Lipoic acid and N-acetylcysteine prevent ammonia-induced inflammatory response in C6 astroglial cells: The putative role of ERK and HO1 signaling pathways
| Autor: | Bernardo Assein Arús, Diogo O. Souza, Camila Leite Santos, Carlos Alberto Gonçalves, André Quincozes-Santos, Larissa Daniele Bobermin, Débora Guerini Souza, Bruna Bellaver, Gabriela Bellaver |
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| Rok vydání: | 2015 |
| Předmět: |
MAPK/ERK pathway
HO1 medicine.medical_treatment Anti-Inflammatory Agents Excitotoxicity S100 Calcium Binding Protein beta Subunit Biology Pharmacology Toxicology medicine.disease_cause Antioxidants Cell Line Acetylcysteine chemistry.chemical_compound Ammonia Glutamine synthetase medicine Animals Extracellular Signal-Regulated MAP Kinases Nitrites NAC Thioctic Acid Inflammatory response Ammonia cytotoxicity Hyperammonemia General Medicine Glutathione medicine.disease Rats ERK Lipoic acid Cytokine Biochemistry chemistry Astrocytes Heme Oxygenase (Decyclizing) Cytokines LA Signal Transduction medicine.drug |
| Zdroj: | Toxicology in Vitro. 29:1350-1357 |
| ISSN: | 0887-2333 |
| Popis: | Hyperammonemia induces significant changes in the central nervous system (CNS) in direct association with astroglial functions, such as oxidative damage, glutamatergic excitotoxicity, and impaired glutamine synthetase (GS) activity and pro-inflammatory cytokine release. Classically, lipoic acid (LA) and N-acetylcysteine (NAC) exhibit antioxidant and anti-inflammatory activities by increasing glutathione (GSH) biosynthesis and decreasing pro-inflammatory mediator levels in glial cells. Thus, we evaluated the protective effects of LA and NAC against ammonia cytotoxicity in C6 astroglial cells. Ammonia decreased GSH levels and increased cytokine release and NFκB transcriptional activation. LA and NAC prevented these effects by the modulation of ERK and HO1 pathways. Taken together, these observations show that LA and NAC prevent the ammonia-induced inflammatory response. |
| Databáze: | OpenAIRE |
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