Tags

Type your tag names separated by a space and hit enter

Isoquercetin protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via suppression of TLR4-NF-кB signal pathway.
Neurochem Int. 2013 Dec; 63(8):741-9.NI

Abstract

In the present study, oxygen-glucose deprivation followed by reperfusion (OGD/R), an in vitro model of ischemia, was used to evaluate the neuroprotective effect of isoquercetin in primary culture of rat cortical neuronal cells. It was found that isoquercetin administered prior to the insult could prevent OGD/R-induced intracellular calcium concentrations ([Ca(2+)]i) increase, lactate dehydrogenase (LDH) release and cell viability decrease. For the first time, isoquercetin is described as a neuroprotective agent that potentially explains the alleviation and prevention from OGD/R-induced injury in neurons. Mechanistic studies showed that the neuroprotective effect of isoquercetin was carried out by anti-inflammatory signaling pathway of inhibiting protein expression of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB), and mRNA expression of TNF-α and IL-6, accompanied by the anti-apoptotic signaling pathway of deactivation of extracellular-regulated kinase (ERK), Jun kinase (JNK) and p38, and inhibition of activity of caspase-3. Therefore, these studies highlighted the confirmation of isoquercetin, a flavonoid compound, as an anti-inflammation and anti-apoptosis factor which might be used as a therapeutic strategy for the ischemia/reperfusion (I/R) brain injury and related diseases.

Authors+Show Affiliations

Jiangsu Key Laboratory of Neuroregeneration, Nantong University, Nantong 226001, PR China.No 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

24099731

Citation

Wang, Cai-Ping, et al. "Isoquercetin Protects Cortical Neurons From Oxygen-glucose Deprivation-reperfusion Induced Injury Via Suppression of TLR4-NF-кB Signal Pathway." Neurochemistry International, vol. 63, no. 8, 2013, pp. 741-9.
Wang CP, Li JL, Zhang LZ, et al. Isoquercetin protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via suppression of TLR4-NF-кB signal pathway. Neurochem Int. 2013;63(8):741-9.
Wang, C. P., Li, J. L., Zhang, L. Z., Zhang, X. C., Yu, S., Liang, X. M., Ding, F., & Wang, Z. W. (2013). Isoquercetin protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via suppression of TLR4-NF-кB signal pathway. Neurochemistry International, 63(8), 741-9. https://doi.org/10.1016/j.neuint.2013.09.018
Wang CP, et al. Isoquercetin Protects Cortical Neurons From Oxygen-glucose Deprivation-reperfusion Induced Injury Via Suppression of TLR4-NF-кB Signal Pathway. Neurochem Int. 2013;63(8):741-9. PubMed PMID: 24099731.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Isoquercetin protects cortical neurons from oxygen-glucose deprivation-reperfusion induced injury via suppression of TLR4-NF-кB signal pathway. AU - Wang,Cai-Ping, AU - Li,Jian-Long, AU - Zhang,Lu-Zhong, AU - Zhang,Xiao-Chuan, AU - Yu,Shu, AU - Liang,Xin-Miao, AU - Ding,Fei, AU - Wang,Zhi-Wei, Y1 - 2013/10/05/ PY - 2013/04/06/received PY - 2013/09/10/revised PY - 2013/09/22/accepted PY - 2013/10/9/entrez PY - 2013/10/9/pubmed PY - 2014/7/23/medline KW - 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide KW - Apoptosis KW - DMEM KW - Dulbecco’s Modified Eagle’s Medium KW - ERK KW - FBS KW - I/R KW - Inflammation KW - Ischemia KW - Isoquercetin KW - JNK KW - Jun kinase KW - LDH KW - MAP KW - MCAO KW - MTT KW - NF-κB KW - OGD/R KW - Oxygen–glucose deprivation followed by reperfusion (OGD/R) KW - PI KW - RT-PCR KW - Reverse Transcription-Polymerase Chain Reaction KW - SD KW - Sprague–Dawley KW - TLR4 KW - TLRs KW - [Ca(2+)](i) KW - extracellular-regulated kinase KW - fetal bovine serum KW - intracellular calcium concentrations KW - ischemia/reperfusion KW - lactate dehydrogenase KW - middle cerebral artery occlusion KW - mitogen-activated protein KW - nuclear factor-kappa B KW - oxygen–glucose deprivation followed by reperfusion KW - propidium iodide KW - toll-like receptor 4 KW - toll-like receptors SP - 741 EP - 9 JF - Neurochemistry international JO - Neurochem. Int. VL - 63 IS - 8 N2 - In the present study, oxygen-glucose deprivation followed by reperfusion (OGD/R), an in vitro model of ischemia, was used to evaluate the neuroprotective effect of isoquercetin in primary culture of rat cortical neuronal cells. It was found that isoquercetin administered prior to the insult could prevent OGD/R-induced intracellular calcium concentrations ([Ca(2+)]i) increase, lactate dehydrogenase (LDH) release and cell viability decrease. For the first time, isoquercetin is described as a neuroprotective agent that potentially explains the alleviation and prevention from OGD/R-induced injury in neurons. Mechanistic studies showed that the neuroprotective effect of isoquercetin was carried out by anti-inflammatory signaling pathway of inhibiting protein expression of toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB), and mRNA expression of TNF-α and IL-6, accompanied by the anti-apoptotic signaling pathway of deactivation of extracellular-regulated kinase (ERK), Jun kinase (JNK) and p38, and inhibition of activity of caspase-3. Therefore, these studies highlighted the confirmation of isoquercetin, a flavonoid compound, as an anti-inflammation and anti-apoptosis factor which might be used as a therapeutic strategy for the ischemia/reperfusion (I/R) brain injury and related diseases. SN - 1872-9754 UR - https://www.unboundmedicine.com/medline/citation/24099731/Isoquercetin_protects_cortical_neurons_from_oxygen_glucose_deprivation_reperfusion_induced_injury_via_suppression_of_TLR4_NF_кB_signal_pathway_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0197-0186(13)00246-5 DB - PRIME DP - Unbound Medicine ER -