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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.

This study is to explore the effect of ginsenoside Rb1 on the process of beta-amyloid peptide(25-35) (Abeta(25-35)) -induced hyperphosphorylation of tau protein, and on the level of cyclin-dependent kinase 5 activator, p25/p35. Western blotting and/or immunocytochemical staining were used to detect the levels of phosphorylation of tau protein at the sites of Thr205, Ser396, Ser404 in hippocampal neurons, cdk5 and p25/p35. After exposure to Abeta(25-35) (20 micromol x L(-1)) for 12 h, the levels of tau protein phosphorylation at the sites of Thr205, Ser396, Ser404 were enhanced, the level of p25 was increased, but the level of protein cdk5 was not changed markedly. Pretreatment with ginsenoside Rb1 reduced Abeta(25-35) -induced hyperphosphorylation of tau protein and decreased the lever of p25, but had no effect on cdk5. Ginsenoside Rb1 can attenuate Abeta(25-35) -induced hyperphosphorylation of tau protein through CDK5 signal pathway.