Protective effects of Scutellaria baicalensis Georgi against hydrogen peroxide-induced DNA damage and apoptosis in HaCaT human skin keratinocytes
| Autor: | Yoon, Jung Jeh, Jeong, Jin-Woo, Choi, Eun Ok, Kim, Min Ju, Hwang-Bo, Hyun, Kim, Hong Jae, Hong, Su Hyun, Park, Cheol, Lee, Dong Hee, Choi, Yung Hyun |
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| Rok vydání: | 2016 |
| Předmět: | |
| Zdroj: | EXCLI Journal |
| ISSN: | 1611-2156 |
| Popis: | Oxidative stress due to excessive accumulation of reactive oxygen species (ROS) is one of the risk factors for the development of several chronic diseases. In this study, we investigated the protective effects of Scutellaria bai- calensis rhizome ethanol extract (SBRE) against oxidative stress-induced cellular damage and elucidated the un- derlying mechanisms in the HaCaT human skin keratinocyte cell line. Our results revealed that treatment with SBRE prior to hydrogen peroxide (H2O2) exposure significantly increased viability of aCaT cells. SBRE also effectively attenuated H2O2-induced comet tail formation and inhibited the H2O2-induced phosphorylation levels of the histone γH2AX, as well as the number of apoptotic bodies and Annexin V-positive cells. In addition, SBRE exhibited scavenging activity against intracellular ROS generation and restored the mitochondrial membrane po- tential loss by H2O2. Moreover, H2O2 enhanced the cleavage of caspase-3 and degradation of poly (ADP-ribose)- polymerase, a typical substrate protein of activated caspase-3, as well as DNA fragmentation; however, these events were almost totally reversed by pretreatment with SBRE. Furthermore, SBRE increased the levels of heme oxygenase-1 (HO-1), which is a potent antioxidant enzyme, associated with the induction of nuclear fac- tor-erythroid 2-related factor 2 (Nrf2). According to our data, SBRE is able to protect HaCaT cells from H2O2- induced DNA damage and apoptosis through blocking cellular damage related to oxidative stress through a mech-anism that would affect ROS elimination and activating the Nrf2/HO-1 signaling pathway. EXCLI Journal;Vol. 16 2017 |
| Databáze: | OpenAIRE |
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