Abstract Title:

Gomisin A modulates aging progress via mitochondrial biogenesis in human diploid fibroblast cells.

Abstract Source:

Clin Exp Pharmacol Physiol. 2018 06 ;45(6):547-555. Epub 2018 Feb 13. PMID: 29319901

Abstract Author(s):

Jeong-Seok Kim, Seon-Hwa Jeong, Sin-Hee Han, Ho-Keun Yi

Article Affiliation:

Jeong-Seok Kim


Gomisin A from the fruit of Schisandra chinensis has many pharmacological properties, including hepato-protective, anti-diabetic, and anti-oxidative stress. However, the potential benefit of gomisin A is still not well understood, especially in aging progression. Therefore, the aim of this study was to clarify whether the promotion of mitochondrial biogenesis and autophagy of gomisin A affects anti-aging progression, and its mechanism. Intermediate (PD32) human diploid fibroblast (HDF) cells were brought to stress-induced premature senescence (SIPS) using hydrogen peroxide. Gomisin A inhibited reactive oxygen species production even in the SIPS-HDF cells. Gomisin A was also able to attenuate the activity of senescence-associatedĪ²-galactosidase and the production of pro-inflammatory molecules in the SIPS as well as aged HDF cells. The antioxidant activity of gomisin A was determined by recovering the Cu/Zn, Mn-SOD, and HO-1 expression in the SIPS-HDF cells. In mechanistic aspect, gomisin A inhibited the mitogen-activated protein kinase pathway and the translocation of nuclear factor kappa B to the nucleus. In addition, gomisin A promoted the autophagy and mitochondrial biogenesis factors through the translocation of nuclear factor erythroid 2-related factor-2, and inhibited aging progression in the SIPS-HDF cells. Insummary, the enhanced properties of mitochondrial biogenesis and autophagy of gomisin A has a benefit to control age-related molecules against SIPS-induced chronic oxidative stress, and gomisin A may be a potential therapeutic compound for the enhancement of intracellular homeostasis to aging progression.

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