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Baicalein Decreases Hydrogen Peroxide-Induced Damage to NG108-15 Cells via Upregulation of Nrf2.
J Cell Physiol. 2015 Aug; 230(8):1840-51.JC

Abstract

Baicalein is a flavonoid inhibitor of 12-lipoxygenase. Here, we investigated its effect on hydrogen peroxide-induced damage to NG108-15 cells. Hydrogen peroxide activated the mitochondrial apoptotic pathway, decreased Nrf2 expression, increased reactive oxygen species (ROS) levels, reduced viability, and increased cell death after 2-24 h treatment of NG108-15 cells. Co-treatment with hydrogen peroxide and baicalein completely suppressed the activation of mitochondrial apoptotic pathway by upregulating Nrf2 expression and reducing ROS stress and partially inhibited the effects on cell viability and cell death. Silencing of 12-lipoxygenase had a similar protective effect to baicalein on hydrogen peroxide-induced damage by blocking the hydrogen peroxide-induced decrease in Nrf2 expression and increase in ROS levels. Neither protective effect was altered by addition of 12-hydroxyeicosatetraenoic acid, the product of 12-lipoxygenase, suggesting that hydrogen peroxide induced damage via 12-lipoxygenase by another, as yet unknown, mechanism, rather than activating it. Co-treatment of cells with hydrogen peroxide and N-acetylcysteine or the Nrf2 inducer sulforaphane reduced hydrogen peroxide-induced damage in a similar fashion to baicalein, while the Nrf2 inhibitor retinoic acid blocked the protective effect of baicalein. Silencing Nrf2 also inhibited the protective effects of baicalein, sulforaphane, and N-acetylcysteine and resulted in high ROS levels, suggesting ROS elimination was mediated by Nrf2. Taken together our results suggest that baicalein protects cells from hydrogen peroxide-induced activation of the mitochondrial apoptotic pathway by upregulating Nrf2 and inhibiting 12-lipoxygenase to block the increase in ROS levels. Hydrogen peroxide also activates a second mitochondrial dysfunction independent death pathway which is resistant to baicalein.

Authors+Show Affiliations

Department of Neurosurgery, Chi Mei Medical Center, Tainan, Taiwan, Republic of China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25557231

Citation

Yeh, Chao-Hung, et al. "Baicalein Decreases Hydrogen Peroxide-Induced Damage to NG108-15 Cells Via Upregulation of Nrf2." Journal of Cellular Physiology, vol. 230, no. 8, 2015, pp. 1840-51.
Yeh CH, Ma KH, Liu PS, et al. Baicalein Decreases Hydrogen Peroxide-Induced Damage to NG108-15 Cells via Upregulation of Nrf2. J Cell Physiol. 2015;230(8):1840-51.
Yeh, C. H., Ma, K. H., Liu, P. S., Kuo, J. K., & Chueh, S. H. (2015). Baicalein Decreases Hydrogen Peroxide-Induced Damage to NG108-15 Cells via Upregulation of Nrf2. Journal of Cellular Physiology, 230(8), 1840-51. https://doi.org/10.1002/jcp.24900
Yeh CH, et al. Baicalein Decreases Hydrogen Peroxide-Induced Damage to NG108-15 Cells Via Upregulation of Nrf2. J Cell Physiol. 2015;230(8):1840-51. PubMed PMID: 25557231.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Baicalein Decreases Hydrogen Peroxide-Induced Damage to NG108-15 Cells via Upregulation of Nrf2. AU - Yeh,Chao-Hung, AU - Ma,Kuo-Hsing, AU - Liu,Pei-Shan, AU - Kuo,Jung-Kuei, AU - Chueh,Sheau-Huei, PY - 2014/03/27/received PY - 2014/12/16/accepted PY - 2015/1/6/entrez PY - 2015/1/6/pubmed PY - 2015/7/16/medline SP - 1840 EP - 51 JF - Journal of cellular physiology JO - J Cell Physiol VL - 230 IS - 8 N2 - Baicalein is a flavonoid inhibitor of 12-lipoxygenase. Here, we investigated its effect on hydrogen peroxide-induced damage to NG108-15 cells. Hydrogen peroxide activated the mitochondrial apoptotic pathway, decreased Nrf2 expression, increased reactive oxygen species (ROS) levels, reduced viability, and increased cell death after 2-24 h treatment of NG108-15 cells. Co-treatment with hydrogen peroxide and baicalein completely suppressed the activation of mitochondrial apoptotic pathway by upregulating Nrf2 expression and reducing ROS stress and partially inhibited the effects on cell viability and cell death. Silencing of 12-lipoxygenase had a similar protective effect to baicalein on hydrogen peroxide-induced damage by blocking the hydrogen peroxide-induced decrease in Nrf2 expression and increase in ROS levels. Neither protective effect was altered by addition of 12-hydroxyeicosatetraenoic acid, the product of 12-lipoxygenase, suggesting that hydrogen peroxide induced damage via 12-lipoxygenase by another, as yet unknown, mechanism, rather than activating it. Co-treatment of cells with hydrogen peroxide and N-acetylcysteine or the Nrf2 inducer sulforaphane reduced hydrogen peroxide-induced damage in a similar fashion to baicalein, while the Nrf2 inhibitor retinoic acid blocked the protective effect of baicalein. Silencing Nrf2 also inhibited the protective effects of baicalein, sulforaphane, and N-acetylcysteine and resulted in high ROS levels, suggesting ROS elimination was mediated by Nrf2. Taken together our results suggest that baicalein protects cells from hydrogen peroxide-induced activation of the mitochondrial apoptotic pathway by upregulating Nrf2 and inhibiting 12-lipoxygenase to block the increase in ROS levels. Hydrogen peroxide also activates a second mitochondrial dysfunction independent death pathway which is resistant to baicalein. SN - 1097-4652 UR - https://www.unboundmedicine.com/medline/citation/25557231/Baicalein_Decreases_Hydrogen_Peroxide_Induced_Damage_to_NG108_15_Cells_via_Upregulation_of_Nrf2_ L2 - https://doi.org/10.1002/jcp.24900 DB - PRIME DP - Unbound Medicine ER -