Protective Role of Psoralea corylifolia L. Seed Extract against Hepatic Mitochondrial Dysfunction Induced by Oxidative Stress or Aging
- Authors
- Seo, Eunhui; Oh, Yoon Sin; Kim, Donghee; Lee, Mi-Young; Chae, Sungwook; Jun, Hee-Sook
- Issue Date
- Aug-2013
- Publisher
- HINDAWI PUBLISHING CORPORATION
- Citation
- EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE, v.2013
- Journal Title
- EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE
- Volume
- 2013
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/15866
- DOI
- 10.1155/2013/678028
- ISSN
- 1741-427X
- Abstract
- The accumulation of oxidative damage and mitochondrial dysfunction is an important factor that contributes to aging. The Psoralea corylifolia seeds (PCS), commonly known as "Boh-Gol-Zhee" in Korea, have been used traditionally as a medicinal remedy. We investigated whether an extract of PCS has protective effects on oxidative stress and mitochondrial function in hepatocytes. The PCS extract showed an antisenescence effect on human diploid fibroblasts as evidenced by a decreased expression of p16(INK4a) mRNA and senescence-associated beta-galactosidase staining. PCS extract treatment reduced H2O2-induced reactive oxygen species (ROS) production in HepG2 cells, inhibited ROS production in hepatocytes of aged mice, and increased superoxide dismutase activity. In H2O2-treated HepG2 cells, PCS extract treatment recovered ATP production. PCS extract treatment recovered the oxygen consumption rate and inhibited reduction of mitochondrial membrane potential induced by oxidative stress, suggesting improvement of mitochondrial function. In addition, PCS extract treatment recovered peroxisome proliferator-activated receptor gamma coactivator 1 alpha and carnitine palmitoyltransferase 1 mRNA and protein expression, and inhibited mitochondrial genome damage. Treatment with the major component of PCS extract, bakuchiol, also recovered mitochondrial dysfunction. On the basis of these results, we conclude that PCS extract inhibits ROS production and mitochondrial dysfunction induced by oxidative stress in hepatocytes.
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