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Hyperoside protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via nitric oxide signal pathway.
Brain Res. 2012 Aug 21; 1469:164-73.BR

Abstract

Hyperoside is a flavonoid compound and widely used in clinic to relieve pain and improve cardiovascular functions. However, the effects of hyperoside on ischemic neurons and the molecular mechanisms remain unclear. Here, we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD-R) to investigate the protective effects of hyperoside on ischemic neuron injury and further explore the possible related mechanisms. Our results demonstrated that hyperoside protected cultured cortical neurons from OGD-R injury, it also relieved glutamate-induced neuronal injury and NMDA-induced [Ca(2+)](i) elevation. As for the mechanisms, hyperoside firstly attenuated the phosphorylation of CaMKII caused by OGD-R lesions. Meanwhile, hyperoside lessened iNOS expression induced by OGD-R via inhibition of NF-κB activation. Furthermore, ameliorating of ERK, JNK and Bcl-2 family-related apoptotic signaling pathways were also involved in the neuroprotection of hyperoside. Taken together, these studies revealed that hyperoside had protective effects on neuronal ischemia-reperfusion impairment, which was related to the regulation of nitric oxide signaling pathway.

Authors+Show Affiliations

Department of Pharmacology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

22771858

Citation

Liu, Rui-Li, et al. "Hyperoside Protects Cortical Neurons From Oxygen-glucose Deprivation-reperfusion Induced Injury Via Nitric Oxide Signal Pathway." Brain Research, vol. 1469, 2012, pp. 164-73.
Liu RL, Xiong QJ, Shu Q, et al. Hyperoside protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via nitric oxide signal pathway. Brain Res. 2012;1469:164-73.
Liu, R. L., Xiong, Q. J., Shu, Q., Wu, W. N., Cheng, J., Fu, H., Wang, F., Chen, J. G., & Hu, Z. L. (2012). Hyperoside protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via nitric oxide signal pathway. Brain Research, 1469, 164-73. https://doi.org/10.1016/j.brainres.2012.06.044
Liu RL, et al. Hyperoside Protects Cortical Neurons From Oxygen-glucose Deprivation-reperfusion Induced Injury Via Nitric Oxide Signal Pathway. Brain Res. 2012 Aug 21;1469:164-73. PubMed PMID: 22771858.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hyperoside protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via nitric oxide signal pathway. AU - Liu,Rui-Li, AU - Xiong,Qiu-Ju, AU - Shu,Qing, AU - Wu,Wen-Ning, AU - Cheng,Jin, AU - Fu,Hui, AU - Wang,Fang, AU - Chen,Jian-Guo, AU - Hu,Zhuang-Li, Y1 - 2012/07/04/ PY - 2012/03/02/received PY - 2012/06/26/revised PY - 2012/06/27/accepted PY - 2012/7/10/entrez PY - 2012/7/10/pubmed PY - 2013/1/15/medline SP - 164 EP - 73 JF - Brain research JO - Brain Res. VL - 1469 N2 - Hyperoside is a flavonoid compound and widely used in clinic to relieve pain and improve cardiovascular functions. However, the effects of hyperoside on ischemic neurons and the molecular mechanisms remain unclear. Here, we used an in vitro ischemic model of oxygen-glucose deprivation followed by reperfusion (OGD-R) to investigate the protective effects of hyperoside on ischemic neuron injury and further explore the possible related mechanisms. Our results demonstrated that hyperoside protected cultured cortical neurons from OGD-R injury, it also relieved glutamate-induced neuronal injury and NMDA-induced [Ca(2+)](i) elevation. As for the mechanisms, hyperoside firstly attenuated the phosphorylation of CaMKII caused by OGD-R lesions. Meanwhile, hyperoside lessened iNOS expression induced by OGD-R via inhibition of NF-κB activation. Furthermore, ameliorating of ERK, JNK and Bcl-2 family-related apoptotic signaling pathways were also involved in the neuroprotection of hyperoside. Taken together, these studies revealed that hyperoside had protective effects on neuronal ischemia-reperfusion impairment, which was related to the regulation of nitric oxide signaling pathway. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/22771858/Hyperoside_protects_cortical_neurons_from_oxygen_glucose_deprivation_reperfusion_induced_injury_via_nitric_oxide_signal_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(12)01119-5 DB - PRIME DP - Unbound Medicine ER -