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The Nrf2-inducible antioxidant defense in astrocytes can be both up- and down-regulated by activated microglia:Involvement of p38 MAPK.

Artikel i vetenskaplig tidskrift
Författare Fernando Correa
Elin Ljunggren
Carina Mallard
Michael Nilsson
Stephen G Weber
Mats Sandberg
Publicerad i Glia
Volym 59
Nummer/häfte 5
Sidor 785-99
ISSN 1098-1136
Publiceringsår 2011
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för farmakologi
Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi
Sidor 785-99
Språk en
Länkar dx.doi.org/10.1002/glia.21151
Ämnesord Analysis of Variance, Animals, Animals, Newborn, Astrocytes, cytology, drug effects, immunology, metabolism, Blotting, Western, Cell Survival, physiology, Cells, Cultured, Cerebral Cortex, cytology, drug effects, metabolism, Culture Media, Conditioned, Down-Regulation, drug effects, physiology, Extracellular Signal-Regulated MAP Kinases, metabolism, Glutathione, metabolism, Hydroquinones, pharmacology, JNK Mitogen-Activated Protein Kinases, metabolism, Microglia, cytology, drug effects, immunology, metabolism, NF-E2-Related Factor 2, metabolism, Oxidative Stress, drug effects, physiology, Rats, Rats, Sprague-Dawley, Up-Regulation, drug effects, physiology, p38 Mitogen-Activated Protein Kinases, metabolism
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

The effects of microglia-conditioned medium (MCM) on the inducible Nrf2 system in astrocyte-rich cultures were investigated by determination of glutathione (GSH) levels, γglutamylcysteine ligase (γGCL) activity, the protein levels of Nrf2, Keap1, the modulatory subunit of γGCL (γGCL-M) and activated MAP kinases (ERK1/2, JNK and p38). Microglia were either cultured for 24 h in serum-free culture medium to achieve microglia-conditioned medium from non-activated cells (MCM(0) ), used as control condition, or activated with different concentrations (0.1-1,000 ng mL(-1) ) of lipopolysaccharide (LPS) to produce MCM(0.1-1,000) . Acute exposure (24 h) to MCM(100) increased GSH, γGCL activity, the protein levels of γGCL-M, Nrf2, and activated JNK and ERK1/2 in astrocyte-rich cultures. In contrast, treatment with MCM(10) for 24 h decreased components of the Nrf2 system in parallel with activation of p38 MAPK. Stimulation of the Nrf2 system by tBHQ was partly intact after 24 h but blocked after 72 h treatment with MCM(10) and MCM(100) . This down-regulation after 72 h correlated with activation of p38 MAPK and lack of ERK1/2 and JNK activation. The negative effects were partly reversed by an inhibitor of p38 which restored tBHQ mediated protection against oxidative stress. In conclusion, the study showed a negative effect of MCM(10) on the inducible anti-oxidant defense in astrocyte-rich cultures at both 24 and 72 h that correlated with activation of p38 and was partly reversed by a p38 inhibitor. A transient protective effect of MCM(100) on astrocyte-rich cultures against H(2)O(2) toxicity was observed at 24 h which coincided with activation of JNK and ERK1/2.

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