Melatonin delays photoreceptor degeneration in a mouse model of autosomal recessive retinitis pigmentosa
Autor: | Shu-Min Wang, Zhizhong Ma, Ying Jin, Yun-Tao Hu, Xiao-Jian Xu, Kang Feng |
---|---|
Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Retinal degeneration medicine.medical_specialty Ependymoglial Cells Drug Evaluation Preclinical CCL2 Biology Neuroprotection Antioxidants Melatonin 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Endocrinology Internal medicine Retinitis pigmentosa medicine CXCL10 Animals Gliosis Glial fibrillary acidic protein Retinal medicine.disease Disease Models Animal 030104 developmental biology chemistry biology.protein Microglia hormones hormone substitutes and hormone antagonists 030217 neurology & neurosurgery Retinitis Pigmentosa medicine.drug Photoreceptor Cells Vertebrate |
Zdroj: | Journal of pineal research. 63(3) |
ISSN: | 1600-079X |
Popis: | Retinitis pigmentosa (RP) comprises a group of incurable inherited retinal degenerations. Targeting common processes, instead of mutation-specific treatment, has proven to be an innovative strategy to combat debilitating retinal degeneration. Growing evidence indicates that melatonin possesses a potent activity against neurodegenerative disorders by mitigating cell damage associated with apoptosis and inflammation. Given the pleiotropic role of melatonin in central nervous system, the aim of the present study was to investigate whether melatonin would afford protection against retinal degeneration in autosomal recessive RP (arRP). Rd10, a well-characterized murine model of human arRP, received daily intraperitoneal injection of melatonin (15 mg/kg) between postnatal day (P) 13 and P30. Retinas treated with melatonin or vehicle were harvested for analysis at P30 and P45, respectively. The findings showed that melatonin could dampen the photoreceptors death and delay consequent retinal degeneration. We also observed that melatonin weakened the expression of glial fibrillary acidic protein (GFAP) in Muller cells. Additionally, melatonin could alleviate retinal inflammatory response visualized by IBA1 staining, which was further corroborated by downregulation of inflammation-related genes, such as tumor necrosis factor alpha (Tnf-α), chemokine (C-C motif) ligand 2 (Ccl2), and chemokine (C-X-C motif) ligand 10 (Cxcl10). These data revealed that melatonin could ameliorate retinal degeneration through potentially attenuating apoptosis, reactive gliosis, and microglial activation in rd10 mice. Moreover, these results suggest melatonin as a promising agent improving photoreceptors survival in human RP. |
Databáze: | OpenAIRE |
Externí odkaz: | |
Nepřihlášeným uživatelům se plný text nezobrazuje | K zobrazení výsledku je třeba se přihlásit. |