Frontiers in pharmacology · 2026
Lycium barbarum glycopeptide confers neuroprotection in chronic ocular hypertensive rats: a study investigating visual function, retinal structure, microcirculation, and pyroptosis.
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Zhao Chunlin, Shi Wei, Lu Xuejing
Аннотация
BACKGROUND: Lycium barbarum glycopeptide (LbGp) has been reported to exert neuroprotective effects, yet its role in chronic ocular hypertension (COH) and the underlying mechanisms remain unclear. This study investigated whether LbGp protects against COH-induced retinal damage by inhibiting pyroptosis.
METHODS: A COH rat model was established, and the animals were randomly assigned to model, LbGp, VX-765 (pyroptosis inhibitor), and VX-765+LbGp groups. After 28 days of treatment, visual function, retinal structure, microcirculation, and pyroptosis-related protein expression were assessed. In parallel, R28 cells subjected to oxygen-glucose deprivation/reperfusion (OGD/R) were used for in vitro validation.
RESULTS: COH model rats exhibited marked visual dysfunction, retinal thinning, microvascular impairment, and upregulation of pyroptosis markers. LbGp treatment significantly attenuated these abnormalities and suppressed pyroptosis activation, showing efficacy comparable to that of VX-765. Notably, combined administration of LbGp and VX-765 produced synergistic effects. In vitro, LbGp similarly reduced pyroptosis-related protein expression in OGD/R-exposed R28 cells.
CONCLUSION: These findings demonstrate that LbGp confers neuroprotection against COH-induced optic nerve injury, at least in part, through inhibition of the pyroptosis pathway. This study provides experimental evidence supporting LbGp as a potential therapeutic candidate for glaucoma.
METHODS: A COH rat model was established, and the animals were randomly assigned to model, LbGp, VX-765 (pyroptosis inhibitor), and VX-765+LbGp groups. After 28 days of treatment, visual function, retinal structure, microcirculation, and pyroptosis-related protein expression were assessed. In parallel, R28 cells subjected to oxygen-glucose deprivation/reperfusion (OGD/R) were used for in vitro validation.
RESULTS: COH model rats exhibited marked visual dysfunction, retinal thinning, microvascular impairment, and upregulation of pyroptosis markers. LbGp treatment significantly attenuated these abnormalities and suppressed pyroptosis activation, showing efficacy comparable to that of VX-765. Notably, combined administration of LbGp and VX-765 produced synergistic effects. In vitro, LbGp similarly reduced pyroptosis-related protein expression in OGD/R-exposed R28 cells.
CONCLUSION: These findings demonstrate that LbGp confers neuroprotection against COH-induced optic nerve injury, at least in part, through inhibition of the pyroptosis pathway. This study provides experimental evidence supporting LbGp as a potential therapeutic candidate for glaucoma.