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Hyperbaric oxygen preconditioning attenuates early apoptosis after spinal cord ischemia in rats.
J Neurotrauma. 2009 Jan; 26(1):55-66.JN

Abstract

This study tested the hypothesis that spinal cord ischemic tolerance induced by hyperbaric oxygen preconditioning (HBO-PC) is mediated by inhibition of early apoptosis. Male Sprague-Dawley rats were preconditioned with consecutive 4 cycles of 1-h HBO exposures (2.5 atmospheres absolute [ATA], 100% O(2)) at a 12-h interval. At 24 h after the last HBO pretreatment, rats underwent 9 min of spinal cord ischemia induced by occlusion of the descending thoracic aorta in combination with systemic hypotension (40 mmHg). Spinal cord ischemia produced marked neuronal death and neurological dysfunction in animals. HBO-PC enhanced activities of Mn-superoxide dismutase (Mn-SOD) and catalase, as well as the expression of Bcl-2 in the mitochondria in the normal spinal cord at 24 h after the last pretreatment (before spinal cord ischemia), and retained higher levels throughout the early reperfusion in the ischemic spinal cord. In parallel, superoxide and hydrogen peroxide levels in mitochondria were decreased, cytochrome c release into the cytosol was reduced at 1 h after reperfusion, and activation of caspase-3 and -9 was subsequently attenuated. HBO-PC improved neurobehavioral scores and reduced neuronal apoptosis in the anterior, intermediate, and dorsal gray matter of lumbar segment at 24 h after spinal cord ischemia. HBO-PC increased nitric oxide (NO) production. L-nitroarginine-methyl-ester (L-NAME; 10 mg/kg), a nonselective NO synthase (NOS) inhibitor, applied before each HBO-PC protocol abolished these beneficial effects of HBO-PC. We conclude that HBO-PC reduced spinal cord ischemia-reperfusion injury by increasing Mn-SOD, catalase, and Bcl-2, and by suppressing mitochondrial apoptosis pathway. NO may be involved in this neuroprotection.

Authors+Show Affiliations

Department of Anesthesiology, Changhai Hospital Affiliated to Second Military Medical University , Shanghai, PR China.No affiliation info availableNo affiliation info availableNo 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

19196076

Citation

Wang, Liping, et al. "Hyperbaric Oxygen Preconditioning Attenuates Early Apoptosis After Spinal Cord Ischemia in Rats." Journal of Neurotrauma, vol. 26, no. 1, 2009, pp. 55-66.
Wang L, Li W, Kang Z, et al. Hyperbaric oxygen preconditioning attenuates early apoptosis after spinal cord ischemia in rats. J Neurotrauma. 2009;26(1):55-66.
Wang, L., Li, W., Kang, Z., Liu, Y., Deng, X., Tao, H., Xu, W., Li, R., Sun, X., & Zhang, J. H. (2009). Hyperbaric oxygen preconditioning attenuates early apoptosis after spinal cord ischemia in rats. Journal of Neurotrauma, 26(1), 55-66. https://doi.org/10.1089/neu.2008.0538
Wang L, et al. Hyperbaric Oxygen Preconditioning Attenuates Early Apoptosis After Spinal Cord Ischemia in Rats. J Neurotrauma. 2009;26(1):55-66. PubMed PMID: 19196076.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Hyperbaric oxygen preconditioning attenuates early apoptosis after spinal cord ischemia in rats. AU - Wang,Liping, AU - Li,Wenxian, AU - Kang,Zhimin, AU - Liu,Yun, AU - Deng,Xiaoming, AU - Tao,Hengyi, AU - Xu,Weigang, AU - Li,Runping, AU - Sun,Xuejun, AU - Zhang,John H, PY - 2009/2/7/entrez PY - 2009/2/7/pubmed PY - 2009/9/26/medline SP - 55 EP - 66 JF - Journal of neurotrauma JO - J. Neurotrauma VL - 26 IS - 1 N2 - This study tested the hypothesis that spinal cord ischemic tolerance induced by hyperbaric oxygen preconditioning (HBO-PC) is mediated by inhibition of early apoptosis. Male Sprague-Dawley rats were preconditioned with consecutive 4 cycles of 1-h HBO exposures (2.5 atmospheres absolute [ATA], 100% O(2)) at a 12-h interval. At 24 h after the last HBO pretreatment, rats underwent 9 min of spinal cord ischemia induced by occlusion of the descending thoracic aorta in combination with systemic hypotension (40 mmHg). Spinal cord ischemia produced marked neuronal death and neurological dysfunction in animals. HBO-PC enhanced activities of Mn-superoxide dismutase (Mn-SOD) and catalase, as well as the expression of Bcl-2 in the mitochondria in the normal spinal cord at 24 h after the last pretreatment (before spinal cord ischemia), and retained higher levels throughout the early reperfusion in the ischemic spinal cord. In parallel, superoxide and hydrogen peroxide levels in mitochondria were decreased, cytochrome c release into the cytosol was reduced at 1 h after reperfusion, and activation of caspase-3 and -9 was subsequently attenuated. HBO-PC improved neurobehavioral scores and reduced neuronal apoptosis in the anterior, intermediate, and dorsal gray matter of lumbar segment at 24 h after spinal cord ischemia. HBO-PC increased nitric oxide (NO) production. L-nitroarginine-methyl-ester (L-NAME; 10 mg/kg), a nonselective NO synthase (NOS) inhibitor, applied before each HBO-PC protocol abolished these beneficial effects of HBO-PC. We conclude that HBO-PC reduced spinal cord ischemia-reperfusion injury by increasing Mn-SOD, catalase, and Bcl-2, and by suppressing mitochondrial apoptosis pathway. NO may be involved in this neuroprotection. SN - 1557-9042 UR - https://www.unboundmedicine.com/medline/citation/19196076/Hyperbaric_oxygen_preconditioning_attenuates_early_apoptosis_after_spinal_cord_ischemia_in_rats_ L2 - https://www.liebertpub.com/doi/full/10.1089/neu.2008.0538?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -