We studied the role of K_ATP channels in the infarct-limiting effect of short-term normobaric hypoxia. Male Wistar rats were subjected to a 45-min coronary artery occlusion followed by a 120-min reperfusion. Normobaric hypoxia was simulated 30 min before coronary artery occlusion: 6 sessions of hypoxia (8% O₂, 10 min) and reoxygenation (21% O₂, 10 min). The following drugs were administered to rats: glibenclamide, 5-hydroxydecanoate, and HMR1098. It was found that normobaric hypoxia contributes to a decrease in myocardial infarct size by 36%. Preliminary administration of glibenclamide or 5-hydroxydecanoate eliminated the infarct-reducing effect of normobaric hypoxia. Activator of mitochondrial K_ATP channel diazoxide limited the infarct size. These findings suggest that mitochondrial K_ATP channels are involved into the cardioprotective effect of normobaric hypoxia.

01 May 2022·Bulletin of Experimental Biology and Medicine

δ2-Opioid Receptors as a Target in Designing New Cardioprotective Drugs: the Role of Protein Kinase C, AMPK, and Sarcolemmal KATP Channels

Article

Author: Mukhomedzyanov, A V ; Maslov, L N ; Popov, S V

In rats anesthetized with α-chloralose, coronary artery occlusion (45 min) and reperfusion (120 min) were modeled. The selective δ₂-opioid receptor agonist deltorphin II was administered 5 min before reperfusion. Protein kinase C inhibitor chelerythrine, AMP-activated protein kinase inhibitor compound C, and ATP-sensitive K⁺ channel blockers glibenclamide, 5-hydroxydecanoate, and HMR 1098 were administered 10 min before reperfusion. It was found that the infarct-limiting effect of deltorphin II is associated with activation of protein kinase C and opening of sarcolemmal ATP-sensitive K⁺ channel.

24 Apr 2021·Clinical Hemorheology and MicrocirculationQ4 · MEDICINE

Effects and mechanism of arachidonic acid against TNF-α induced apoptosis of endothelial cells

Q4 · MEDICINE

Article

Author: Chen, Ji-Xiong ; Xu, Wen-Xing ; Lin, Wen-Ting ; Wang, Ping ; Zeng, Min ; Huang, Xiao-Yan

This study aimed to investigate the effects of arachidonic acid metabolite epoxyeicosatrienoic acid (EETs) in the apoptosis of endothelial cells induced by tumor necrosis factor-alpha (TNF-α). After human umbilical vein endothelial cells were cultured, TNF-α/ActD, 14, 15-EET, and HMR-1098 were added, respectively, into the culture medium. The apoptosis level of endothelial cells was detected by flow cytometry. After TNF-α/ActD induced endothelial cell apoptosis, flow cytometry staining showed that endothelial cell apoptosis increased significantly, and the apoptotic cells were significantly reduced after the addition of 14, 15-EET. However, the apoptotic cells significantly increased after the addition of HMR-1098. Western Blot results showed that the phosphorylation levels of LC3-II and AMPK were increased after TNF-α/ActD induction, and the increase was noticeable after the addition of 14, 15-EET. However, the phosphorylation levels of LC3-II and AMPK significantly decreased after the addition of HMR-1098. The activity of Caspase-8 and -9 decreased significantly after the addition of 14, 15-EET but increased after the addition of HMR-1098. Arachidonic acid can inhibit TNF-α induced endothelial cell apoptosis by upregulating autophagy.

100 Deals associated with Clamikalant sodium

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Indication	Highest Phase	Country/Location	Organization	Date
Arrhythmias, Cardiac	Phase 2	US	-	-
Heart Arrest	Phase 2	US	-	-
Myocardial Infarction	Phase 2	-	Sanofi	-
Ventricular Arrhythmia	Phase 2	-	Sanofi	-

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