Neuroprotective Effects of Hydroxysafflor Yellow A Against Excitotoxic Neuronal Death Partially Through Down-Regulation of NR2B-Containing NMDA Receptors

Yang, Qi; Yang, Zhiming; Liu, S.-B.; Zhang, X.-N.; Ying, Hanjie; Li, X.-Q.; Wu, Yumei; Wen, Aidong; Zhao, Ming

doi:10.1007/s11064-010-0191-6

Cited by 57 publications

(28 citation statements)

References 44 publications

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“…Hydroxysafflor yellow A (HSYA), the major active chemical component of the yellow color pigments extracted from the safflower, has strong effects to scavenge oxygen-free radicals and inhibition apoptosis (Tian et al 2008;Ji et al 2008Ji et al , 2009Yang et al 2010). It has been shown that HSYA can alleviate spinal cord and brain damage induced by I/R (Shan et al 2010;Wei et al 2005), but the molecular pathways is still unclear.…”

Section: Introductionmentioning

confidence: 99%

Hydroxysafflor Yellow A Protects PC12 Cells Against the Apoptosis Induced by Oxygen and Glucose Deprivation

et al. 2011

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Hydroxysafflor yellow A (HSYA) was reported neuroprotective under several ischemic models in vivo. In this study, the direct effect of HSYA against oxygen-glucose deprivation (OGD) inducing acute neuronal injury and the underling mechanisms in vitro were investigated. Four-hour oxygen and glucose deprivation (OGD) followed by 20 h reperfusion (adding back oxygen and glucose, OGD-R) was used to induce in vitro ischemia reperfusion injury in differentiated rat pheochromocytoma PC12 cells. HSYA (1, 10, and 100 μmol/l) was added to the cultures 30 min prior to the ischemic insult and was present during OGD and reoxygenation phases. The survival rate of PC12 cells was detected by MTT assay. The contents of malondialdehyde (MDA), superoxide dismutase (SOD) activity were elevated by biochemical method. Hoechst 33258 staining and flow cytometric analysis were used to detect apoptosis; western blotting was used to detect the expression of Bcl-2, Bax, and Cytochrome C protein. The activity of caspase-3 was assessed by colorimetry. HSYA concentration-dependently attenuated neuronal damage with characteristics of increasing injured neuronal absorbance of MTT, decreasing cell apoptosis, and antagonizing decreases in SOD activity and increase in MDA level induced by OGD-R. Moreover, the down-regulation of Bcl-2, up-regulation of Bax and the release of mitochondrial cytochrome c to cytosol and the consequent activation of caspase-3 were reversed by HSYA in a dose-dependent manner. These results suggest that apoptosis is an important characteristic of OGD-R-induced PC 12 death and that treatment of PC12 cells with HSYA can block OGD-R-induced apoptosis through suppression of intracellular oxidative stress and mitochondria dependent caspase cascade.

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Section: Introductionmentioning

confidence: 99%

Hydroxysafflor Yellow A Protects PC12 Cells Against the Apoptosis Induced by Oxygen and Glucose Deprivation

et al. 2011

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“…Additionally, EGF might also regulate Bcl-2 expression through the EGFR/Bcl-2 signaling pathway in P5 rat cochlear sensory epithelial cells [Zheng et al, 2008]. The increased expression of Bcl-2 inhibits NR2B mRNA and protein expression [Yang et al, 2010]. Therefore, we hypothesized that Id1 downregulates NR2B by regulating EGFR.…”

Section: Id1/nr2b Receptor Pathway Is Involved In Oc1 Cell Radiation-mentioning

confidence: 99%

Id1/NR2B Receptor Pathway Regulates Rat Cochlear Sensory Epithelial Cell Survival after Radiation

Chen¹,

Zhou²,

Zou³

et al. 2018

Audiol Neurotol

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Survival of cochlear sensory epithelial cells may be regulated by inhibitor of differentiation-1 (Id1) and the N-methyl-D-aspartic acid (NMDA) receptor. However, it is unclear whether Id1 and the NMDA receptor are involved in the radiation-mediated survival of rat cochlear sensory epithelial cells. Here, we show that the percentage of apoptotic cells increased, the percentage of cells in the S phase decreased, Id1 mRNA and protein expression decreased and the NMDA receptor subtype 2B (NR2B) mRNA and protein level increased in OC1 cells after radiation. Cells infected with the Id1 gene exhibited higher Id1 mRNA and protein levels and lower NR2B mRNA and protein levels than the control cells. In contrast, after transfection of the Id1 siRNA into OC1 cells, Id1 mRNA and protein expression decreased and NR2B mRNA and protein expression increased relative to that of the control group. Additionally, treatment with ifenprodil for 24 h before radiation reduced apoptosis and increased the percentage of cells in the S phase. Our results suggest that Id1 and NR2B might regulate the survival of OC1 cells following radiation.

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“…With NR1 activated, LTP is established and the negative effects of NMDARs on spatial learning and memory are thus inhibited and reduced [28][29][30] . Yang studied cortical neurons from rats pre-treated with NMDA in vitro, and revealed that HSYA reduces Bax expression, restores the balance between pro-and anti-apoptotic proteins, and reverses the up-regulation of NR2B mediated by NMDA, while NR2A is not affected in this process [19] . In our study, Western blot showed that HSYA increased the expression of NR1 in the hippocampus of VaD rats, which facilitated the enhancement of LTP.…”

Section: Assessment Of Protein Expression By Western Blotmentioning

confidence: 99%

“…Its effects on angiogenesis and neuroprotective action in cerebrovascular and neurodegenerative diseases have become hot topics in recent years [14,15] . In addition to antiinfl ammatory and antioxidant effects, its protection against apoptosis and effects on NMDARs have been found important for neuroprotection [14][15][16][17][18][19] .…”

Section: Introductionmentioning

confidence: 99%

Hydroxysafflor yellow A improves learning and memory in a rat model of vascular dementia by increasing VEGF and NR1 in the hippocampus

et al. 2013

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Hydroxysafflor yellow A (HSYA) has angiogenesisregulating and neuro-protective effects, but its effects on vascular dementia (VaD) are unknown. In this study, 30 adult Sprague-Dawley rats were randomly allocated to fi ve groups: normal, sham-operation, VaD alone (bilateral carotid artery occlusion), VaD plus saline (control), and VaD plus HSYA. One week after operation, the HSYA group received one daily tail-vein injection of 0.6 mg/100 g HSYA for two weeks. Five weeks after operation, the spatial memory of all fi ve groups was evaluated by the water maze task, and synaptic plasticity in the hippocampus was assessed by the long-term potentiation (LTP) method. Vascular endothelial growth factor (VEGF) and N-methyl-Daspartic acid receptor 1 (NR1) expression in the hippocampus was detected via Western blot. We found that, compared with the group with VaD alone, the group with HSYA had a reduced escape latency in the water maze (P <0.05), and the LTP at CA3-CA1 synapses in the hippocampus was enhanced (P <0.05). Western blot in the late-phase VaD group showed slight up-regulation of VEGF and downregulation of NR1 in the hippocampus, while HSYA signifi cantly up-regulated both VEGF and NR1. These results suggested that HSYA promotes angiogenesis and increases synaptic plasticity, thus improving spatial learning and memory in the rat model of VaD.

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Neuroprotective Effects of Hydroxysafflor Yellow A Against Excitotoxic Neuronal Death Partially Through Down-Regulation of NR2B-Containing NMDA Receptors

Cited by 57 publications

References 44 publications

Hydroxysafflor Yellow A Protects PC12 Cells Against the Apoptosis Induced by Oxygen and Glucose Deprivation

Hydroxysafflor Yellow A Protects PC12 Cells Against the Apoptosis Induced by Oxygen and Glucose Deprivation

Id1/NR2B Receptor Pathway Regulates Rat Cochlear Sensory Epithelial Cell Survival after Radiation

Hydroxysafflor yellow A improves learning and memory in a rat model of vascular dementia by increasing VEGF and NR1 in the hippocampus

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