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Different doses of dexmedetomidine reduce plasma cytokine production, brain oxidative injury, PARP and caspase expression levels but increase liver oxidative toxicity in cerebral ischemia-induced rats.
Brain Res Bull. 2017 04; 130:1-9.BR

Abstract

Cerebral ischemia-induced progression of brain, liver, and erythrocyte oxidative injuries might be modulated by dexmedetomidine (DEX) as a potent antioxidant and anti-inflammatory drug. The present study was conducted to explore whether two different doses of DEX protect against plasma cytokine and brain, liver and erythrocyte oxidative toxicity and apoptosis in cerebral ischemia-induced rats. Forty-two rats were equally divided into 7 groups. The first and second groups were used as untreated and sham controls, respectively. The third (DEX4) and fourth (DEX40) groups received 4mg/kg and 40mg/kg DEX treatments. The fifth, sixth and seventh group were operated on to induce cerebral ischemia. The fifth, sixth and seventh groups are used to represent cerebral ischemia, cerebral ischemia+DEX4, and cerebral ischemia+DEX40, respectively. DEX was intraperitoneally given to the DEX groups at the 3rd, 24th and 48th hour. Brain and erythrocyte lipid peroxidation (MDA) levels and plasma IL-1β and TNF-α levels were high in the cerebral ischemia group although they were low in the DEX4 and DEX40 groups. Decreased glutathione peroxidase (GSH-Px) and reduced glutathione (GSH) values in the brain and erythrocyte of the cerebral ischemia group were increased by the DEX treatments, although PARP, and the caspase 3 and 9 expressions in the brain were further decreased. Conversely, the cerebral ischemia-induced decrease in the liver vitamin A, vitamin E, GSH, and GSH-Px were further decreased by the DEX treatments, although MDA level, PARP, and caspase 3 and 9 expressions were further increased by the DEX treatments. In conclusion, DEX induced protective effects against cerebral ischemia-induced brain and erythrocyte oxidative injuries through regulation of the antioxidant level and cytokine production. However, both doses of DEX induced oxidative toxicity and apoptotic effects in the rats' livers.

Authors+Show Affiliations

Unit of Microbiology, Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Suleyman Demirel University, Isparta, Turkey.Neuroscience Research Center, University of Suleyman Demirel, Isparta, Turkey. Electronic address: mustafanaziroglu@sdu.edu.tr.Unit of Anesthesiology and Reanimation, Department of Oral and Maxillofacial Surgery, Faculty of Dentistry, Suleyman Demirel University, Isparta, Turkey.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28007581

Citation

Akpınar, Orhan, et al. "Different Doses of Dexmedetomidine Reduce Plasma Cytokine Production, Brain Oxidative Injury, PARP and Caspase Expression Levels but Increase Liver Oxidative Toxicity in Cerebral Ischemia-induced Rats." Brain Research Bulletin, vol. 130, 2017, pp. 1-9.
Akpınar O, Nazıroğlu M, Akpınar H. Different doses of dexmedetomidine reduce plasma cytokine production, brain oxidative injury, PARP and caspase expression levels but increase liver oxidative toxicity in cerebral ischemia-induced rats. Brain Res Bull. 2017;130:1-9.
Akpınar, O., Nazıroğlu, M., & Akpınar, H. (2017). Different doses of dexmedetomidine reduce plasma cytokine production, brain oxidative injury, PARP and caspase expression levels but increase liver oxidative toxicity in cerebral ischemia-induced rats. Brain Research Bulletin, 130, 1-9. https://doi.org/10.1016/j.brainresbull.2016.12.005
Akpınar O, Nazıroğlu M, Akpınar H. Different Doses of Dexmedetomidine Reduce Plasma Cytokine Production, Brain Oxidative Injury, PARP and Caspase Expression Levels but Increase Liver Oxidative Toxicity in Cerebral Ischemia-induced Rats. Brain Res Bull. 2017;130:1-9. PubMed PMID: 28007581.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Different doses of dexmedetomidine reduce plasma cytokine production, brain oxidative injury, PARP and caspase expression levels but increase liver oxidative toxicity in cerebral ischemia-induced rats. AU - Akpınar,Orhan, AU - Nazıroğlu,Mustafa, AU - Akpınar,Hatice, Y1 - 2016/12/19/ PY - 2016/08/24/received PY - 2016/12/09/accepted PY - 2016/12/23/pubmed PY - 2018/2/23/medline PY - 2016/12/24/entrez KW - Brain KW - Cerebral ischemia KW - Cytokine KW - Dexmedetomidine KW - Liver KW - Oxidative stress SP - 1 EP - 9 JF - Brain research bulletin JO - Brain Res Bull VL - 130 N2 - Cerebral ischemia-induced progression of brain, liver, and erythrocyte oxidative injuries might be modulated by dexmedetomidine (DEX) as a potent antioxidant and anti-inflammatory drug. The present study was conducted to explore whether two different doses of DEX protect against plasma cytokine and brain, liver and erythrocyte oxidative toxicity and apoptosis in cerebral ischemia-induced rats. Forty-two rats were equally divided into 7 groups. The first and second groups were used as untreated and sham controls, respectively. The third (DEX4) and fourth (DEX40) groups received 4mg/kg and 40mg/kg DEX treatments. The fifth, sixth and seventh group were operated on to induce cerebral ischemia. The fifth, sixth and seventh groups are used to represent cerebral ischemia, cerebral ischemia+DEX4, and cerebral ischemia+DEX40, respectively. DEX was intraperitoneally given to the DEX groups at the 3rd, 24th and 48th hour. Brain and erythrocyte lipid peroxidation (MDA) levels and plasma IL-1β and TNF-α levels were high in the cerebral ischemia group although they were low in the DEX4 and DEX40 groups. Decreased glutathione peroxidase (GSH-Px) and reduced glutathione (GSH) values in the brain and erythrocyte of the cerebral ischemia group were increased by the DEX treatments, although PARP, and the caspase 3 and 9 expressions in the brain were further decreased. Conversely, the cerebral ischemia-induced decrease in the liver vitamin A, vitamin E, GSH, and GSH-Px were further decreased by the DEX treatments, although MDA level, PARP, and caspase 3 and 9 expressions were further increased by the DEX treatments. In conclusion, DEX induced protective effects against cerebral ischemia-induced brain and erythrocyte oxidative injuries through regulation of the antioxidant level and cytokine production. However, both doses of DEX induced oxidative toxicity and apoptotic effects in the rats' livers. SN - 1873-2747 UR - https://www.unboundmedicine.com/medline/citation/28007581/Different_doses_of_dexmedetomidine_reduce_plasma_cytokine_production_brain_oxidative_injury_PARP_and_caspase_expression_levels_but_increase_liver_oxidative_toxicity_in_cerebral_ischemia_induced_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(16)30219-2 DB - PRIME DP - Unbound Medicine ER -