Modulation of PARP-1 and PARP-2 expression by L-carnosine and trehalose after LPS and INFγ-induced oxidative stress (549 views)
Neurochemical Research (ISSN: 0364-3190, 1573-6903), 2010 Dec; 35(12): 2144-2153.
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Paper type: Journal Article,
Impact factor: 2.608, 5-year impact factor: 2.573
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-78651326306&partnerID=40&md5=84d7cb8162b8caed925c6fd7f3229f8f
Keywords: Astrocytes, Inos, L-Carnosine, Oligodendrocytes, Parp, Trehalose, Gamma Interferon, Inducible Nitric Oxide Synthase, Lactate Dehydrogenase, Lipopolysaccharide, Nicotinamide Adenine Dinucleotide Adenosine Diphosphate Ribosyltransferase 1, Animal Cell, Article, Cell Viability, Cellular Stress Response, Controlled Study, Down Regulation, Drug Mechanism, Enzyme Activity, Enzyme Release, Gene Expression Regulation, Nerve Cell Necrosis, Neuroprotection, Nonhuman, Nucleotide Sequence, Oligodendroglia, Oxidative Stress, Phenotype, Polymerase Chain Reaction, Priority Journal, Protein Expression, Western Blotting, Base Sequence, Cultured, Dna Primers, Interferon-Gamma, Poly(adp-Ribose) Polymerases, Rattus, Poly (adp-Ribose) Polymerases,
Affiliations:
*** IBB - CNR ***
Department of Chemical Sciences, Section of Biochemistry and Molecular Biology, University of Catania, Viale A. Doria 6, Catania 95125, Italy
Istituto Biostrutture e Bioimmagini CNR Sez. di Catania, Viale A.Doria 6, Catania 95125, Italy
References:
Not available.
Neurochemical Research (ISSN: 0364-3190, 1573-6903), 2010 Dec; 35(12): 2144-2153.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 2.608, 5-year impact factor: 2.573
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-78651326306&partnerID=40&md5=84d7cb8162b8caed925c6fd7f3229f8f
Keywords: Astrocytes, Inos, L-Carnosine, Oligodendrocytes, Parp, Trehalose, Gamma Interferon, Inducible Nitric Oxide Synthase, Lactate Dehydrogenase, Lipopolysaccharide, Nicotinamide Adenine Dinucleotide Adenosine Diphosphate Ribosyltransferase 1, Animal Cell, Article, Cell Viability, Cellular Stress Response, Controlled Study, Down Regulation, Drug Mechanism, Enzyme Activity, Enzyme Release, Gene Expression Regulation, Nerve Cell Necrosis, Neuroprotection, Nonhuman, Nucleotide Sequence, Oligodendroglia, Oxidative Stress, Phenotype, Polymerase Chain Reaction, Priority Journal, Protein Expression, Western Blotting, Base Sequence, Cultured, Dna Primers, Interferon-Gamma, Poly(adp-Ribose) Polymerases, Rattus, Poly (adp-Ribose) Polymerases,
Affiliations:
*** IBB - CNR ***
Department of Chemical Sciences, Section of Biochemistry and Molecular Biology, University of Catania, Viale A. Doria 6, Catania 95125, Italy
Istituto Biostrutture e Bioimmagini CNR Sez. di Catania, Viale A.Doria 6, Catania 95125, Italy
References:
Not available.
Modulation of PARP-1 and PARP-2 expression by L-carnosine and trehalose after LPS and INFγ-induced oxidative stress
Poly(ADP-ribose) polymerases (PARPs) play a crucial role in DNA damage surveillance through their nick sensor functions. Since PARPs' over activation leads to an excessive consumption of NAD + and ATP depletion, these enzymes also are involved in the early events of programmed cell death as well as in necrosis. In order to verify the protective action of L-carnosine and trehalose against NO induced cell death, in the present study we examined their effects on the expression of PARP-1, PARP-2 and iNOS in primary rat astrocyte and oligodendrocyte cells, treated with lipopolysaccharide (LPS) and interferon gamma (INFγ), through semi-quantitative PCR and western analysis. To further characterize the molecular mechanisms underlying L-carnosine and trehalose action, we measured cell viability, nitrite production and LDH release. The data obtained clearly demonstrate that in the stress model employed L-carnosine and trehalose down regulate PARP-1 and PARP-2 expression in both cell phenotypes, thus suggesting their possible application in clinical trials. © 2010 Springer Science+Business Media, LLC.
Poly(ADP-ribose) polymerases (PARPs) play a crucial role in DNA damage surveillance through their nick sensor functions. Since PARPs' over activation leads to an excessive consumption of NAD + and ATP depletion, these enzymes also are involved in the early events of programmed cell death as well as in necrosis. In order to verify the protective action of L-carnosine and trehalose against NO induced cell death, in the present study we examined their effects on the expression of PARP-1, PARP-2 and iNOS in primary rat astrocyte and oligodendrocyte cells, treated with lipopolysaccharide (LPS) and interferon gamma (INFγ), through semi-quantitative PCR and western analysis. To further characterize the molecular mechanisms underlying L-carnosine and trehalose action, we measured cell viability, nitrite production and LDH release. The data obtained clearly demonstrate that in the stress model employed L-carnosine and trehalose down regulate PARP-1 and PARP-2 expression in both cell phenotypes, thus suggesting their possible application in clinical trials. © 2010 Springer Science+Business Media, LLC.
Modulation of PARP-1 and PARP-2 expression by L-carnosine and trehalose after LPS and INFγ-induced oxidative stress
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Modulation of PARP-1 and PARP-2 expression by L-carnosine and trehalose after LPS and INFγ-induced oxidative stress
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18 Records (16 excluding Abstracts).
Total impact factor: 91.012 (86.798 excluding Abstracts).
Total 5 year impact factor: 92.852 (88.594 excluding Abstracts).
Total impact factor: 91.012 (86.798 excluding Abstracts).
Total 5 year impact factor: 92.852 (88.594 excluding Abstracts).
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