Panaxatriol Saponins Attenuated Oxygen-Glucose Deprivation Injury in PC12 Cells via Activation of PI3K/Akt and Nrf2 Signaling Pathway

Huang, Yong‐Liang; Li, Jingling; Wan, Fang; Zhang, Wenwu; Yang, Huiru; Wang, Li; Hu, Qi; Wu, Chunjie

doi:10.1155/2014/978034

Cited by 33 publications

(29 citation statements)

References 28 publications

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“…The results indicated that PTS at the concentrations ranging from 0.03 to 2 mg/ml significantly ameliorated the cell growth inhibition and apoptosis induced by 6-OHDA in PC12 cells (Fig. 1B and C), which was in line with the previous reports that PTS protected PC12 cells against oxygen-glucose deprivation reperfusion- and 1-methyl-4-phenylpyridinium ion-induced cell damage1819. However, relatively high concentration of PTS (4 mg/ml) did not show neuroprotective activity but enhanced the cytotoxicity of 6-OHDA (Fig.…”

Section: Discussionsupporting

confidence: 92%

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Hormetic effect of panaxatriol saponins confers neuroprotection in PC12 cells and zebrafish through PI3K/AKT/mTOR and AMPK/SIRT1/FOXO3 pathways

Zhang

Chen

et al. 2017

Sci Rep

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Hormesis is an adaptive response of living organisms to a moderate stress. However, its biomedical implication and molecular mechanisms remain to be intensively investigated. Panaxatriol saponins (PTS) is the major bioactive components extracted from Panax notoginseng, a widely used herbal medicine for cerebrovascular diseases. This study aims to examine the hormetic and neuroprotective effects of PTS in PC12 cells and zebrafish Parkinson’s disease (PD) models. Our results demonstrated that PTS stimulated PC12 cell growth by about 30% at low doses, while PTS at high doses inhibited cell growth, which is a typical hormetic effect. Moreover, we found that low dose PTS pretreatment significantly attenuated 6-OHDA-induced cytotoxicity and up-regulated PI3K/AKT/mTOR cell proliferation pathway and AMPK/SIRT1/FOXO3 cell survival pathway in PC12 cells. These results strongly suggested that neuroprotective effects of PTS may be attributable to the hormetic effect induced by PTS through activating adaptive response-related signaling pathways. Notably, low dose PTS could significantly prevent the 6-OHDA-induced dopaminergic neuron loss and improve the behavior movement deficiency in zebrafish, whereas relative high dose PTS exhibited neural toxicity, further supporting the hormetic and neuroprotective effects of PTS. This study indicates that PTS may have the potential in the development of future therapeutic medicines for PD.

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Section: Discussionsupporting

confidence: 92%

“…. PTS have been reported to exhibit neuroprotective effects on oxygen-glucose deprivation-reperfusion induced PC12 cell death18 and 1-methyl-4-phenylpyridinium ion-induced neurotoxicity in mice19. However, the cellular and molecular mechanisms remain to be elucidated.…”

mentioning

confidence: 99%

Hormetic effect of panaxatriol saponins confers neuroprotection in PC12 cells and zebrafish through PI3K/AKT/mTOR and AMPK/SIRT1/FOXO3 pathways

Zhang

Chen

et al. 2017

Sci Rep

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“…19) In brief, PC12 cells were first incubated in glucose-free DMEM and subsequently transferred into a Tri-Gas incubator (Heal Force, HF100) with 1% O 2 , 94% N 2 and 5% CO 2 for 9 h at 37°C. Sham OGD cultures were maintained in a normal oxygenated DMEM.…”

Section: Methodsmentioning

confidence: 99%

Protective HSP70 Induction by Z-Ligustilide against Oxygen–Glucose Deprivation Injury <i>via</i> Activation of the MAPK Pathway but Not of HSF1

Jiang

Ning

et al. 2015

Biological & Pharmaceutical Bulletin

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Key words Z-ligustilide; heat-shock protein 70; mitogen-activated protein kinase; oxygen-glucose deprivation-reoxygenation; heat-shock factor 1The World Health Organization (WHO) Global Infobase reports that stroke has become the second leading cause of mortality in the world, causing around 6000000 deaths annually. 1)However, there are currently relatively few treatment options available to minimize damage or death following a stroke. Protein aggregates containing ubiquitinated proteins are commonly present in neurodegenerative disorders and have been considered to cause neuronal degeneration. The previous study also showed that transient cerebral ischemia caused severe protein aggregation in hippocampal CA1 neurons which appeared at 4 h and progressively accumulated at 24 and 48 h. 2)Therefore, control of protein aggregation may represent an alternative treatment to neurological damage caused by ischemic stroke.Heat shock proteins (HSPs) are a group of phylogenetically and ubiquitous cytoprotective proteins found in all prokaryotic and eukaryotic cells, many of which are chaperone molecules that facilitate protein folding, trafficking and also prevent their aggregation and degradation.3) Heat shock protein 70 (HSP70) is a major inducible heat shock protein that basically functions as a molecular chaperone and plays an important role in preventing protein aggregation, degrading unstable and misfolded proteins and transporting proteins between cellular compartments.4) It's reported that over-expression of HSP70 via transgenes and viruses or systemic administration of HSP70 fusion proteins that allow it to cross the blood brain barrier protects the brain against ischemia, 5,6) suggesting that increasing HSP70 level or activity may be a potential therapeutic target for pharmacological intervention of ischemic diseases.Ligusticum chuanxiong is a commonly used Chinese herbal medicine with its empiric treatment of cardiovascular and cerebrovascular diseases.7) Z-Ligustilide as the major bioactive phthalide compound of Rhizoma chuanxiong was previously suggested for the prevention and treatment of ischemic stroke. 8,9) Our and others' studies showed that Z-ligustilide could protect ischemic injury both in vitro and in vivo via the induction of direct and indirect antioxidant response. 8,10,11) However, its effect on the heat shock response, a highly conserved and fundamental cytoprotective mechanism, under ischemic stress remains unexplored. Along this line, we characterized the effect of Z-ligustilide on HSP70 and explored the potential role of HSP70 in the protection of Z-ligustilide against oxygen-glucose deprivation and reoxygenation (OGDReoxy) induced injury in this study.

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“…Panaxatriol saponins may activate endogenous cytoprotective mechanism against oxygen-Glc deprivation-reperfusion-induced oxidative injury via the activation of PI3K/AKT and Nrf2 signaling pathway (Huang et al, 2014). Panaxatriol saponins may activate endogenous cytoprotective mechanism against oxygen-Glc deprivation-reperfusion-induced oxidative injury via the activation of PI3K/AKT and Nrf2 signaling pathway (Huang et al, 2014).…”

Section: Antioxidant and Anti-inflammatory Effectsmentioning

confidence: 99%

Phytochemical and biological research of Panax medicinal resources

Hao¹

2015

Medicinal Plants

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Panaxatriol Saponins Attenuated Oxygen-Glucose Deprivation Injury in PC12 Cells via Activation of PI3K/Akt and Nrf2 Signaling Pathway

Cited by 33 publications

References 28 publications

Hormetic effect of panaxatriol saponins confers neuroprotection in PC12 cells and zebrafish through PI3K/AKT/mTOR and AMPK/SIRT1/FOXO3 pathways

Hormetic effect of panaxatriol saponins confers neuroprotection in PC12 cells and zebrafish through PI3K/AKT/mTOR and AMPK/SIRT1/FOXO3 pathways

Protective HSP70 Induction by Z-Ligustilide against Oxygen–Glucose Deprivation Injury <i>via</i> Activation of the MAPK Pathway but Not of HSF1

Phytochemical and biological research of Panax medicinal resources

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