naa a22 4500 510805507 CHVBK 20180411083416.0 cr unu---uuuuu 180411e20130101xx s 000 0 eng 10.1007/s12576-012-0228-5 doi (NATIONALLICENCE)springer-10.1007/s12576-012-0228-5 Anandamide enhances expression of heat shock protein 72 to protect against ischemia-reperfusion injury in rat heart [Elektronische Daten] [Qian Li, Min Shi, Bo Li] Anandamide (AEA), one of endocannabinoids, has been reported to exhibit a cardioprotective ability to limit the damage produced by ischemia-reperfusion injury. AEA reportedly enhanced heat shock protein 72 (HSP72) and HSP25 expression in lungs to protect against lung inflammation. This study tested the hypothesis that intravenously injected AEA would induce HSP72 in the heart and thus render cardioprotection against ischemia-reperfusion injury in rats. Cardiac expression of HSPs was quantitatively evaluated in rats by Western blot analysis. That intravenously injected AEA 1mg/kg in vivo induced expression of HSP72, which peaked at 24h after administration. The enhancement of HSP72 by AEA was blocked by cannabinoid 2 (CB2) receptor antagonist AM630, but not cannabinoid 1 (CB1) receptor antagonist AM251. Therefore, the rats were induced with a 30-min coronary occlusion followed by a 120-min reperfusion in vivo at 24h after administration of drugs or vehicle, and then the infarct size was measured. AEA reduced myocardial infarct size compared to control group. Pretreatment with AM630 but not AM251 abolished the infarct size-limiting effect of AEA. Further study demonstrated pretreatment with phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin, Akt inhibitor MK-2206 and AM630 attenuated phosphorylation of Akt and AEA-induced HSP72 expression. The results suggest that AEA is cardioprotective against ischemia-reperfusion insult through its induction of HSP72, which might be mediated by the PI3K/Akt signaling pathway. These effects were mediated by CB2 but not CB1 receptors. The Physiological Society of Japan and Springer, 2012 Anandamide nationallicence Heat shock protein 72 nationallicence Ischemia-reperfusion nationallicence Heart nationallicence Phosphatidylinositol 3-kinase nationallicence Akt nationallicence Li Qian Department of Physiology, Hebei Medical University, 050017, Shijiazhuang, China aut Shi Min Department of Clinical Laboratory, Second Hospital, Hebei Medical University, 050000, Shijiazhuang, China aut Li Bo Department of Clinical Laboratory, Shijiazhuang Center for Disease Control and Prevention, 050011, Shijiazhuang, China aut The Journal of Physiological Sciences Springer Japan 63/1(2013-01-01), 47-53 1880-6546 63:1<47 2013 63 12576 https://doi.org/10.1007/s12576-012-0228-5 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s12576-012-0228-5 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Li Qian Department of Physiology, Hebei Medical University, 050017, Shijiazhuang, China aut NATIONALLICENCE 700 1- Shi Min Department of Clinical Laboratory, Second Hospital, Hebei Medical University, 050000, Shijiazhuang, China aut NATIONALLICENCE 700 1- Li Bo Department of Clinical Laboratory, Shijiazhuang Center for Disease Control and Prevention, 050011, Shijiazhuang, China aut NATIONALLICENCE 773 0- The Journal of Physiological Sciences Springer Japan 63/1(2013-01-01), 47-53 1880-6546 63:1<47 2013 63 12576 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer