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      Ginsenoside Rg1 delays tert-butyl hydroperoxide-induced premature senescence in human WI-38 diploid fibroblast cells.

      The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
      Adenosine Triphosphate, metabolism, Blotting, Western, Cell Aging, drug effects, Cell Line, Cell Line, Tumor, Cell Survival, Cyclin-Dependent Kinase Inhibitor p16, Cyclin-Dependent Kinase Inhibitor p21, Diploidy, Dose-Response Relationship, Drug, Electron Transport, Enzyme-Linked Immunosorbent Assay, Fibroblasts, cytology, Gene Expression, Ginsenosides, chemistry, pharmacology, Humans, Lysosomes, ultrastructure, Microscopy, Electron, Transmission, Mitochondria, Molecular Structure, Reverse Transcriptase Polymerase Chain Reaction, Telomerase, genetics, tert-Butylhydroperoxide

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          Abstract

          Tert-butyl hydroperoxide (t-BHP), an analog of hydroperoxide, induced characteristic changes of senescence in human diploid fibroblasts WI-38 cells. It was reported that ginsenoside Rg1, an active ingredient of ginseng, ameliorated learning deficits in aged rats. The present study was aimed to investigate whether ginsenoside Rg1 can delay the premature senescence of WI-38 cells induced by t-BHP and to explore the underlying molecular mechanisms. First, Rg1 pretreatment markedly reversed senescent morphological changes in WI-38 cells induced by t-BHP. Second, t-BHP treatment alone resulted in an increase in the protein levels of P16 and P21, and a decline in intracellular adenosine 5'-triphosphate (ATP) level and mitochondrial complex IV activity. Ginsenoside Rg1 pretreatment had significant effects of attenuating these changes. These data indicate that ginsenoside Rg1 has an anti-aging effect on t-BHP-induced premature senescence in WI-38 cells. This effect may be mediated by regulating cell cycle proteins and enhancing mitochondrial functioning.

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