BPC 157 Protects Retina from Ischemic Damage in Rat Model

Retinal ischemia, a condition where blood flow to the retina is insufficient, is a major cause of vision loss and contributes to severe eye diseases like glaucoma and diabetic retinopathy. This lack of oxygen and nutrients leads to irreversible damage to retinal cells. Current therapeutic options are often limited in their ability to fully restore function or prevent progressive damage, highlighting a critical need for novel neuroprotective and vasoprotective strategies to preserve retinal integrity.

The L-NAME treatment successfully induced significant retinal ischemia, characterized by reduced retinal blood flow and functional impairment. However, BPC 157 treatment at both tested doses significantly mitigated these detrimental effects. BPC 157 administered intraperitoneally at 10 µg/kg notably preserved retinal function, showing a significant increase in electroretinogram (ERG) b-wave amplitude by approximately 45% compared to L-NAME-treated controls (p<0.01), indicating improved photoreceptor and bipolar cell activity. Histological examination revealed that BPC 157 treatment significantly reduced retinal ganglion cell loss by around 35% and preserved overall retinal thickness by about 28% in the ischemic eyes (p<0.05). Furthermore, markers of oxidative stress, such as malondialdehyde (MDA), were significantly reduced by BPC 157 by over 20% (p<0.05), suggesting an antioxidant mechanism. The local retrobulbar administration of BPC 157 (10 µg/kg) also demonstrated comparable protective effects, indicating its potential for direct ocular delivery.