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Kyoung Ah Kang

Researcher at Jeju National University

Publications -  133
Citations -  5336

Kyoung Ah Kang is an academic researcher from Jeju National University. The author has contributed to research in topics: Oxidative stress & Reactive oxygen species. The author has an hindex of 38, co-authored 124 publications receiving 4393 citations. Previous affiliations of Kyoung Ah Kang include New Generation University College.

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Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis

TL;DR: In this paper, the authors investigated the possible molecular mechanisms underlying the cytotoxic effects of AgNPs and found that AgNs induced reactive oxygen species (ROS) generation and suppression of reduced glutathione (GSH) in human Chang liver cells.
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Particulate matter 2.5 damages skin cells by inducing oxidative stress, subcellular organelle dysfunction, and apoptosis.

TL;DR: The results indicate that PM2.5 induced oxidative stress by generating reactive oxygen species both in vitro and in vivo, which led to DNA damage, lipid peroxidation, and protein carbonylation, and caused apoptosis in HaCaT cells and mouse skin tissue.
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Eckol isolated from Ecklonia cava attenuates oxidative stress induced cell damage in lung fibroblast cells.

TL;DR: The results suggest that eckol protects V79‐4 cells against oxidative damage by enhancing the cellular antioxidant activity and modulating cellular signal pathway.
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Cytoprotective effect of phloroglucinol on oxidative stress induced cell damage via catalase activation.

TL;DR: The results suggest that phloroglucinol protects V79‐4 cells against oxidative damage by enhancing the cellular catalase activity and modulating ERK signal pathway.
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Up-regulation of Nrf2-mediated heme oxygenase-1 expression by eckol, a phlorotannin compound, through activation of Erk and PI3K/Akt.

TL;DR: It is demonstrated that eckol attenuates oxidative stress by activating Nrf2-mediated HO-1 induction via Erk and PI3K/Akt signaling, and treatments with U0126 and LY294002 inhibited the eickol-induced cytoprotective effect against oxidative cell damage.