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China Journal of Chinese Materia Medica ; (24): 1554-1559, 2015.
Artigo em Chinês | WPRIM | ID: wpr-351309

RESUMO

<p><b>OBJECTIVE</b>To investigate the protective effect of ginsenoside Rg1 on oxygen-glucose deprivation (OGD) in PC-12 cells, and preliminarily discuss the potential molecular mechanism of mTOR/Akt/FoxO3 signaling pathway.</p><p><b>METHOD</b>The OGD PC-12 cell model was established. The cell viability was measured by MTT assay. After the pretreatment with Rg1 with the concentration of 10, 20, 40 micromol x L(-1) for 24 h, the cell viability was observed. Lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) ac- tivity and malondialdehyde (MDA) level were detected by colorimetry assay. mTOR, p-Akt(ser473), p-Akt(tjr308), Akt, p-FoxO3, FoxO3 in cytoplasm and nucleus, and total FoxO3 protein expression were detected by Western blot assay.</p><p><b>RESULT</b>OGD could significantly in- hibit cell proliferation in 4-24 h in a time-dependent manner. After pretreatment for 24 h, Rg1 (20, 40 micromol x L(-1)) could notably elevate the cell viability and SOD viability and reduce the LDH release and MDA content. Besides, Rg1 also inhibited OGD-induced mTOR and p-Akt(ser473) decreases. After treatment for 6 h, OGD could reduce FoxO3 phosphorylation and promote FoxO3 in cytoplasm. This data suggested that Rg1 could protect PC-12 cell injury through mTOR/p-Akt/FoxO3 signaling pathway.</p><p><b>CONCLUSION</b>Ginsenoside Rg1 could attenuate OGD-induced PC-12 cell injury. Its action mechanism may be closely related to activation of mTOR/p-Akt/FoxO3 signaling pathway.</p>


Assuntos
Animais , Ratos , Apoptose , Proliferação de Células , Sobrevivência Celular , Medicamentos de Ervas Chinesas , Farmacologia , Proteína Forkhead Box O3 , Fatores de Transcrição Forkhead , Genética , Metabolismo , Ginsenosídeos , Farmacologia , Glucose , Metabolismo , Oxigênio , Metabolismo , Células PC12 , Substâncias Protetoras , Farmacologia , Proteínas Proto-Oncogênicas c-akt , Genética , Metabolismo , Transdução de Sinais , Serina-Treonina Quinases TOR , Genética , Metabolismo
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