The Effect of NaHS on Behavioral Neurological Dysfunction Following Focal Cerebral Ischemia in Rats
DOI:
https://doi.org/10.22100/jkh.v9i1.465Keywords:
NaHS, Brain edema, Behavioral neurological dysfunction, Transient focal cerebral ischemia, RatAbstract
Introduction: Stroke is the third leading cause of death and the second cause of neurological disabilities,after alzheimer's disease in the world. NaHS in biological systems produce hydrogen sulfide (H2S), which will reduce damage after ischemia in different tissues. According to previous studies, NaHS protects cardiomyocytes from ischemic injury. In addition, this peptide has neuroprotective effect on mouse hippocampal and cultured cortical neurons. The present study was conducted to determine whether NaHS provides protection in transient focal cerebral ischemia.
Methods: Transient focal cerebral ischemia was induced in male Wistar rats by 60 minutes middle cerebral artery occlusion (MCAO) through using a filament method, followed by 23 hour reperfusion. Saline as a vehicle and NaHS at doses of 1, 5 and 10mg were injected intraperitoneally (IP) at the beginning of ischemia. Brain edema and motor dysfunction were assessed 24 h after MCAO.
Results: Our results indicated that administration of NaHS at doses of 1 and 5 mg markedly reduced brain edema (P<0.01); NaHS did not significantly change neurological dysfunction (P>0.05).
Conclusion: Our present findings demonstrate that treatment with NaHS exerts its protective effects in focal cerbral ischemic models in rat.
References
Tamura A, Graham DI, McCulloch J, Teasdale GM. Focal cerebral ischaemia in the rat: 1. Description of technique and early neuropathological consequences following middle cerebral artery occlusion. J Cereb Blood Flow Metab 1981;1(1):53-60.
Little JR. Implanted device for middle cerebral artery occlusion in conscious cats. Stroke 1977;8(2):258-60.
Bederson JB, Pitts LH, Tsuji M, Nishimura MC, Davis RL, Bartkowski H. Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. Stroke 1986;17(3):472-6.
Vakili A, Kataoka H, Plesnila N. Role of arginine vasopressin V1 and V2 receptors for brain damage after transient focal cerebral ischemia. Journal of Cerebral Blood Flow & Metabolism 2005;25(8):1012-9.
Lin TN, He YY, Wu G, Khan M, Hsu CY. Effect of brain edema on infarct volume in a focal cerebral ischemia model in rats. Stroke 1993;24(1):117-21.
Slivka A, Murphy E, Horrocks L. Cerebral edema after temporary and permanent middle cerebral artery occlusion in the rat. Stroke 1995;26(6):1061-6.
Sugawara T, Fujimura M, Noshita N, Kim GW, Saito A, Hayashi T, et al. Neuronal death/survival signaling pathways in cerebral ischemia. NeuroRx 2004;1(1):17-25.
Oliver CN, Starke-Reed PE, Stadtman ER, Liu GJ, Carney JM, Floyd RA. Oxidative damage to brain proteins, loss of glutamine synthetase activity, and production of free radicals during ischemia/reperfusion-induced injury to gerbil brain. Proceedings of the National Academy of Sciences 1990;87(13):5144.
Hossmann KA. Glutamate-mediated injury in focal cerebral ischemia: the excitotoxin hypothesis revised. Brain Pathology 1994;4(1):23-36.
Ankarcrona M, Dypbukt JM, Bonfoco E, Zhivotovsky B, Orrenius S, Lipton SA, et al. Glutamate-induced neuronal death: a succession of necrosis or apoptosis depending on mitochondrial function. Neuron 1995;15(4):961.
Ohansen D, Ytrehus K. Exogenous hydrogen sulfide (H2S) protects against regional myocardial ischemia–reperfusion injury. Basic Research in Cardiology 2006;101(1):53-60.
Zhang LM, Jiang CX, Liu DW. Hydrogen sulfide attenuates neuronal injury induced by vascular dementia via inhibiting apoptosis in rats. Neurochemical Research 2009;34(11):1984-1992.
Heo JH, Han SW, Lee SK. Free radicals as triggers of brain edema formation after stroke. Free Radical Biology and Medicine 2005;39(1):51-70.
Valen G, Vaage J. Toxic oxygen metabolites and leukocytes in reperfusion injury: a review. Scandinavian Cardiovascular Journal 1993;27(S41):19-29.
Longa EZ, Weinstein PR, Carlson S, Cummins R. Reversible middle cerebral artery occlusion without craniectomy in rats. Stroke 1989;20(1):84-91.
Aboutaleb N, Khaksari M. Apelin-13 protects the brain against ischemic reperfusion injury and cerebral edema in a transient model of focal cerebral ischemia. Journal of Molecular Neuroscience 2012;48(1):201-208.
Aboutaleb N, Khaksari M .Apelin-13 inhibits apoptosis of cortical neurons following brain ischemic reperfusion injury in a transient model of focal cerebral ischemia. International Journal of Peptide Research and Therapeutics: DOI 10.1007/s10989-013-9374-8.
Wahl F, Allix M, Plotkine M, Boulu RG. Neurological and behavioral outcomes of focal cerebral ischemia in rats. Stroke 1992;23(2):267-72.
Yang Y, Li Q, Miyashita H, Howlett W, Siddiqui M, Shuaib A. Usefulness of postischemic thrombolysis with or without neuroprotection in a focal embolic model of cerebral ischemia. Journal of neurosurgery 2000;92(5):841-7.
Yamamoto M, Tamura A, Kirino T, Shimizu-Sasamata M, Sano K. Effects of thyrotropin-releasing hormone on behavioral disturbances in middle cerebral artery-occluded rats. European Journal of Pharmacology 1991;197(2-3):117-23.
Kawamata T, Alexis NE, Dietrich WD, Finklestein SP. Intracisternal basic fibroblast growth factor (bFGF) enhances behavioral recovery following focal cerebral infarction in the rat. Journal of Cerebral Blood Flow & Metabolism 1996;16(4):542-7.
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