Shevelev O B, Illarionova N B, Petrovski D V, Sarapultsev A P, Chupakhin O N, Moshkin M P
The federal research center Institute of Cytology and Genetics Siberian Branch of the Russian Academy of Sciences, Novosibirsk, Russia.
Institute of Immunology and Physiology of the Ural Branch of the Russian Academy of Sciences, Ekaterinburg, Russia.
PLoS One. 2017 Jul 5;12(7):e0180739. doi: 10.1371/journal.pone.0180739. eCollection 2017.
The aim of the present study was to examine how administration of a compound of 1,3,4- thiadiazine class 2-morpholino-5-phenyl-6H-1,3,4-thiadiazine, hydrobromide (L-17) with hypothermia inducing properties affects the brain metabolism. The mechanism by which L-17 induces hypothermia is unknown; it may involve hypothalamic central thermoregulation as well as act via inhibition of energy metabolism. We tested the hypothesis that L-17 may induce hypothermia by directly inhibiting energy metabolism. The study in vivo was carried out on Sprague-Dawley adult rats. Two doses of L-17 were administered (190 mg/kg and 760 mg/kg). Brain metabolites were analyzed in control and treated groups using magnetic resonance spectroscopy, along with blood flow rate measurements in carotid arteries and body temperature measurements. Further in vitro studies on primary cultures from rat hippocampus were carried out to perform a mitochondria function test of L-17 pre-incubation (100 μM, 30 min). Analysis of brain metabolites showed no significant changes in 190 mg/kg treated group along with a significant reduction in body temperature by 1.5°C. However, administration of L-17 in higher dose 760 mg/kg provoked changes in brain metabolites indicative of neurotoxicity as well as reduction in carotid arteries flow rate. In addition, a balance change of excitatory and inhibitory neurotransmitters was observed. The L-17 pre-incubation with cell primary cultures from rat brain showed no significant changes in mitochondrial function. The results obtained in the study indicate that acute administration of L-17 190 mg/kg in rats induces mild hypothermia with no adverse effects onto brain metabolism.
本研究的目的是考察具有诱导体温降低特性的1,3,4 -噻二嗪类化合物2 -吗啉代- 5 -苯基- 6H - 1,3,4 -噻二嗪氢溴酸盐(L - 17)的给药对脑代谢的影响。L - 17诱导体温降低的机制尚不清楚;它可能涉及下丘脑中枢体温调节,也可能通过抑制能量代谢起作用。我们检验了L - 17可能通过直接抑制能量代谢诱导体温降低的假说。在成年Sprague - Dawley大鼠上进行了体内研究。给予了两剂L - 17(190毫克/千克和760毫克/千克)。使用磁共振波谱分析对照组和处理组的脑代谢物,同时测量颈动脉血流速率和体温。对大鼠海马原代培养物进行了进一步的体外研究,以对L - 17预孵育(100μM,30分钟)进行线粒体功能测试。脑代谢物分析显示,190毫克/千克处理组无显著变化,同时体温显著降低了1.5°C。然而,给予760毫克/千克的高剂量L - 17引发了指示神经毒性的脑代谢物变化以及颈动脉血流速率降低。此外,观察到兴奋性和抑制性神经递质的平衡变化。L - 17与大鼠脑原代培养细胞预孵育未显示线粒体功能有显著变化。该研究获得的结果表明,在大鼠中急性给予190毫克/千克的L - 17会诱导体温轻度降低,且对脑代谢无不良影响。