Antioxidant and cytoprotective effects of Stachys riederi var. japonica ethanol extract on UVA‑irradiated human dermal fibroblasts

Hwang,Ji Yeon; Yadav,Anil Kumar; Jang,Byeong‑Churl; Kim,Young Chul

doi:10.3892/ijmm.2019.4048

Antioxidant and cytoprotective effects of Stachys riederi var. japonica ethanol extract on UVA‑irradiated human dermal fibroblasts

Authors:
- Ji Yeon Hwang
- Anil Kumar Yadav
- Byeong‑Churl Jang
- Young Chul Kim
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Affiliations: Department of Research and Development, Research Center for Natural Ingredients and New Materials, Daepyung Co., Ltd., Sangju 37112, Republic of Korea, Department of Molecular Medicine, College of Medicine, Keimyung University, Daegu 42601, Republic of Korea, Department of Public Health, Faculty of Food and Health Sciences, Keimyung University, Daegu 42601, Republic of Korea
Published online on: January 2, 2019 https://doi.org/10.3892/ijmm.2019.4048
Pages: 1497-1504

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Abstract

Stachys riederi is one of the largest genera in the flowering plant family Lamiaceae. The aqueous extract of Stachys riederi var. japonica is known for its anti‑allergic effect. In the present study, the antioxidant and cytoprotective effects of Stachys riederi var. japonica ethanol extract (SREE) on ultraviolet A (UVA)‑irradiated human dermal fibroblasts (HDFs) were evaluated. At 100 µg/ml, SREE significantly inhibited production of reactive oxygen species (ROS) in UVA‑irradiated HDFs. SREE at 100 µg/ml additionally markedly interfered with the loss of mitochondrial membrane potential (ΔΨm) in these cells. In addition, SREE at 100 µg/ml attenuated UVA‑induced DNA fragmentation and caspase‑3 activation in HDFs. SREE at 100 µg/ml additionally increased mRNA and protein expressions of Bcl‑2 and decreased those of Bax and cytochrome c in UVA‑irradiated HDFs. In summary, to the best of our knowledge, these results demonstrate for the first time that SREE exhibited antioxidant and cytoprotective effects on UVA‑irradiated HDFs, which may be mediated through suppression of ROS generation, inhibition of the loss of ΔΨm and inhibition of apoptosis.

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