Effects of Salidroside on Cobalt Chloride-Induced Hypoxia Damage and mTOR Signaling Repression in PC12 Cells

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  • Zhong Xiaoyong
    College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine Key Laboratory of TCM Rehabilitation of State Administration of Traditional Chinese Medicine, Fujian University of Traditional Chinese Medicine Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine
  • Lin Ruhui
    MOE Key Laboratory of Traditional Chinese Medicine on Osteology & Traumatology and Exercise Rehabilitation, Fujian University of Traditional Chinese Medicine Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine
  • Li Zuanfang
    Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine
  • Mao Jingjie
    Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine
  • Chen Lidian
    College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine Key Laboratory of TCM Rehabilitation of State Administration of Traditional Chinese Medicine, Fujian University of Traditional Chinese Medicine MOE Key Laboratory of Traditional Chinese Medicine on Osteology & Traumatology and Exercise Rehabilitation, Fujian University of Traditional Chinese Medicine

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  • Effects of <i>Salidroside</i> on Cobalt Chloride-Induced Hypoxia Damage and mTOR Signaling Repression in PC12 Cells

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Salidroside (SA), a phenylpropanoid glycoside isolated from Rhodiola rosea L., has been documented to exert a broad spectrum of pharmacological properties, including protective effects against neuronal death induced by various stresses. To provide further insights into the neuroprotective functions of SA, this study examined whether SA can attenuate cobalt chloride (CoCl2)-induced hypoxia damage and mammalian target of rapamycin (mTOR) signaling repression in PC12 differentiated cells. Differentiated PC12 cells were exposed to CoCl2 for 12 h to mimic hypoxic/ischemic conditions and treated with SA at the same time, followed by electron microscopy and analysis of cell viability, intracellular reactive oxygen species (ROS) level, hypoxia-inducible factor-1α (HIF-1α) level, and the regulated in development and DNA damage responses (REDD1)/mTOR/ p70 ribosomal S6 kinase (p70S6K) signaling pathway. Our data indicated that SA can dramatically attenuate the ultrastructural damage of mitochondria induced by CoCl2 and significantly decrease CoCl2-induced ROS production. Moreover, phosphorylated mammalian target of rapamycin (p-mTOR) was significantly reduced by CoCl2, and this inhibition was relieved by the treatment of SA in PC12 cells, as evidenced by immunoblot and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analyses. The SA effects were blocked by pretreatment of RAD001. The results indicate that SA can rescue CoCl2-induced repression of REDD1/mTOR/ p70S6K signal transduction in PC12 cells. Our data demonstrate that SA is able to attenuate CoCl2-induced hypoxia damage and mTOR signaling repression, suggesting that SA may protect brain neurons from ischemic injury through mTOR signaling, and provide new insights into the prevention and treatment of cerebral ischemic.

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