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Inhibition of apoptosis by hyperbaric oxygen in a rat focal cerebral ischemic model.
J Cereb Blood Flow Metab. 2003 Jul; 23(7):855-64.JC

Abstract

The hypothesis was tested that hyperbaric oxygen therapy (HBO) reduced brain infarction by preventing apoptotic death in ischemic cortex in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) and subsequently were exposed to HBO (2.5 atmospheres absolute) for 2 h, at 6 h after reperfusion. Rats were killed and brain samples were collected at 24, 48, 72 h, and 7 days after reperfusion. Neurologic deficits, infarction area, and apoptotic changes were evaluated by clinical scores, 2,3,7-triphenyltetrazolium chloride staining, caspase-3 expression, DNA fragmentation assay, and terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling (TUNEL)-hematoxylin and eosin (H&E) costaining. In MCAO/R without HBO treatment animals, DNA fragmentation was observed in injured cortex at 24, 48, and 72 h but not in samples at 7 days after reperfusion. Double labeling of brain slides with NeuN and caspase-3 demonstrated neurons in the injured cortex labeled with caspase-3. TUNEL+H&E costaining revealed morphologic apoptotic changes at 24, 48, and 72 h after reperfusion. Hyperbaric oxygen therapy abolished DNA fragmentation and reduced the number of TUNEL-positive cells. Hyperbaric oxygen therapy reduced infarct area and improved neurologic scores at 7 days after reperfusion. One of the molecular mechanisms of HBO-induced brain protection is to prevent apoptosis, and this effect of HBO might preserve more brain tissues and promote neurologic functional recovery.

Authors+Show Affiliations

Department of Neurosurgery, University of Mississippi Medical Center, Jackson, Mississippi, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

12843789

Citation

Yin, Dali, et al. "Inhibition of Apoptosis By Hyperbaric Oxygen in a Rat Focal Cerebral Ischemic Model." Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, vol. 23, no. 7, 2003, pp. 855-64.
Yin D, Zhou C, Kusaka I, et al. Inhibition of apoptosis by hyperbaric oxygen in a rat focal cerebral ischemic model. J Cereb Blood Flow Metab. 2003;23(7):855-64.
Yin, D., Zhou, C., Kusaka, I., Calvert, J. W., Parent, A. D., Nanda, A., & Zhang, J. H. (2003). Inhibition of apoptosis by hyperbaric oxygen in a rat focal cerebral ischemic model. Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, 23(7), 855-64.
Yin D, et al. Inhibition of Apoptosis By Hyperbaric Oxygen in a Rat Focal Cerebral Ischemic Model. J Cereb Blood Flow Metab. 2003;23(7):855-64. PubMed PMID: 12843789.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of apoptosis by hyperbaric oxygen in a rat focal cerebral ischemic model. AU - Yin,Dali, AU - Zhou,Changman, AU - Kusaka,Ikuyo, AU - Calvert,John W, AU - Parent,Andrew D, AU - Nanda,Anil, AU - Zhang,John H, PY - 2003/7/5/pubmed PY - 2003/8/27/medline PY - 2003/7/5/entrez SP - 855 EP - 64 JF - Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism JO - J. Cereb. Blood Flow Metab. VL - 23 IS - 7 N2 - The hypothesis was tested that hyperbaric oxygen therapy (HBO) reduced brain infarction by preventing apoptotic death in ischemic cortex in a rat model of focal cerebral ischemia. Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion/reperfusion (MCAO/R) and subsequently were exposed to HBO (2.5 atmospheres absolute) for 2 h, at 6 h after reperfusion. Rats were killed and brain samples were collected at 24, 48, 72 h, and 7 days after reperfusion. Neurologic deficits, infarction area, and apoptotic changes were evaluated by clinical scores, 2,3,7-triphenyltetrazolium chloride staining, caspase-3 expression, DNA fragmentation assay, and terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling (TUNEL)-hematoxylin and eosin (H&E) costaining. In MCAO/R without HBO treatment animals, DNA fragmentation was observed in injured cortex at 24, 48, and 72 h but not in samples at 7 days after reperfusion. Double labeling of brain slides with NeuN and caspase-3 demonstrated neurons in the injured cortex labeled with caspase-3. TUNEL+H&E costaining revealed morphologic apoptotic changes at 24, 48, and 72 h after reperfusion. Hyperbaric oxygen therapy abolished DNA fragmentation and reduced the number of TUNEL-positive cells. Hyperbaric oxygen therapy reduced infarct area and improved neurologic scores at 7 days after reperfusion. One of the molecular mechanisms of HBO-induced brain protection is to prevent apoptosis, and this effect of HBO might preserve more brain tissues and promote neurologic functional recovery. SN - 0271-678X UR - https://www.unboundmedicine.com/medline/citation/12843789/Inhibition_of_apoptosis_by_hyperbaric_oxygen_in_a_rat_focal_cerebral_ischemic_model_ L2 - http://journals.sagepub.com/doi/full/10.1097/01.WCB.0000073946.29308.55?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -