J Mol Neurosci DOI 10.1007/s12031-014-0284-9
Hydrogen Sulfide Protects the Brain Against Ischemic Reperfusion Injury in a Transient Model of Focal Cerebral Ischemia Sevda Gheibi & Nahid Aboutaleb & Mehdi Khaksari & Hamid Kalalian-Moghaddam & Abedin Vakili & Yasin Asadi & Fatemeh Zare Mehrjerdi & Azam Gheibi
Received: 26 January 2014 / Accepted: 4 March 2014 # Springer Science+Business Media New York 2014
Abstract Hydrogen sulfide (H2S), a well-known toxic gas, is regarded as endogenous neuromodulator and plays multiple roles in the central nervous system under physiological and pathological states, especially in secondary neuronal injury. Recent studies have shown relatively high concentrations of hydrogen sulfide (H2S) in the brain and also cytoprotective effects of endogenous and exogenous H2S in models of in vitro and in vivo ischemic injury. H2S protects neurons by functioning as an anti-oxidant, anti-inflammatory, and antiapoptotic mediator and by improving neurological function. Moreover, it protects neurons from glutamate toxicity. Therefore, the present study aimed to determine whether H2S provides protection in transient focal cerebral ischemia. Focal ischemia was induced by 60-min middle cerebral artery occlusion (MCAO), followed by 23-h reperfusion. Saline as a S. Gheibi Dept. of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran N. Aboutaleb Physiology Research Center and Physiology Department, School of Medicine, Iran University of Medical Sciences, Tehran, Iran M. Khaksari (*) : H. Kalalian-Moghaddam Dept. of Physiology, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran e-mail: [email protected] A. Vakili : Y. Asadi Physiology Research Center and Physiology Department, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran F. Z. Mehrjerdi Dept of physiology, School of Medicine, Shahid Sadoghi University of Medical Sciences, Yazd, Iran A. Gheibi Dept. of Medical Biotechnology, School of Advanced Medical Technologies, Tehran University of Medical Sciences, Tehran, Iran
vehicle and NaHS (H2S donor; 1 and 5 mg) were intraperitoneally injected (IP) at the beginning of ischemia. Infarct volume, brain edema, and apoptosis were assessed 24 h after MCAO. Treatment with NaHS at doses of 1 and 5 mg markedly reduced total infarct volumes by 29 and 51 %, respectively (P
Hydrogen Sulfide Protects the Brain Against Ischemic Reperfusion Injury in a Transient Model of Focal Cerebral Ischemia Sevda Gheibi & Nahid Aboutaleb & Mehdi Khaksari & Hamid Kalalian-Moghaddam & Abedin Vakili & Yasin Asadi & Fatemeh Zare Mehrjerdi & Azam Gheibi
Received: 26 January 2014 / Accepted: 4 March 2014 # Springer Science+Business Media New York 2014
Abstract Hydrogen sulfide (H2S), a well-known toxic gas, is regarded as endogenous neuromodulator and plays multiple roles in the central nervous system under physiological and pathological states, especially in secondary neuronal injury. Recent studies have shown relatively high concentrations of hydrogen sulfide (H2S) in the brain and also cytoprotective effects of endogenous and exogenous H2S in models of in vitro and in vivo ischemic injury. H2S protects neurons by functioning as an anti-oxidant, anti-inflammatory, and antiapoptotic mediator and by improving neurological function. Moreover, it protects neurons from glutamate toxicity. Therefore, the present study aimed to determine whether H2S provides protection in transient focal cerebral ischemia. Focal ischemia was induced by 60-min middle cerebral artery occlusion (MCAO), followed by 23-h reperfusion. Saline as a S. Gheibi Dept. of Physiology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran N. Aboutaleb Physiology Research Center and Physiology Department, School of Medicine, Iran University of Medical Sciences, Tehran, Iran M. Khaksari (*) : H. Kalalian-Moghaddam Dept. of Physiology, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Iran e-mail: [email protected] A. Vakili : Y. Asadi Physiology Research Center and Physiology Department, School of Medicine, Semnan University of Medical Sciences, Semnan, Iran F. Z. Mehrjerdi Dept of physiology, School of Medicine, Shahid Sadoghi University of Medical Sciences, Yazd, Iran A. Gheibi Dept. of Medical Biotechnology, School of Advanced Medical Technologies, Tehran University of Medical Sciences, Tehran, Iran
vehicle and NaHS (H2S donor; 1 and 5 mg) were intraperitoneally injected (IP) at the beginning of ischemia. Infarct volume, brain edema, and apoptosis were assessed 24 h after MCAO. Treatment with NaHS at doses of 1 and 5 mg markedly reduced total infarct volumes by 29 and 51 %, respectively (P
