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protective effects of 17β‑estradiol on benzo(e) pyrene[b(e)p]‑induced toxicity in arpe‑19 cells
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نویسنده
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sapkal ashish u. ,nashine sonali ,mansoor saffar ,sharma vishal r. ,ramirez claudio a. ,migon rafael z. ,gupta navin k. ,chwa marilyn ,kuppermann baruch d. ,kenney m. cristina
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منبع
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journal of ophthalmic and vision research - 2018 - دوره : 13 - شماره : 4 - صفحه:418 -425
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چکیده
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Purpose: the aim of this study was to examine the effect of 17β‑estradiol on benzo(e)pyrene [b(e)p]‑induced toxicity in arpe‑19 cells. methods: we pretreated arpe‑19 cells with 20 nm and 40 nm 17β‑estradiol for 6 hours, followed by addition of 300 µm b(e)p for additional 24 hours. cell viability was measured using trypan blue dye‑exclusion assay. jc‑1 assay was performed to measure mitochondrial membrane potential (δψm). for a quantitative estimation of cell death, apoptotic markers such as caspase‑3/7, caspase‑9, and caspase‑12 were measured. results: our results demonstrated that when treated with b(e)p, the viability and δψm of arpe‑19 cells declined by 25% and 63%, respectively (p < 0.05). however, pretreating with 17β‑estradiol increased the viability of arpe‑19 cells by 21% (20 nm) and 10% (40 nm) (p < 0.05). furthermore, the significantly reduced δψm in βe+b(e)p treated cells arpe‑19 cells was restored by pre‑treatment with 17β‑estradiol‑ δψm was increased by 177% (20 nm) and 158% (40 nm) (p < 0.05). we further observed a significant up‑regulation in the activity of caspases‑3/7, ‑9, and ‑12 in b(e)p‑treated arpe‑19 cells. however, 17β‑estradiol treatment significantly reduced the activity of all apoptotic markers (p < 0.05). conclusion: in conclusion, our results demonstrate that 17β‑estradiol protects arpe‑19 cells against b(e) p‑induced toxicity by decreasing apoptosis, preventing cell death, and restoring mitochondrial membrane potential.
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کلیدواژه
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17β‑estradiol ,benzo(e)pyrene ,age‑related macular degeneration ,apoptosis ,retinal pigment epithelial cells ,smoking
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آدرس
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university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, usa, university of california, gavin herbert eye institute, department of ophthalmology, department of pathology and laboratory medicine, usa
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پست الکترونیکی
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mkenney@uci.edu
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Authors
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