further elucidation.
Purpose of the Study:
- To investigate the role and mechanism of galectin-1 (Gal-1) in traumatic optic neuropathy (TON) induced by optic nerve crush (ONC).
- To evaluate the therapeutic potential of Gal-1 overexpression in a mouse model of TON.
Main Methods:
- Establishment of a mouse model of TON via optic nerve crush (ONC).
- Intravitreal injection of phosphate-buffered saline (PBS) or adeno-associated virus carrying Gal-1 gene for overexpression.
- Assessment of galectin-1 expression, retinal ganglion cell (RGC) survival, retinal function (flash electroretinography), and visual function (optomotor response).
- Western blotting to analyze molecular mechanisms involving p38/mitogen-activated protein kinase and nuclear factor-κB pathways.
Main Results:
- Optic nerve crush (ONC) significantly reduced RGC survival, retinal function, and visual function in mice.
- Galectin-1 (Gal-1) overexpression counteracted ONC-induced RGC death and functional deficits.
- Gal-1 upregulation led to decreased expression of p38/mitogen-activated protein kinase and nuclear factor-κB, indicating reduced inflammatory signaling.
Conclusions:
- Galectin-1 (Gal-1) demonstrates a protective effect against traumatic optic neuropathy (TON) in a mouse model.
- Gal-1 mitigates TON by inhibiting inflammatory responses, preserving retinal ganglion cell survival, and restoring visual function.
