English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

The development of septic shock is a common and frequently lethal consequence of gram-negative infection. Mediators released by lung macrophages activated by bacterial products such as lipopolysaccharide (LPS) contribute to shock symptoms. We have shown that insulin down-regulates LPS-induced TNF production by alveolar macrophages (AMs). In the present study, we investigated the effect of insulin on the LPS-induced production of nitric oxide (NO) and prostaglandin (PG)-E(2), on the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and on nuclear factor kappa B (NF-kappaB) activation in AMs. Resident AMs from male Wistar rats were stimulated with LPS (100 ng/mL) for 30 minutes. Insulin (1 mU/mL) was added 10 min before LPS. Enzymes expression, NF-kappaB p65 activation and inhibitor of kappa B (I-kappaB)alpha phosphorylation were assessed by immunobloting; NO by Griess reaction and PGE(2) by enzyme immunoassay (EIA). LPS induced in AMs the expression of iNOS and COX-2 proteins and production of NO and PGE(2), and, in parallel, NF-kappaB p65 activation and cytoplasmic I-kappaBalpha phosphorylation. Administration of insulin before LPS suppressed the expression of iNOS and COX-2, of NO and PGE(2) production and Nuclear NF-kappaB p65 activation. Insulin also prevented cytoplasmic I-kappaBalpha phosphorylation. These results show that in AMs stimulated by LPS, insulin prevents nuclear translocation of NF-kappaB, possibly by blocking I-kappaBalpha degradation, and supresses the production of NO and PGE(2), two molecules that contribute to septic shock.

Insulin Suppresses LPS-induced iNOS and COX-2 Expression and NF-&kappa;B Activation in Alveolar Macrophages and

Insulin Suppresses LPS-induced iNOS and COX-2 Expression and NF-κB Activation in Alveolar Macrophages and