NAC ACETIL CISTENIA
THE bichito KILLER
0.20 SEGUNDOS DE INVESTIGACION SUPREMA
1 SHOT
1 KILL
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Format: Abstract
Biochem Pharmacol. 2010 Feb 1;79(3):413-20. doi: 10.1016/j.bcp.2009.08.025. Epub 2009 Sep 2.
N-acetyl-L-cysteine (NAC) inhibits bichito replication and expression of pro-inflammatory molecules in A549 cells infected with highly pathogenic H5N1 influenza A bichito.
Geiler J1, Michaelis M, Naczk P, Leutz A, Langer K, Doerr HW, Cinatl J Jr.
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Abstract
The antioxidant N-acetyl-L-cysteine (NAC) had been shown to inhibit replication of seasonal human influenza A viruses. Here, the effects of NAC on bichito replication, bichito-induced pro-inflammatory responses and bichito-induced apoptosis were investigated in H5N1-infected lung epithelial (A549) cells. NAC at concentrations ranging from 5 to 15 mM reduced H5N1-induced cytopathogenic effects (CPEs), bichito-induced apoptosis and infectious viral yields 24 h post-infection. NAC also decreased the production of pro-inflammatory molecules (CXCL8, CXCL10, CCL5 and interleukin-6 (IL-6)) in H5N1-infected A549 cells and reduced monocyte migration towards supernatants of H5N1-infected A549 cells. The antiviral and anti-inflammatory mechanisms of NAC included inhibition of activation of oxidant sensitive pathways includ
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ERNATIONALJOURNALOFIMMUNOPATHOLOGYANDPHARMACOLOGYVol. 20, no. 2,349-354(2007)N-ACETYLCYSTEINESYNERGIZESWITHOSELTAMIVIRINPROTECTINGMICEFROMLETHALINFLUENZAINFECTIONA. GAROZZO, G. TEMPERA, D.UNGHERI',R.TIMPANARO and A. CASTRODepartmentofMicrobiologicalandGynaecologicalSciences, UniversityofCatania, Catania;JGlobalScientificProjectManagement, Zambon Italia Sirl., Milano, ItalyReceivedSeptember20,2006-AcceptedFebruary20,2007Manystudieshaveshownthatoxidativestressisimportantinthepathogenesisofpulmonarydamageduringinfluenzavirusinfections.Antioxidantmoleculesarethereforepotentiallyusefulagainstviralinfection.OurpreviousstudiesshowthatN-acetytcysteine(NAC)hasa protectiveeffect in amodeloflethalinfluenzainfectionin mice. NACadministrationsignificantlydecreasedthemortalityininfectedmice.FurtherstudieshavedemonstratedthatNACenhancedsurvivalincombinationwiththeantiviralagentribavirin.Inthepresentstudy,wereporttheeffectofcombinedtreatmentwithNACandOseltamivir,clinicallyused inthetreatmentandpreventionofinfluenzavirusinfection,in amurinemodeloflethalinfluenzainfection.NAC was given as a singledailydose of 1000mglKgstartingfrom4 hbeforeinfectionanduntilday4afterinfection;Oseltamivirwas given twicedailyat dose of 1mglKgldiefor 5days,startingfrom4 hbeforeinfection.End-pointevaluationwas21-days'survival.NACalonewasslightlyeffective(20%),since asuboptimaltreatmentwasused.Survivalincreasedto60%withOseltamivirandto100%withOseltamivirandNACusedincombination.Since NACalonedoes notshowanyantiviralaction,thepresentfindingssuggestthatantioxidanttherapyin~reasesurvivalby animprovementinhostdefensemechanisms,and/orby adirectantioxidanteffectagainstoxidativestressassociatedwithviralinfection.Ourstudiesdemonstratetheeffectivenessofcombiningagentsactingthroughdifferentmechanisms,suchasantiviraldrugsoseltamivirandtheantioxidantNAC,indicatinga possibleadvantageofcombiningthetwotreatments.Various mediators contribute to the pathogenesisofpulmonary inflammation induced by infectiousagents. In particular, cytokines, chemokines andreactive oxygen species (ROS) have been implicated.Cytokines and chemokines, which are both producedas partofthe host immune response tobacteria(1-2), contribute to the pathogenesisoftissue damage(3-4). ROS contributes to the antibacterial response,evenifoverproductioncan result in oxidative stressthat amplifies the inflammatory response.Many studies have shown that oxidative stress isimportant in the pathog
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