Neuroprotective effects of ginsenoside Rd against oxygen-glucose deprivation in cultured hippocampal neurons

Ye, Richard D.; Li, Nanlin; Han, Junliang; Kong, Xiangdong; Cao, Rong; Rao, Zhi-Ren; Zhao, Gang

doi:10.1016/j.neures.2009.03.016

Cited by 114 publications

(88 citation statements)

References 25 publications

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“…We have previously reported that Rd protects against neuronal oxidative damage induced by hydrogen peroxide [5] and oxygen-glucose deprivation [6]. More recently, we suggested that Rd exerts neuroprotection against transient focal ischemia in an integrated process of free radicals scavenging, mitochondrial protection, energy restoration, and apoptosis inhibition [7,8].…”

Section: Discussionmentioning

confidence: 97%

“…Previously, we found that Rd could protect against neuronal oxidative damage induced by hydrogen peroxide [5] and oxygen-glucose deprivation [6], an in vitro model of cerebral ischemia. More recently, Rd was reported to ameliorate histological and functional outcome after focal cerebral ischemia [7][8][9], which is associated with mitochondrial protection and energy restoration.…”

Section: (S)-triol-(20-o-b-d-glucopyranosyl)-3-o-b-d-glucopyranosyl-(mentioning

confidence: 98%

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Ginsenoside Rd in Experimental Stroke: Superior Neuroprotective Efficacy with a Wide Therapeutic Window

Kong

Yang

et al. 2011

Neurotherapeutics

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Ginsenoside Rd (Rd), one of the main active ingredients in Panax ginseng, has been demonstrated to protect against ischemic cerebral damage in vitro and in vivo. In this study, we aimed to further define the preclinical characteristics of Rd. We show that Rd passes the intact blood-brain barrier and exerts protection in both transient and permanent middle cerebral artery occlusion (MCAO) in rats. In the dose-response study, Rd (10-50 mg/Kg) significantly reduced the infarct volume on postoperative days (PODs) 1, 3, and 7. This protection was associated with an improved neurological outcome for as many as 6 weeks after transient MCAO, as assessed by modified neurological severity score, modified sticky-tape test, and corner test. For comparison, Rd was significantly more effective than edaravone and slightly more effective than Ntert-butyl-alpha-phenylnitrone (PBN). In the therapeutic window study, Rd exhibited remarkable neuroprotection, even when administered for as many as 4 h after the recirculation of transient MCAO or after the onset of permanent MCAO. Furthermore, in female rats or 16-month-old male rats, the salutary effects of Rd were also observed. These findings suggest Rd is a promising neuroprotectant and provide support for future clinical studies to confirm whether Rd is beneficial in ischemic stroke.

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Section: Discussionmentioning

confidence: 97%

Section: (S)-triol-(20-o-b-d-glucopyranosyl)-3-o-b-d-glucopyranosyl-(mentioning

confidence: 98%

Ginsenoside Rd in Experimental Stroke: Superior Neuroprotective Efficacy with a Wide Therapeutic Window

Kong

Yang

et al. 2011

Neurotherapeutics

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“…The cultured hippocampal neurons were stained with 10 mM Hoechst 33342 dye for 5 min followed by observing nuclear condensation/aggregation under a fluorescence microscope (Olympus, Tokyo, Japan) to obtain morphological evidence for apoptotic nuclei (Ye et al, 2009). …”

Section: Morphological Detectionmentioning

confidence: 99%

Neuroprotective effects of oxysophocarpine on neonatal rat primary cultured hippocampal neurons injured by oxygen-glucose deprivation and reperfusion

Zhu

Zhou

et al. 2014

Pharmaceutical Biology

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Objective: This study investigated the protective effects of OSC on neonatal rat primary-cultured hippocampal neurons were injured by oxygen-glucose deprivation and reperfusion (OGD/RP). Materials and methods: Cultured hippocampal neurons were exposed to OGD for 2 h followed by a 24 h RP. OSC (1, 2, and 5 mmol/L) and nimodipine (Nim) (12 mmol/L) were added to the culture after OGD but before RP. The cultures of the control group were not exposed to OGD/ RP. MTT and LDH assay were used to evaluate the protective effects of OSC. The concentration of intracellular-free calcium [Ca 2+ ] i and mitochondrial membrane potential (MMP) were determined to evaluate the degree of neuronal damage. Morphologic changes of neurons following OGD/RP were observed with a microscope. The expression of caspase-3 and caspase-12 mRNA was examined by real-time quantitative PCR. Results: The IC 50 of OSC was found to be 100 mmol/L. Treatment with OSC (1, 2, and 5 mmol/L) attenuated neuronal damage (p50.001), with evidence of increased cell viability (p50.001) and decreased cell morphologic impairment. Furthermore, OSC increased MMP (p50.001), but it inhibited [Ca 2+ ] i (p50.001) elevation in a dose-dependent manner at OGD/RP. OSC (5 mmol/L) also decreased the expression of caspase-3 (p50.05) and caspase-12 (p50.05). Discussion and conclusion: The results suggested that OSC has significant neuroprotective effects that can be attributed to inhibiting endoplasmic reticulum (ER) stress-induced apoptosis.

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“…However, in order to efficiently characterize such compounds, it is desirable to have a model that allows researchers to rapidly determine efficacy as well as to determine mechanism of action of the compounds. The most common models currently used in stroke research include: in vivo focal ischemia models (Weng and Kriz, 2007;Saleh et al, 2009), in vitro dissociated cell models (Larsen et al, 2005;Ye et al, 2009) and in vitro brain slice models (Garcia de Arriba et al, 1999;Jarvis et al, 2001). In vivo focal ischemia models (whole animal models) are used extensively to study stroke and involve invasive surgery to expose and occlude a cerebral artery (Saleh et al, 2009).…”

Section: E-mail Address: Tsaleh@upeica (Tm Saleh)mentioning

confidence: 99%

“…As well, using this type of model, it is difficult to determine the mechanism of action of therapeutic interventions. The use of in vitro models where oxygen-glucose deprivation (OGD) is used to mimic stroke (Jarvis et al, 2001;Wise-Faberowski et al, 2009;Ye et al, 2009) overcomes many of these problems. Of the in vitro models, the dissociated cell models are popular for screening due to their high throughput, low cost and ease of use.…”

Section: E-mail Address: Tsaleh@upeica (Tm Saleh)mentioning

confidence: 99%

A novel method for inducing focal ischemia in vitro

Richard

Saleh

Bahh³

et al. 2010

Journal of Neuroscience Methods

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Current in vitro models of stroke involve applying oxygen-glucose deprived (OGD) media over an entire brain slice or plate of cultured neurons. Thus, these models fail to mimic the focal nature of stroke as observed clinically and with in vivo rodent models of stroke. Our aim was to develop a novel in vitro brain slice model of stroke that would mimic focal ischemia and thus allow for the investigation of events occurring in the penumbra. This was accomplished by focally applying OGD medium to a small portion of a brain slice while bathing the remainder of the slice with normal oxygenated media. This technique produced a focal infarct on the brain slice that increased as a function of time. Electrophysiological recordings made within the flow of the OGD solution ("core") revealed that neurons rapidly depolarized (anoxic depolarization; AD) in a manner similar to that observed in other stroke models. Edaravone, a known neuroprotectant, significantly delayed this onset of AD. Electrophysiological recordings made outside the flow of the OGD solution ("penumbra") revealed that neurons within this region progressively depolarized throughout the 75 min of OGD application. Edaravone attenuated this depolarization and doubled neuronal survival. Finally, synaptic transmission in the penumbra was abolished within 50 min of focal OGD application. These results suggest that this in vitro model mimics events that occur during focal ischemia in vivo and can be used to determine the efficacy of therapeutics that target neuronal survival in the core and/or penumbra.

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Neuroprotective effects of ginsenoside Rd against oxygen-glucose deprivation in cultured hippocampal neurons

Cited by 114 publications

References 25 publications

Ginsenoside Rd in Experimental Stroke: Superior Neuroprotective Efficacy with a Wide Therapeutic Window

Ginsenoside Rd in Experimental Stroke: Superior Neuroprotective Efficacy with a Wide Therapeutic Window

Neuroprotective effects of oxysophocarpine on neonatal rat primary cultured hippocampal neurons injured by oxygen-glucose deprivation and reperfusion

A novel method for inducing focal ischemia in vitro

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