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The neuroprotective action of dexmedetomidine on apoptosis, calcium entry and oxidative stress in cerebral ischemia-induced rats: Contribution of TRPM2 and TRPV1 channels.
Sci Rep. 2016 11 22; 6:37196.SR

Abstract

Dexmedetomidine (DEX) may act as an antioxidant through regulation of TRPM2 and TRPV1 channel activations in the neurons by reducing cerebral ischemia-induced oxidative stress and apoptosis. The neuroprotective roles of DEX were tested on cerebral ischemia (ISC) in the cultures of rat primary hippocampal and DRG neurons. Fifty-six rats were divided into five groups. A placebo was given to control, sham control, and ISC groups, respectively. In the third group, ISC was induced. The DEX and ISC+DEX groups received intraperitoneal DEX (40 μg/kg) 3, 24, and 48 hours after ISC induction. DEX effectively reversed capsaicin and cumene hydroperoxide/ADP-ribose-induced TRPV1 and TRPM2 densities and cytosolic calcium ion accumulation in the neurons, respectively. In addition, DEX completely reduced ISC-induced oxidative toxicity and apoptosis through intracellular reactive oxygen species production and depolarization of mitochondrial membrane. The DEX and ISC+DEX treatments also decreased the expression levels of caspase 3, caspase 9, and poly (ADP-ribose) polymerase in the hippocampus and DRG. In conclusion, the current results are the first to demonstrate the molecular level effects of DEX on TRPM2 and TRPV1 activation. Therefore, DEX can have remarkable neuroprotective impairment effects in the hippocampus and DRG of ISC-induced rats.

Authors+Show Affiliations

Unit of Anesthesiology and Reanimation, Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Süleyman Demirel, Isparta, Turkey.Department of Neuroscience, Institute of Health Science, University of Süleyman Demirel, Isparta, Turkey. Center of Neuroscience, University of Süleyman Demirel, Isparta, Turkey.Department of Neuroscience, Institute of Health Science, University of Süleyman Demirel, Isparta, Turkey.Department of Neuroscience, Institute of Health Science, University of Süleyman Demirel, Isparta, Turkey.Unit of Microbiology, Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, University of Süleyman Demirel, Isparta, Turkey.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

27872485

Citation

Akpınar, Hatice, et al. "The Neuroprotective Action of Dexmedetomidine On Apoptosis, Calcium Entry and Oxidative Stress in Cerebral Ischemia-induced Rats: Contribution of TRPM2 and TRPV1 Channels." Scientific Reports, vol. 6, 2016, p. 37196.
Akpınar H, Nazıroğlu M, Övey İS, et al. The neuroprotective action of dexmedetomidine on apoptosis, calcium entry and oxidative stress in cerebral ischemia-induced rats: Contribution of TRPM2 and TRPV1 channels. Sci Rep. 2016;6:37196.
Akpınar, H., Nazıroğlu, M., Övey, İ. S., Çiğ, B., & Akpınar, O. (2016). The neuroprotective action of dexmedetomidine on apoptosis, calcium entry and oxidative stress in cerebral ischemia-induced rats: Contribution of TRPM2 and TRPV1 channels. Scientific Reports, 6, 37196. https://doi.org/10.1038/srep37196
Akpınar H, et al. The Neuroprotective Action of Dexmedetomidine On Apoptosis, Calcium Entry and Oxidative Stress in Cerebral Ischemia-induced Rats: Contribution of TRPM2 and TRPV1 Channels. Sci Rep. 2016 11 22;6:37196. PubMed PMID: 27872485.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The neuroprotective action of dexmedetomidine on apoptosis, calcium entry and oxidative stress in cerebral ischemia-induced rats: Contribution of TRPM2 and TRPV1 channels. AU - Akpınar,Hatice, AU - Nazıroğlu,Mustafa, AU - Övey,İshak Suat, AU - Çiğ,Bilal, AU - Akpınar,Orhan, Y1 - 2016/11/22/ PY - 2016/09/07/received PY - 2016/10/25/accepted PY - 2016/11/23/entrez PY - 2016/11/23/pubmed PY - 2018/5/19/medline SP - 37196 EP - 37196 JF - Scientific reports JO - Sci Rep VL - 6 N2 - Dexmedetomidine (DEX) may act as an antioxidant through regulation of TRPM2 and TRPV1 channel activations in the neurons by reducing cerebral ischemia-induced oxidative stress and apoptosis. The neuroprotective roles of DEX were tested on cerebral ischemia (ISC) in the cultures of rat primary hippocampal and DRG neurons. Fifty-six rats were divided into five groups. A placebo was given to control, sham control, and ISC groups, respectively. In the third group, ISC was induced. The DEX and ISC+DEX groups received intraperitoneal DEX (40 μg/kg) 3, 24, and 48 hours after ISC induction. DEX effectively reversed capsaicin and cumene hydroperoxide/ADP-ribose-induced TRPV1 and TRPM2 densities and cytosolic calcium ion accumulation in the neurons, respectively. In addition, DEX completely reduced ISC-induced oxidative toxicity and apoptosis through intracellular reactive oxygen species production and depolarization of mitochondrial membrane. The DEX and ISC+DEX treatments also decreased the expression levels of caspase 3, caspase 9, and poly (ADP-ribose) polymerase in the hippocampus and DRG. In conclusion, the current results are the first to demonstrate the molecular level effects of DEX on TRPM2 and TRPV1 activation. Therefore, DEX can have remarkable neuroprotective impairment effects in the hippocampus and DRG of ISC-induced rats. SN - 2045-2322 UR - https://www.unboundmedicine.com/medline/citation/27872485/The_neuroprotective_action_of_dexmedetomidine_on_apoptosis_calcium_entry_and_oxidative_stress_in_cerebral_ischemia_induced_rats:_Contribution_of_TRPM2_and_TRPV1_channels_ DB - PRIME DP - Unbound Medicine ER -