Brimonidine Can Prevent In Vitro Hydroquinone Damage on Retinal Pigment Epithelium Cells and Retinal Müller Cells
| Autor: | Claudio Ramírez, Javier Cáceres-del-Carpio, Justin Chu, Joshua Chu, M. Tarek Moustafa, Marilyn Chwa, G. Astrid Limb, Baruch D. Kuppermann, M. Cristina Kenney |
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| Rok vydání: | 2015 |
| Předmět: |
0301 basic medicine
Ependymoglial Cells Apoptosis Retinal Pigment Epithelium Pharmacology In Vitro Techniques medicine.disease_cause 03 medical and health sciences chemistry.chemical_compound Brimonidine Tartrate Lactate dehydrogenase medicine Humans Pharmacology (medical) Viability assay Antihypertensive Agents Cells Cultured Membrane Potential Mitochondrial Retinal pigment epithelium L-Lactate Dehydrogenase business.industry Brimonidine Original Articles Hydroquinones Ophthalmology Oxidative Stress 030104 developmental biology medicine.anatomical_structure chemistry Cell culture Cytoprotection business Reactive Oxygen Species Oxidative stress medicine.drug |
| Zdroj: | Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics. 32(2) |
| ISSN: | 1557-7732 |
| Popis: | Purpose: Brimonidine is a selective alpha-2 adrenergic agonist used to reduce intraocular pressure and it has been shown to have some neuroprotective effects. Hydroquinone (HQ) is a toxicant present in cigarette smoke, and other sources. In this study, we investigated the cyto-protective effects in vitro of Brimonidine on human retinal pigment epithelium cells (ARPE-19) and human retinal Müller cells (MIO-M1) that had been treated with HQ. Methods: Cells were pretreated for 6 h with different doses of Brimonidine tartrate 0.1% (1/2×, 1×, 5×, 10×), followed by a 24-h exposure to 100 μM of HQ, while the Brimonidine was still present. Assays were used to measure cell viability, mitochondrial membrane potential (ΔΨm), reactive oxygen species (ROS) production, and lactate dehydrogenase (LDH) release. Results: Brimonidine increased the cell viability at all concentrations studied in both cell lines studied. ΔΨm also improved at all Brimonidine doses in ARPE-19 cells and in the 5× and 10× dosages MIO-M1 cells. The ROS levels decreased at 1×, 5×, and 10× doses of Brimonidine in ARPE-19 but only at 10× on MIO-M1 cells. The 10×-Brimonidine ARPE-19 cells had decreased LDH release, but no LDH changes were observed on MIO-M1 cells. Conclusion: HQ-induced toxicity is mediated through mitochondrial damaging, oxidative stress-related and necrosis-related pathways; Brimonidine significantly prevented the mitochondrial damaging and oxidative stress-related effects but had little effect on blocking the necrosis component of HQ-toxicity. Brimonidine protective effects differ between the different retinal cell types and high concentrations of Brimonidine (10×) have minimal damaging effects on human retinal cells. |
| Databáze: | OpenAIRE |
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