scholarly journals Study of antihypoxic activities of metal complex selenium containing substances after their parenteral and enteralintroductions

2012 ◽  
Vol 10 (3) ◽  
pp. 28-34
Author(s):  
Denis Vladimirovich Sosin ◽  
Andrey Viktorovich Yevseyev ◽  
Edgar Andreyevich Parfenov ◽  
Vitaliy Andreyevich Pravdivtsev ◽  
Marina Anatolyevna Yevseyeva ◽  
...  

In experiments on mice undergone to an acute hypercapnic hypoxia and an acute hypobaric hypoxia a screening of antihypoxants among new selenium containing metal complex substances was performed after their intra-abdominal and oral introductions. It was found that substances πQ1983 and πQ2170 on both models of hypoxia make the defensive effects surpassing actions well-known antihypoxants such as amthizole and bemythil. It was shown that antihypoxiс affects of studied substances depend on their caused hypothermia. For the first time the protective action of selenium containing metal complex compounds was demonstrated after their introduction per os.

2017 ◽  
Vol 23 (3) ◽  
pp. 148-151
Author(s):  
S. A Shakhmardanova ◽  
P. A Galenko-Yaroshevsky ◽  
L. N Parshina ◽  
B. A Trofimov ◽  
V. V Tarasov ◽  
...  

The pharmacotherapy of hypoxia is an important task of modern experimental and clinical pharmacology. The medications with anti-hypoxic effect implemented into clinical practice unfortunately do not meet requirements of physicians due to poor efficiency, narrow range of active dosages and undesirable side effects. The complexes of zinc with N-alkenylimidazole demonstrated anti-hypoxic activity at various models of acute hypoxia within large range of dosage. Therefore, further studying of zinc-contained compounds as possible correctors of hypoxia is of particular interest. The experiments with white nonlinear male mice were used for comparative investigation of ant-hypoxic effect of complex compounds of zinc acetate with N-propargylimidazole and 3-hydroxipyridine, including complexes immobilized on sulfated arabinogalaсtan and also well-known anti-hypoxants and/or anti-oxidants: etomerzol, mexidol, nooglutil and hypoxen. It is demonstrated that anti-hypoxic effect of complex of zinc acetate with N-propargylimidazolein conditions of acute hypobaric hypoxia, acute hypoxia with hypercapnia acute hematic hypoxia by width of active dosages (1-100 mg/kg, intraperitoneally) and degree of expression (19-317% in comparison with control groups of animals) excels the similar effect in well-known anti-hypoxants and/or anti-oxidants: etomerzol (25-100 mg/kg, intraperitoneally), mexidol (100 mk per kg, intraperitoneally), nooglutil (25-100 mg/kg, intraperitoneally) and hypoxen (50-150 mg/kg, intraperitoneally). The protective effect of complex of zinc acetate with 3-hydroxipyridine by width of active dosages (25-100 mg/kg, intraperitoneally) and degree of expression (27-167% in comparison with control groups of animals) in conditions of exogenous hypoxia (acute hypobaric hypoxia and acute hypoxia with hypercapnia) excels similar effect of etomerzol and mexidol ans is comparable with effect of nooglutil and hypoxen. The complexes immobilized on sulfated arabinogalactan were ineffective.


2007 ◽  
Vol 8 (4) ◽  
pp. 312-321 ◽  
Author(s):  
Barbara J. Engebretsen ◽  
David Irwin ◽  
Maria E. Valdez ◽  
Mary K. O'Donovan ◽  
Alan Tucker ◽  
...  

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Yajing Wang ◽  
Wayne Lau ◽  
Erhe Gao ◽  
Walter Koch ◽  
Xin Ma

Anti-inflammatory and vascular protective actions of adiponectin (APN) are well-recognized. However, many fundamental questions remain unanswered. The current study attempted to identify the APN receptor subtype responsible for APN’s vascular protective action, and investigate the role of ceramidase activation in APN anti-inflammatory signaling. Wild type (WT) or gene manipulated HUVEC were treated with TNFα in the presence and absence of APN. The effect of APN on TNFα-induced inflammatory and oxidative/nitrative stress was determined. In WT HUVEC, APN significantly reduced TNFα-induced ICAM-1 expression and attenuated TNFα-induced superoxide and peroxynitrite formation (P<0.01). These anti-inflammatory actions were virtually abolished by AdipoR1-, but not AdipoR2-, knockdown (KD). Treatment with APN significantly increased neutral ceramidase (nCDase) activity (3.7-fold, P<0.01). AdipoR1-KD markedly (P0.05), reduced APN-induced nCDase activation. More importantly, siRNA mediated nCDase-KD markedly blocked the effect of APN upon TNFα-induced ICAM-1 expression (P0.05), and modestly inhibited APN anti-inflammatory effect (P87% of APN-induced nCDase activation was lost. Whereas APN treatment failed to inhibit TNFα-induced ICAM-1 expression, treatment with S1P or SEW (S1P receptor agonist) remained effective in Cav1-KD cells in reducing TNFα-induced ICAM-1 expression (P<0.01). AdipoR1 and Cav1 co-localized and co-precipitated in HUVECs. APN treatment did not affect this interaction. Moreover, re-expression of WT Cav1 in Cav1-KD cells restored nCDase activation in response to APN (P<0.01 vs. vehicle), whereas re-expression of a mutated Cav1 blocking AdipoR1/Cav1 interaction failed to restore APN-mediated nCDase activation. Finally, there is weak basal Cav1/nCDase interaction, which significantly increased following APN treatment. These results demonstrate for the first time that APN inhibits TNFα-induced inflammatory response via Cav1-mediated ceramidase recruitment and activation in an AdipoR1- dependent fashion.


2008 ◽  
Vol 18 (3) ◽  
pp. 434-442 ◽  
Author(s):  
Julia Serrano ◽  
Ana Patricia Fernández ◽  
Jaime Sánchez ◽  
José Rodrigo ◽  
Alfredo Martínez

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