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We aimed to investigate whether the cardioprotection of sevoflurane against ischemia-reperfusion (IR) injury is via inhibiting endoplasmic reticulum stress. The rat in vivo model of myocardial IR injury was induced by ligation of the left anterior descending coronary artery. Sevoflurane significantly ameliorated the reduced cardiac function, increased infarct size, and elevated troponin I level and lactate dehydrogenase activity in plasma induced by IR injury. Sevoflurane suppressed the IR-induced myocardial apoptosis. The increased protein levels of glucose-regulated protein 78 and C/EBP homologous protein (CHOP) after myocardial IR were significantly reduced by sevoflurane. The protein levels of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK), phosphorylated eukaryotic initiation factor 2 (eIF2a), and activating transcription factor 4 (ATF4) were significantly increased in rats with IR and attenuated by sevoflurane treatment. The phosphorylation of Akt was further activated by sevoflurane. The cardioprotection of sevoflurane could be blocked by wortmannin, a PI3K/Akt inhibitor. Our results suggest that the cardioprotection of sevoflurane against IR injury might be mediated by suppressing PERK/eIF2a/ATF4/CHOP signaling via activating the Akt pathway, which helps in understanding the novel mechanism of the cardioprotection of sevoflurane. Key words: sevoflurane, cardioprotection, ischemia-reperfusion injury, endoplasmic reticulum stress, Akt. Nous avons vise a etudier si l'effet cardioprotecteur du sevoflurane contre les lesions d'ischemie/reperfusion (IR) est lie a l'inhibition du stress du reticulum endoplasmique. Nous avons obtenu un modele de lesions d'IR myocardique in vivo chez le rat par l'occlusion de l'artere coronaire interventriculaire anterieure. Le sevoflurane a nettement permis d'attenuer le dysfonctionnement cardiaque engendre par les lesions d'IR, ainsi que de faire diminuer le degre d'augmentation de la taille de l'infarctus, des taux de troponine I et de l'activite de la deshydrogenase lactique plasmatiques engendres par les lesions d'IR. Le sevoflurane a permis de faire disparaitre l'apoptose engendree par l'IR dans le myocarde. Le sevoflurane a nettement permis faire diminuer le degre d'augmentation des taux de la proteine 78 regulee par le glucose et de la proteine homologue de la C/EBP (pour << CCAAT/enhancer-binding protein >>) ou CHOP observes apres l'IR myocardique. L'administration de sevoflurane a permis de faire diminuer le degre d'augmentation des taux de proteine PERK (pour << protein kinase RNA-like endoplasmic reticulum kinase >>) phosphorylee, de facteur eIF2a (pour << eukaryotic initiation factor 2 >>) phosphoryle et d'ATF4 (pour << activating transcription factor 4 >>) observees de facon notable chez les rats soumis a l'IR. Le sevoflurane permettait d'activer davantage la phosphorylation de l'Akt. Il etait possible d'inhiber les effets cardioprotecteurs du sevoflurane par la wortmannine, un inhibiteur de la voie de signalisation PI3K/Akt. Nos resultats laissent entendre que les effets cardioprotecteurs du sevoflurane contre les lesions d'IR pourraient etre medies par l'inhibition de l'axe PERK/eIF2a/ATF4/CHOP par l'intermediaire de l'activation de la voie de signalisation de l'Akt, ce qui contribue a la comprehension du nouveau mode d'action des effets cardioprotecteurs du sevoflurane. [Traduit par la Redaction] Mots-cles: sevoflurane, cardioprotection, lesions d'ischemie-reperfusion, stress du reticulum endoplasmique, Akt., Introduction Ischemic heart disease is still one of the leading causes of mortality and morbidity worldwide (Ferdinandy et al. 2007; Xia et al. 2016). Despite the development and improvement of [...]

The chemical functionalization process of carbon nanotubes(CNTs) by hydrothermal treatments was investigated systematically under various reaction conditions, including different reagents, treatment time, and temperature. The treated samples were characterized by the FTIR, XPS and Raman spectroscopy. The results revealed that the hydrothermal technology is an effective method for the functionalization of CNTs and the control of the resulting chemical groups.