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Neuroprotective effects of ginsenoside Rg1 against oxygen-glucose deprivation in cultured hippocampal neurons.
J Chin Med Assoc. 2014 Mar; 77(3):142-9.JC

Abstract

BACKGROUND

Ginsenoside Rg1 (Rg1) is believed to be one of the main active principles in ginseng, a traditional Chinese medicine extensively used to enhance stamina and deal with fatigue as well as physical stress. It has been reported that Rg1 performs multiple biological activities, including neuroprotective activity. In this study, we investigated the efficacy of ginsenoside Rg1 on ischemia-reperfusion injury in cultured hippocampal cells and also probed its possible mechanisms.

METHODS

To establish a model of oxygen-glucose deprivation (OGD) and reperfusion, cultured hippocampal neurons were exposed to OGD for 2.5 hours, followed by a 24-hour reoxygenation. Cultured hippocampal neurons were randomly divided into control group, model group (vehicle), and ginsenoside Rg1 treatment groups (5μM, 20μM, 60μM). At 24 hours post-OGD, the intracellular free calcium concentration was detected using Furo-3/AM-loaded hippocampal neurons deprived of oxygen and glucose. Neuronal nitric oxide synthase (nNOS) activity was measured by chemical colorimetry. Cell apoptosis was evaluated by Hoechst staining, and the neuron viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.

RESULTS

Excitotoxic neuronal injury of OGD was demonstrated by the increase of intracellular free calcium concentrations and elevated nNOS activity in the model group compared with the control group. The intracellular free calcium concentrations and the nNOS activity in the groups receiving intermediate and high dose of ginsenoside Rg1 were significantly lower than those of the control group (p < 0.05). In addition, intermediate and high dose of ginsenoside Rg1 administration could also attenuate the cell viability loss (p < 0.05) and cell apoptosis induced by OGD.

CONCLUSION

Ginsenoside Rg1 has neuroprotective effect on ischemia-reperfusion injury in cultured hippocampal cells mediated by blocking calcium over-influx into neuronal cells and decreasing the nNOS activity after OGD exposure. We infer that ginsenoside Rg1 may serve as a potential therapeutic agent for cerebral ischemia injury.

Authors+Show Affiliations

Department of Neurology, The First Hospital of Xuzhou, Xuzhou, Jiangsu, China.Department of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.Department of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.Department of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.Emergency Center, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China. Electronic address: hbhbwywy34@sina.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24548377

Citation

He, Qing, et al. "Neuroprotective Effects of Ginsenoside Rg1 Against Oxygen-glucose Deprivation in Cultured Hippocampal Neurons." Journal of the Chinese Medical Association : JCMA, vol. 77, no. 3, 2014, pp. 142-9.
He Q, Sun J, Wang Q, et al. Neuroprotective effects of ginsenoside Rg1 against oxygen-glucose deprivation in cultured hippocampal neurons. J Chin Med Assoc. 2014;77(3):142-9.
He, Q., Sun, J., Wang, Q., Wang, W., & He, B. (2014). Neuroprotective effects of ginsenoside Rg1 against oxygen-glucose deprivation in cultured hippocampal neurons. Journal of the Chinese Medical Association : JCMA, 77(3), 142-9. https://doi.org/10.1016/j.jcma.2014.01.001
He Q, et al. Neuroprotective Effects of Ginsenoside Rg1 Against Oxygen-glucose Deprivation in Cultured Hippocampal Neurons. J Chin Med Assoc. 2014;77(3):142-9. PubMed PMID: 24548377.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective effects of ginsenoside Rg1 against oxygen-glucose deprivation in cultured hippocampal neurons. AU - He,Qing, AU - Sun,Jianguo, AU - Wang,Qin, AU - Wang,Wei, AU - He,Bin, Y1 - 2014/02/16/ PY - 2013/01/20/received PY - 2013/09/13/accepted PY - 2014/2/20/entrez PY - 2014/2/20/pubmed PY - 2014/11/18/medline KW - calcium overload KW - cerebral ischemia KW - ginsenoside Rg1 KW - hippocampal neurons KW - nitric oxide synthase SP - 142 EP - 9 JF - Journal of the Chinese Medical Association : JCMA JO - J Chin Med Assoc VL - 77 IS - 3 N2 - BACKGROUND: Ginsenoside Rg1 (Rg1) is believed to be one of the main active principles in ginseng, a traditional Chinese medicine extensively used to enhance stamina and deal with fatigue as well as physical stress. It has been reported that Rg1 performs multiple biological activities, including neuroprotective activity. In this study, we investigated the efficacy of ginsenoside Rg1 on ischemia-reperfusion injury in cultured hippocampal cells and also probed its possible mechanisms. METHODS: To establish a model of oxygen-glucose deprivation (OGD) and reperfusion, cultured hippocampal neurons were exposed to OGD for 2.5 hours, followed by a 24-hour reoxygenation. Cultured hippocampal neurons were randomly divided into control group, model group (vehicle), and ginsenoside Rg1 treatment groups (5μM, 20μM, 60μM). At 24 hours post-OGD, the intracellular free calcium concentration was detected using Furo-3/AM-loaded hippocampal neurons deprived of oxygen and glucose. Neuronal nitric oxide synthase (nNOS) activity was measured by chemical colorimetry. Cell apoptosis was evaluated by Hoechst staining, and the neuron viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. RESULTS: Excitotoxic neuronal injury of OGD was demonstrated by the increase of intracellular free calcium concentrations and elevated nNOS activity in the model group compared with the control group. The intracellular free calcium concentrations and the nNOS activity in the groups receiving intermediate and high dose of ginsenoside Rg1 were significantly lower than those of the control group (p < 0.05). In addition, intermediate and high dose of ginsenoside Rg1 administration could also attenuate the cell viability loss (p < 0.05) and cell apoptosis induced by OGD. CONCLUSION: Ginsenoside Rg1 has neuroprotective effect on ischemia-reperfusion injury in cultured hippocampal cells mediated by blocking calcium over-influx into neuronal cells and decreasing the nNOS activity after OGD exposure. We infer that ginsenoside Rg1 may serve as a potential therapeutic agent for cerebral ischemia injury. SN - 1728-7731 UR - https://www.unboundmedicine.com/medline/citation/24548377/Neuroprotective_effects_of_ginsenoside_Rg1_against_oxygen_glucose_deprivation_in_cultured_hippocampal_neurons_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1726-4901(14)00017-3 DB - PRIME DP - Unbound Medicine ER -