Melatonin delays photoreceptor degeneration in a mouse model of autosomal recessive retinitis pigmentosa.

摘要: Retinitis pigmentosa (RP) comprises a group of incurable inherited retinal degenerations. Targeting common processes, instead mutation-specific treatment, has proven to be an innovative strategy combat debilitating degeneration. Growing evidence indicates that melatonin possesses potent activity against neurodegenerative disorders by mitigating cell damage associated with apoptosis and inflammation. Given the pleiotropic role in central nervous system, aim present study was investigate whether would afford protection degeneration autosomal recessive RP (arRP). Rd10, well-characterized murine model human arRP, received daily intraperitoneal injection (15 mg/kg) between postnatal day (P) 13 P30. Retinas treated or vehicle were harvested for analysis at P30 P45, respectively. The findings showed could dampen photoreceptors death delay consequent We also observed weakened expression glial fibrillary acidic protein (GFAP) Muller cells. Additionally, alleviate inflammatory response visualized IBA1 staining, which further corroborated downregulation inflammation-related genes, such as tumor necrosis factor alpha (Tnf-α), chemokine (C-C motif) ligand 2 (Ccl2), (C-X-C 10 (Cxcl10). These data revealed ameliorate through potentially attenuating apoptosis, reactive gliosis, microglial activation rd10 mice. Moreover, these results suggest promising agent improving survival RP.