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Anthocyanins from Hibiscus syriacus L. Inhibit Oxidative Stress-mediated Apoptosis by Activating the Nrf2/HO-1 Signaling Pathway

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2019 한국자원식물학회 정기총회 및 추계학술대회 ‘한반도 내륙생물자원 활용 전략’ 91

F-P-30

Anthocyanins from Hibiscus syriacus L. Inhibit Oxidative

Stress-mediated Apoptosis by Activating the Nrf2/HO-1

Signaling Pathway

Ilandarage Menu Neelaka Molagoda

1

,

Wisurumuni Arachchilage Hasitha Maduranga Karunarathne

1

,

Kyoung Tae Lee

2

,

Yung Hyun Choi

3

,

Rajapaksha Gedara Prasad Tharanga Jayasooriya

4

and Gi-Young Kim

1

*

1Department of Marine Life Science, Jeju National University

2Department of Biochemistry, College of Oriental Medicine, Dong-Eui University 3Forest Biomaterials Research Center, National Institute of Forest Science

4Department of Food Technology, Faculty of Technology, Rajarata University of Sri Lanka

Hibiscus syriacus L. is widely distributed throughout Eastern and Southern Asia and its root bark has been used as a traditional remedy. Recently, the extracts of H. syriacus L. exerts anti-cancerous, anti-microbial, and anti-inflammatory activities. However, the effect of anthocyanin-rich fraction of H. syriacus L. petals (PS) has not been studied under excessive oxidative stress. In this study, we evaluated the cellular protective effect of PS in HaCaT human skin keratinocytes under hydrogen peroxide (H2O2)-induced oxidative stress conditions. PS at below 400 µg/ml did not show any cell death; however,

over 800 µg/ml of PS gradually increased cell death. PS at below 400 µg/ml significantly inhibited H2O2-induced apoptosis in HaCaT cells concomitant with downregulation of Bax and upregulation of

pro-PARP and p-Bcl-2. Additionally, PS remarkably reversed H2O2-induced excessive reactive oxygen

species (ROS) production and apoptosis, and also significantly inhibited mitochondrial ROS production concomitant with suppression of H2O2-induced mitochondrial depolarization. H2O2-mediated ratio of Bax

to Bcl-2, and caspase-3 activation were markedly abolished in the presence of PS. Moreover, the inhibition of HO-1 function using zinc protoporphyrin, an HO-1 inhibitor, significantly attenuated the cellular protective effects of PS against H2O2, indicating the significance of HO-1 in PS mediated

cytoprotective effect, which was mediated by activating nuclear factor erythroid 2-related factor-2 (Nrf2). Taken together, our results suggest that cytoprotective effect of PS in HaCaT keratinocytes against oxidative stress-induced apoptosis is mediated by inhibiting cellular and mitochondrial ROS production, which is downregulated by activating Nrf2/HO-1 axis.

[This research was supported by Basic Science Research Program to RIBS of Jeju National University through the National Research Foundation of Korea (NRF) funded by the Ministry of Education (2019 R1A6A1A10072987).]

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