Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt-0

<p><b>Copyright information:</b></p><p>Taken from "Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt"</p><p>Journal of Neuroinflammation 2008;5():4-4.</p><p>Published online 18 Jan 2008</p><p>PMCID:PMC2254610.</p><p></p>ignificantly induced NO generation, and pretreatment with pioglitazone inhibited this LPS-induced NO production in a dose-dependent manner. Data presented are representative of three independent experiments (n = 3). (***< 0.001 vs. control ###< 0.001 vs. LPS

Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt-4

<p><b>Copyright information:</b></p><p>Taken from "Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt"</p><p>Journal of Neuroinflammation 2008;5():4-4.</p><p>Published online 18 Jan 2008</p><p>PMCID:PMC2254610.</p><p></p>tivation was assessed after 10 min, and P13K and Akt were assessed after 60 min. PPAR-γ activation, PI3K and Akt expression were observed in the pioglitazone-treated cultures, compared to control and LPS-only groups. Data presented are representative of three independent experiments (n = 3). (*< 0.05 vs. control, #< 0.05 vs. LPS, ##< 0.01 vs. LPS)

Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt-6

<p><b>Copyright information:</b></p><p>Taken from "Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt"</p><p>Journal of Neuroinflammation 2008;5():4-4.</p><p>Published online 18 Jan 2008</p><p>PMCID:PMC2254610.</p><p></p>ignificantly induced NO generation, and pretreatment with pioglitazone inhibited this LPS-induced NO production in a dose-dependent manner. Data presented are representative of three independent experiments (n = 3). (***< 0.001 vs. control ###< 0.001 vs. LPS

Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt-1

<p><b>Copyright information:</b></p><p>Taken from "Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt"</p><p>Journal of Neuroinflammation 2008;5():4-4.</p><p>Published online 18 Jan 2008</p><p>PMCID:PMC2254610.</p><p></p>ent with pioglitazone (10 μM), 1 hr before LPS, prevents its expression. : Rat mesencephalic mixed cultures were treated with the selective iNOS inhibitor 1400 W, with different doses from 1 ng/ml to 10 μM/ml, 1 hr before a 72 hr LPS exposure. The number of TH-positive neurons was determined by immunocytochemistry. Data presented are representative of three independent experiments (n = 3). (**< 0.01 vs. control, ***< 0.001 vs. control, #< 0.05 vs. LPS, ##< 0.01 vs. LPS, ###< 0.001 vs. LPS)

Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt-5

<p><b>Copyright information:</b></p><p>Taken from "Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt"</p><p>Journal of Neuroinflammation 2008;5():4-4.</p><p>Published online 18 Jan 2008</p><p>PMCID:PMC2254610.</p><p></p>azone followed by LPS 60 mins later in microglia-enriched culture, and after 48 hrs NO levels were measured. The results show that the LPS-induced NO level was significantly higher than control (< 0.01), and that pretreatment with pioglitazone inhibits LPS-induced NO (< 0.01). In contrast, pretreatment with wortmannin enhanced the LPS-induced increase in NO generation (< 0.05), and this pretreatment prevented the inhibitory effect of pioglitazone on LPS-induced NO generation. Data presented are representative of three independent experiments (n = 3).). (**< 0.01 vs. control, #< 0.05 vs. LPS, ##< 0.01 vs. LPS, &&< 0.01 vs. Piog plus LPS)

Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt-2

<p><b>Copyright information:</b></p><p>Taken from "Pioglitazone inhibition of lipopolysaccharide-induced nitric oxide synthase is associated with altered activity of p38 MAP kinase and PI3K/Akt"</p><p>Journal of Neuroinflammation 2008;5():4-4.</p><p>Published online 18 Jan 2008</p><p>PMCID:PMC2254610.</p><p></p>(1 μg/ml) exposure and, after 24 hrs, NO levels were measured. Only the p38 MAPK inhibitor prevented NO production. : Pretreatment with pioglitazone inhibited LPS-induced phosphorylation of p38 MAPK in mesencephalic neuronal-microglia mixed cultures. Pioglitazone was added 1 hr before LPS treatment (1 μg/ml) and, after 30 mins, p38 MAPK was immunobloted. As shown in 3B, LPS increased phosphorylation of p38 MAPK, and pretreatment with pioglitazone inhibited this expression. Data presented are representative of three independent experiments (n = 3). (*< 0.05 vs. control, ***< 0.001 vs. control, #< 0.05 vs. LPS)