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001-es BibID:BIBFORM014257
Első szerző:Faro, R.
Cím:Myocardial protection by PJ34, a novel potent poly (ADP-ribose) synthetase inhibitor / Faro, R., Toyoda, Y., McCully, J. D., Jagtap, P., Szabo, E., Virag, L., Bianchi, C., Levitsky, S., Szabo, C., Sellke, F. W.
Dátum:2002
ISSN:0003-4975 (Print)
Megjegyzések:The activation of poly (ADP-ribose) synthetase plays an important role in the pathogenesis leading to myocardial ischemia-reperfusion injury. The aim of this study was to determine if a novel potent inhibitor of poly (ADP-ribose) synthetase, PJ34, provides myocardial protection. METHODS: Pigs were subjected to 60 minutes of regional ischemia followed by 180 minutes of reperfusion. Ten mg/kg of PJ34 (PJ34; n = 6) was administrated intravenously (treated group) from 15 to 5 minutes before reperfusion followed by 3 mg/kg/hour of PJ34 from 5 minutes before reperfusion to the end of 180 minutes reperfusion. Control pigs (n = 7) received vehicle only. Arterial and left ventricular pressure and coronary flow were monitored. RESULTS: The PJ34 showed significant reduction on infarct size (37.5%+/-4.5% and 50.5%+/-4.8% of the area at risk) for PJ34 and control pigs groups, respectively, (p < 0.05). Significant reduction in postsystolic shortening, as well as improvement on segment shortening, and positive first derivative of pressure over time (+dP/dt) maximum were also observed in PJ34 versus control pigs (p < 0.05). CONCLUSIONS: Our results suggest that PJ34 provides cardioprotection by decreasing myocardial infarct size and enhancing postischemic regional and global functional recovery.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Animals
Blood Pressure
Coronary Circulation
Enzyme Inhibitors
Female
Hemodynamics
Male
Myocardial Contraction
Myocardial Infarction
Myocardial Reperfusion Injury
Myocardium
külföldön készült közlemény
Phenanthrenes
Poly(ADP-ribose) Polymerases
Swine
Megjelenés:The Annals of Thoracic Surgery. - 73 : 2 (2002), p. 575-581. -
További szerzők:Toyoda, Y. McCully, J. D. Jagtap, Prakash Szabó Éva (1965-) (bőrgyógyász, kozmetológus) Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Bianchi, C. Levitsky, S. Szabó Csaba Sellke, F. W.
Internet cím:elektronikus változat
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2.

001-es BibID:BIBFORM028548
Első szerző:Liaudet, Lucas
Cím:Inosine exerts a broad range of antiinflammatory effects in a murine model of acute lung injury / Lucas Liaudet, Jon G. Mabley, Pál Pacher, László Virág, Francisco G. Soriano, Anita Marton, György Haskó, Edwin A. Deitch, Csaba Szabó
Dátum:2002
ISSN:0003-4932
Megjegyzések:OBJECTIVE: To investigate the effects of inosine on the acute lung inflammation induced by lipopolysaccharide (LPS) in vivo and on the activation and cytotoxicity elicited by proinflammatory cytokines on human lung epithelial (A549) cells in vitro. SUMMARY BACKGROUND DATA: Inosine is an endogenous purine recently shown to exert immunomodulatory and antiinflammatory effects. METHODS: Mice challenged with intratracheal LPS (50 microg) were treated after 1, 6, and 12 hours with inosine (200 mg/kg intraperitoneal) or vehicle. After 24 hours, bronchoalveolar lavage fluid was obtained to measure proinflammatory (tumor necrosis factor-alpha [TNF-alpha], interleukin [IL]-1beta, IL-6), and antiinflammatory (IL-10, IL-4) cytokines, chemokines (MIP-1alpha and MIP-2), myeloperoxidase activity and total cell counts, nitric oxide production, and proteins. Lung histology and immunohistochemical detection of 3-nitrotyrosine, a marker of nitrosative stress, were performed in inflated-fixed lungs. In vitro, cell viability and production of the chemokine IL-8 were evaluated in A549 cells stimulated with a mixture of cytokines in the presence or absence of inosine. RESULTS: Inosine downregulated the LPS-induced expression of TNF-alpha, IL-1beta, IL-6 and MIP-2 and tended to reduce MIP-1alpha, whereas it enhanced the production of IL-4. Total leukocyte counts, myeloperoxidase, nitric oxide production, and proteins were all significantly decreased by inosine. The purine also improved lung morphology and suppressed 3-nitrotyrosine staining in the lungs after LPS. Inosine attenuated the cytotoxicity and the expression of IL-8 induced by proinflammatory cytokines in A549 cells. CONCLUSIONS: Inosine largely suppressed LPS-induced lung inflammation in vivo and reduced the toxicity of cytokines in lung cells in vitro. These data support the proposal that inosine might represent a useful adjunct in the therapy of acute respiratory distress syndrome.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
külföldön készült közlemény
Megjelenés:Annals of Surgery 235 : 4 (2002), p. 568-578. -
További szerzők:Mabley, Jon G. Pacher Pál Virág László (1965-) (biokémikus, sejtbiológus, farmakológus) Soriano, Francisco Garcia Marton Anita Haskó György (1967-) (biokémikus) Deitch, Edwin A. Szabó Csaba (1967-) (orvos)
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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