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KMID : 0613820170270111349
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Journal of Life Science
2017 Volume.27 No. 11 p.1349 ~ p.1356
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The Ca2+-activated K+ (BK) Channel-opener NS 1619 Prevents Hydrogen Peroxide-induced Cell Death and Mitochondrial Dysfunction in Retinal Pigment Epithelial Cells
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Kang Jae-Hoon
Woo Jae-Seok
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Abstract
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Potassium channel openers (KCOs) produce physiological and pharmacological defense mechanisms against cell injuries caused by oxidative stress of diverse origins. Openings of mitochondrial and plasmalemmal K+ channels are involved in the defense mechanisms. This study tested whether NS 1619, an opener of large-conductance BK channels, has a similar beneficial influence on the pigment epithelial cells of retinas. The human retinal pigment epithelial cell line ARPE-19 was exposed to H2O2-induced oxidative stress in the absence and presence of NS 1619. The degrees of the cells' injuries were assessed by analyzing the cells' trypan-blue exclusion abilities and TUNEL staining. NS 1619 produced remarkable protections against cell injuries caused by H2O2. It prevented apoptotic and necrotic cell deaths. The protective effect of NS 1619 was significantly diminished when the cells were treated with NS 1619 in combination with the BK channel-blocker paxilline. NS 1619 significantly ameliorated cellular ATP deprivations in H2O2-treated cells. It helped mitochondria preserve their functional integrity, which was estimated by their MTT reduction abilities and mitochondrial membrane potential. In conclusion, it was suggested that NS 1619 had a beneficial effect on mitochondria in regards to preserving their functional integrity under oxidative stress, and it produces defense mechanisms against oxidant-induced cell injuries in ARPE-19 cells.
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KEYWORD
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Cell death, KCOs, mitochondria, oxidative stress, RPE cells
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