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Autophagy activation is involved in neuroprotection induced by hyperbaric oxygen preconditioning against focal cerebral ischemia in rats.
Brain Res. 2011 Jul 21; 1402:109-21.BR

Abstract

Our previous studies have demonstrated that hyperbaric oxygen (HBO) preconditioning induces tolerance to focal cerebral ischemia. The present study aimed to investigate whether autophagy is involved in the neuroprotection elicited by HBO preconditioning in a rat model of transient focal cerebral ischemia. Twenty-four hours after the completion of HBO preconditioning (2.5 atm absolute in 100% oxygen for 60 min per day for 5 consecutive days), male Sprague-Dawley rats were subjected to focal cerebral ischemia by middle cerebral artery occlusion (MCAO) for 120 min. The neurobehavioral score and infarct volume were used to evaluate cerebral ischemic injury. An intracerebroventricular injection of the autophagy inhibitor 3-methyladenine (3-MA) or the autophagy inducer rapamycin was administered before HBO preconditioning or MCAO. We found that after reperfusion the protein expression of LC3-II and Beclin 1 and the formation of autophagosomes were increased by HBO preconditioning or ischemia, but the increase following HBO preconditioning was higher than the increase following ischemia. 3-MA suppressed the increases in LC3-II and Beclin 1 induced by HBO preconditioning and attenuated the neuroprotection of HBO preconditioning against cerebral ischemia. Furthermore, 3-MA treatment before MCAO aggravated subsequent cerebral ischemic injury. In contrast, pretreatment with rapamycin up-regulated LC3-II and Beclin 1 after reperfusion and mimicked the neuroprotective effect of HBO preconditioning. These results indicate that HBO preconditioning elevates autophagic activity, which elicits a neuroprotective effect against ischemic injury in the brain, and suggest a novel mechanism of HBO preconditioning-induced tolerance against transient focal cerebral ischemia.

Authors+Show Affiliations

Department of Anesthesiology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.No 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

21684529

Citation

Yan, Wenjun, et al. "Autophagy Activation Is Involved in Neuroprotection Induced By Hyperbaric Oxygen Preconditioning Against Focal Cerebral Ischemia in Rats." Brain Research, vol. 1402, 2011, pp. 109-21.
Yan W, Zhang H, Bai X, et al. Autophagy activation is involved in neuroprotection induced by hyperbaric oxygen preconditioning against focal cerebral ischemia in rats. Brain Res. 2011;1402:109-21.
Yan, W., Zhang, H., Bai, X., Lu, Y., Dong, H., & Xiong, L. (2011). Autophagy activation is involved in neuroprotection induced by hyperbaric oxygen preconditioning against focal cerebral ischemia in rats. Brain Research, 1402, 109-21. https://doi.org/10.1016/j.brainres.2011.05.049
Yan W, et al. Autophagy Activation Is Involved in Neuroprotection Induced By Hyperbaric Oxygen Preconditioning Against Focal Cerebral Ischemia in Rats. Brain Res. 2011 Jul 21;1402:109-21. PubMed PMID: 21684529.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Autophagy activation is involved in neuroprotection induced by hyperbaric oxygen preconditioning against focal cerebral ischemia in rats. AU - Yan,Wenjun, AU - Zhang,Haopeng, AU - Bai,Xiaoguang, AU - Lu,Yan, AU - Dong,Hailong, AU - Xiong,Lize, Y1 - 2011/05/27/ PY - 2011/03/11/received PY - 2011/04/30/revised PY - 2011/05/20/accepted PY - 2011/6/21/entrez PY - 2011/6/21/pubmed PY - 2012/5/15/medline SP - 109 EP - 21 JF - Brain research JO - Brain Res. VL - 1402 N2 - Our previous studies have demonstrated that hyperbaric oxygen (HBO) preconditioning induces tolerance to focal cerebral ischemia. The present study aimed to investigate whether autophagy is involved in the neuroprotection elicited by HBO preconditioning in a rat model of transient focal cerebral ischemia. Twenty-four hours after the completion of HBO preconditioning (2.5 atm absolute in 100% oxygen for 60 min per day for 5 consecutive days), male Sprague-Dawley rats were subjected to focal cerebral ischemia by middle cerebral artery occlusion (MCAO) for 120 min. The neurobehavioral score and infarct volume were used to evaluate cerebral ischemic injury. An intracerebroventricular injection of the autophagy inhibitor 3-methyladenine (3-MA) or the autophagy inducer rapamycin was administered before HBO preconditioning or MCAO. We found that after reperfusion the protein expression of LC3-II and Beclin 1 and the formation of autophagosomes were increased by HBO preconditioning or ischemia, but the increase following HBO preconditioning was higher than the increase following ischemia. 3-MA suppressed the increases in LC3-II and Beclin 1 induced by HBO preconditioning and attenuated the neuroprotection of HBO preconditioning against cerebral ischemia. Furthermore, 3-MA treatment before MCAO aggravated subsequent cerebral ischemic injury. In contrast, pretreatment with rapamycin up-regulated LC3-II and Beclin 1 after reperfusion and mimicked the neuroprotective effect of HBO preconditioning. These results indicate that HBO preconditioning elevates autophagic activity, which elicits a neuroprotective effect against ischemic injury in the brain, and suggest a novel mechanism of HBO preconditioning-induced tolerance against transient focal cerebral ischemia. SN - 1872-6240 UR - https://www.unboundmedicine.com/medline/citation/21684529/Autophagy_activation_is_involved_in_neuroprotection_induced_by_hyperbaric_oxygen_preconditioning_against_focal_cerebral_ischemia_in_rats_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(11)00983-8 DB - PRIME DP - Unbound Medicine ER -