3-O-Demethylswertipunicoside Protects against Oxidative Toxicity in PC12 Cells

Zhang, Shiping; Du, Xingang; Pu, Xiaoping

doi:10.1248/bpb.33.1529

Cited by 10 publications

(13 citation statements)

References 49 publications

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“…Oxidative stress has been implicated in a wide variety of diseases, including atherosclerosis, diabetes, pulmonary fibrosis, arthritis, and neurodegenerative disorders such as Parkinson’s disease (PD), and is also believed to be a major factor in ageing 11 . PD affects 1–2% of the population over the age of 50 years, or approximately 6 million people worldwide 15 . Many studies have shown that E2 can protect nerve cells from excitotoxicity induced by N ‐Methyl‐ d ‐aspartate, oxidative toxicity or other forms of damage by activating genomic signalling pathways, such as those mediated by ERα and ERβ.…”

Section: Discussionmentioning

confidence: 99%

“…Generation of hydroxyls and other free radicals induces apoptosis by inducing mitochondrial dysfunction and by damaging DNA, proteins and lipids 14 . Therefore, H 2 O 2 has been extensively used as an inducer of oxidative stress in in vitro models of oxidative damage and neuronal apoptosis 15 . It is generally accepted that H 2 O 2 stimulation also induces total nitric oxide (NO) production and inducible NO synthase (iNOS) activity.…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotective effects of oestrogen against oxidative toxicity through activation of G‐protein‐coupled receptor 30 receptor

Liu¹,

Jy²,

Zhang

et al. 2011

Clin Exp Pharma Physio

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1. 17-β-oestradiol (E2) plays a critical role in neuroprotection through both genomic and non-genomic mechanisms. The aim of the present study was to investigate the role of G-protein-coupled receptor 30 (GPR30), a new kind of oestrogen receptor, in the neuroprotection against oxidative insult. 2. The neuroprotection evoked by GPR30 stimulation was examined in cultured cortical neurons. Hoechst 33258/propidium iodide double staining, flow cytometric analysis and western blotting were applied to assess neuronal apoptosis induced by H(2)O(2) . 3. We found that the GPR30 agonist, G1, and E2 attenuated apoptosis induced by H(2)O(2) exposure. Furthermore, G1 (1 nmol/L) or E2 (1 nmol/L) significantly increased the levels of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2), Bcl-2 and pro-caspase-3. Pretreatment with ICI182780, a highly selective nuclear oestrogen receptor antagonist that is used to block the classical ERα and ERβ receptors, did not totally block the neuroprotective effects of E2 (1 nmol/L) and had no effect on the neuroprotective effects of G1 (1 nmol/L). 4. Our data suggest that GPR30 is involved in the neuroprotection against oxidative insult. The neuroprotection evoked by GPR30 stimulation was associated with the signalling through the ERK1/2 kinase pathway. In addition, the anti-apoptotic activity of GPR30 was dependent on the expression of Bcl-2 and pro-caspase-3. GPR30 might be a potential therapeutic target for neuroprotection and oxidative stress.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuroprotective effects of oestrogen against oxidative toxicity through activation of G‐protein‐coupled receptor 30 receptor

Liu¹,

Jy²,

Zhang

et al. 2011

Clin Exp Pharma Physio

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“…The controls were exposed to the same solvent. Cell viability was measured using the MTT assay [17]. …”

Section: Methodsmentioning

confidence: 99%

Neuroprotective Effects of Protocatechuic Aldehyde against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease

et al. 2013

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Protocatechuic aldehyde (PAL) has been reported to bind to DJ-1, a key protein involved in Parkinson’s disease (PD), and exerts potential neuroprotective effects via DJ-1 in SH-SY5Y cells. In this study, we investigated the neuroprotective pharmacological effects of PAL against neurotoxin-induced cell and animal models of PD. In cellular models of PD, PAL markedly increased cell viability rates, mitochondrial oxidation-reduction activity and mitochondrial membrane potential, and reduced intracellular ROS levels to prevent neurotoxicity in PC12 cells. In animal models of PD, PAL reduced the apomorphine injection, caused turning in 6-OHDA treated rats, and increased the motor coordination and stride decreases in MPTP treated mice. Meanwhile, in an MPTP mouse model, PAL prevented a decrease of the contents of dopamine (DA) and its metabolites in the striatum and TH-positive dopaminergic neuron loss in the substantia nigra (SN). In addition, PAL increased the protein expression of DJ-1 and reduced the level of α-synuclein in the SN of MPTP lesioned mice. PAL also increased the spine density in hippocampal CA1 neurons. The current study demonstrates that PAL can efficiently protect dopaminergic neurons against neurotoxin injury in vitro and in vivo, and that the potential mechanisms may be related to its effects in increasing DJ-1, decreasing α-synuclein and its growth-promoting effect on spine density.

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“…Mitochondrial membrane perturbation, oxidative stress, and proteasome dysfunction are among the several hypotheses suggested to explain the molecular basis of neuronal damage (Dawson and Dawson, 2003). DJ-1 protects several kinds of cancer cells such as pancreatic (Inberg and Linial, 2010), neuronal (Yokota et al , 2003; Zhang et al , 2010), leukaemic (Liu et al , 2008), lung (MacKeigan et al , 2003), and breast (Ismail et al , 2012) against oxidative stress-induced apoptosis. DJ-1 is reported to modulate the PTEN/Akt survival pathway inactivation (Kim et al , 2005).…”

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confidence: 99%

DJ-1 upregulates breast cancer cell invasion by repressing KLF17 expression

Ismail

Lee

et al. 2014

Br J Cancer

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Background:DJ-1 (PARK7) was reported as an oncogene in a Ras-dependent manner. Recent studies have shown that DJ-1 stimulates cell proliferation, cell invasion, and cancer metastasis. However, the molecular mehchanism by which DJ-1 induces cancer cell invasion and metastasis remains unclear.Methods:Breast cancer cells were transfected with DJ-1 siRNA or DJ-1 overexpression to investigate the effect of DJ-1 on KLF17 expression. ID-1 luciferase promoter assay was performed to evaluate DJ-1-dependent KLF17 expression changes. In addition, Epistasis analysis of DJ-1 and KLF17 was performed to evaluate their regulatory interactions. Ras inhibitors were pretreated to determine whether DJ-1 regulates cell invasion in a Ras-dependent manner.Results:In the present study, we found increased DJ-1 expression in highly invasive breast cancer cells as compared with non-metastatic cells. Furthermore, DJ-1 promoted breast cancer cell invasion by downregulating E-cadherin and increasing Snail expression. Interestingly, exogenous DJ-1 overexpression markedly decreased mRNA and protein expression of KLF17, the EMT negative regulator. These data were confirmed by ID-1 promoter activity, which is directly regulated by DJ-1-dependent KLF17 transcription factor. Epistasis analysis showed that KLF17 overexpression overcomes increased cell invasion by DJ-1, suggesting that KLF17 might be one of the downstream signalling molecules of DJ-1. Acceleration of cell invasion by DJ-1 was alleviated by Ras inhibitors, suggesting that DJ-1 cooperates with Ras to increase cell invasion.Conclusion:Altogether, these data suggest for the first time that DJ-1 acts as an EMT-positive regulator in breast cancer cells via regulation of the KLF17/ID-1 pathway.

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3-O-Demethylswertipunicoside Protects against Oxidative Toxicity in PC12 Cells

Cited by 10 publications

References 49 publications

Neuroprotective effects of oestrogen against oxidative toxicity through activation of G‐protein‐coupled receptor 30 receptor

Neuroprotective effects of oestrogen against oxidative toxicity through activation of G‐protein‐coupled receptor 30 receptor

Neuroprotective Effects of Protocatechuic Aldehyde against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease

DJ-1 upregulates breast cancer cell invasion by repressing KLF17 expression

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