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<p>Background and purpose Optic neuritis (ON) is an inflammatory condition of the optic nerve, characterized by peri- or retro-ocular pain accentuated by eye movement, reduced colour vision, abnormal visual acuity and field, a relative afferent pupillary defect, and abnormal visual evoked potentials (VEPs). We have developed an experimental model of primary ON in rats through a single microinjection of 4.5&#xa0;µg of bacterial lipopolysaccharide (LPS) into the optic nerve. Since metformin acts as a pleiotropic therapeutic agent in various neurodegenerative diseases, we analyzed the effect of metformin on LPS-induced ON. Experimental approach : LPS or vehicle were injected into the optic nerve from adult male Wistar rats. One group of animals received an intraperitoneal injection of metformin (100&#xa0;mg/kg), 24&#xa0;h before and 2-, 4- and 6-days post-vehicle or LPS injection in the optic nerve, while another group was injected with vehicle. Key results : Metformin prevented blood-brain barrier disruption, optic nerve cell infiltration, macro and microgliosis, retinal ganglion cell and optic nerve axon loss, and consensual pupillary light-reflex (PLR) and VEP alterations induced by LPS, likely through AMP-activated kinase (AMPK)-dependent and antioxidant mechanisms. When metformin was administered at 4-days post-LPS, it was able to reverse the alterations in PLR and VEPs induced by LPS. Conclusions and implications : We found that metformin prevented structural and functional damage of the optic nerve induced by experimental primary ON. Moreover, metformin was able to protect ongoing visual dysfunction. These data suggest that metformin could be a promising candidate for ON treatment. </p>

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Neuroprotective effect of metformin in experimental optic neuritis in rats

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月31日

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  • Nathaly A. Bernal Aguirre,
  • Marco A. García Tovar,
  • Ignacio L. Caballero Lescano,
  • Diego Cifarelli,
  • Juan S. Calanni,
  • Hernan H. Dieguez,
  • Ruth E. Rosenstein,
  • Damian Dorfman

摘要

Background and purpose Optic neuritis (ON) is an inflammatory condition of the optic nerve, characterized by peri- or retro-ocular pain accentuated by eye movement, reduced colour vision, abnormal visual acuity and field, a relative afferent pupillary defect, and abnormal visual evoked potentials (VEPs). We have developed an experimental model of primary ON in rats through a single microinjection of 4.5 µg of bacterial lipopolysaccharide (LPS) into the optic nerve. Since metformin acts as a pleiotropic therapeutic agent in various neurodegenerative diseases, we analyzed the effect of metformin on LPS-induced ON. Experimental approach : LPS or vehicle were injected into the optic nerve from adult male Wistar rats. One group of animals received an intraperitoneal injection of metformin (100 mg/kg), 24 h before and 2-, 4- and 6-days post-vehicle or LPS injection in the optic nerve, while another group was injected with vehicle. Key results : Metformin prevented blood-brain barrier disruption, optic nerve cell infiltration, macro and microgliosis, retinal ganglion cell and optic nerve axon loss, and consensual pupillary light-reflex (PLR) and VEP alterations induced by LPS, likely through AMP-activated kinase (AMPK)-dependent and antioxidant mechanisms. When metformin was administered at 4-days post-LPS, it was able to reverse the alterations in PLR and VEPs induced by LPS. Conclusions and implications : We found that metformin prevented structural and functional damage of the optic nerve induced by experimental primary ON. Moreover, metformin was able to protect ongoing visual dysfunction. These data suggest that metformin could be a promising candidate for ON treatment.