Neuroprotective effects of salidroside against beta-amyloid-induced oxidative stress in SH-SY5Y human neuroblastoma cells

Zhang, Li; Yu, Huixin; Zhao, Xin-Can; Lin, Xiao; Tan, Chen; Cao, Guo-xian; Wang, Zhengwu

doi:10.1016/j.neuint.2010.06.021

Cited by 192 publications

(118 citation statements)

References 37 publications

Supporting

Mentioning

114

Contrasting

Order By: Relevance

“…1a), has been documented to possess neuroprotective effects against neuronal damage induced by various insults. [19][20][21][22][23][24][25][26][27][28][29][30][31][32][33] However, the underlying mechanisms are still not well understood.…”

Section: Discussionmentioning

confidence: 99%

“…SA can reduce the degree of cerebral edema and the brain infarct size of rats with global cerebral ischemia, relieve the metabolism abnormity of free radicals and improve the function of cognition as well as behavioral and histological outcomes. [20][21][22] [23][24][25][26][27][28][29][30][31][32][33] In addition, it has been reported that SA may regulate mTOR signaling in cultured human umbilical vein endothelial cells (HUVECs) or in bladder cancer cell lines. 34,35) However, whether the neuroprotective effects of SA involve regulation of the mTOR signaling pathway in PC12 cells is still unknown.…”

mentioning

confidence: 99%

See 1 more Smart Citation

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

Zhong

Lin

et al. 2014

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

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 (CoCl 2 )-induced hypoxia damage and mammalian target of rapamycin (mTOR) signaling repression in PC12 differentiated cells. Differentiated PC12 cells were exposed to CoCl 2 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 ( Key words salidroside; ischemic; mammalian target of rapamycin (mTOR); hypoxia; cobalt chloride; PC12 cell Focal cerebral ischemia or stroke is characterized by obstruction of blood flow to the brain, resulting in deficient supply of oxygen, glucose, serum, and nutrient that are indispensable for the energy generation. Since central nervous system is most susceptible to hypoxia conditions, the continuous oxygen and energy deprivation results in cognitive disturbances and decreased motor control, leading to fainting, long term loss of consciousness, coma, seizures, cessation of brain stem reflexes, and brain death. Ischemic stroke is currently a leading cause of disability and mortality in the aged population, due to limited medication and therapy, and new therapeutic strategies for this devastating disease are urgently needed.Recently, the role of mammalian target of rapamycin (mTOR) signaling in neurodegenerative and cerebrovascular diseases has attracted great attention.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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

Zhong

Lin

et al. 2014

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…The crucial role of Bax/Bcl-2 in mitochondrial permeability and ΔΨm loss has been well established [27,28]. The downregulation of the Bcl-2 protein level observed in many different models of apoptosis, neuronal and non-neuronal, decreases its capacity to form heterodimers with the related pro-apoptotic protein Bax, or to link with specific molecules, thus of Bcl-2, thus preventing its anti-apoptotic activity [29][30][31]. This decrease in Bcl-2 protein level also occurs in SH- in addition it has been shown previously that p38MAPK and JNK1/2 contributes to SH-SY5Y cell apoptosis [31].…”

Section: Discussionmentioning

confidence: 99%

The signalling axis mediating neuronal apoptosis in response to [Pt(O,O′-acac)(γ-acac)(DMS)]

Muscella

Calabriso

Vetrugno

et al. 2011

Biochemical Pharmacology

View full text Add to dashboard Cite

“…In nonstimulated microglial cells, c-enolase localization was mainly seen in the cytoplasm. However, in cells treated with fibrilar Ab that exerts neurotoxical properties of the native full-length Ab peptide (Zhang et al, 2010), more peripheral localization pattern was observed. This suggests that c-enolase is released from microglia as described for other neurotrophic factors.…”

Section: The Neuroprotection Conferred By Microglial Medium Is Mediatmentioning

confidence: 94%

Neuroprotective role of γ‐enolase in microglia in a mouse model of Alzheimer's disease is regulated by cathepsin X

et al. 2013

View full text Add to dashboard Cite

Summaryc-Enolase is a neurotrophic-like factor promoting growth, differentiation, survival and regeneration of neurons. Its neurotrophic activity is regulated by cysteine protease cathepsin X which cleaves the C-terminal end of the molecule. We have investigated the expression and colocalization of c-enolase and cathepsin X in brains of Tg2576 mice overexpressing amyloid precursor protein.In situ hybridization of c-enolase and cathepsin X revealed that mRNAs for both enzymes were expressed abundantly around amyloid plaques. Immunostaining demonstrated that the C-terminally cleaved form of c-enolase was present in the immediate plaque vicinity, whereas the intact form, exhibiting neurotrophic activity, was observed in microglia cells in close proximity to senile plaque. The upregulation of c-enolase in microglial cells in response to amyloid-b peptide (Ab) was confirmed in mouse microglial cell line EOC 13.31 and primary microglia and medium enriched with c-enolase proved to be neuroprotective against Ab toxicity; however, the effect was reversed by cathepsin X proteolytic activity. These results demonstrate an upregulation of c-enolase in microglia cells surrounding amyloid plaques in Tg2576 transgenic mice and demonstrate its neuroprotective role in amyloid-b-related neurodegeneration.

show abstract

Neuroprotective effects of salidroside against beta-amyloid-induced oxidative stress in SH-SY5Y human neuroblastoma cells

Cited by 192 publications

References 37 publications

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

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

The signalling axis mediating neuronal apoptosis in response to [Pt(O,O′-acac)(γ-acac)(DMS)]

Neuroprotective role of γ‐enolase in microglia in a mouse model of Alzheimer's disease is regulated by cathepsin X

Contact Info

Product

Resources

About