The Akt-Endothelial Nitric Oxide Synthase Pathway in Lipopolysaccharide Preconditioning-Induced Hypoxic-Ischemic Tolerance in the Neonatal Rat Brain | Zendy

Hsiang-Yin Lin | Zendy; ChaoLiang Wu | Zendy; Chao Huang | Zendy

Open Access

The Akt-Endothelial Nitric Oxide Synthase Pathway in Lipopolysaccharide Preconditioning-Induced Hypoxic-Ischemic Tolerance in the Neonatal Rat Brain

Author(s) -

Hsiang-Yin Lin,

ChaoLiang Wu,

Chao Huang

Publication year - 2010

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.109.574004

Subject(s) - enos , medicine , protein kinase b , endocrinology , nitric oxide synthase , lipopolysaccharide , nitric oxide , downregulation and upregulation , wortmannin , ischemia , neuroprotection , nitric oxide synthase type iii , biology , signal transduction , microbiology and biotechnology , biochemistry , gene

Low-dose lipopolysaccharide (LPS) preconditioning provides neonatal rats long-term neuroprotection against hypoxic ischemia (HI). Upregulating endothelial nitric oxide synthase (eNOS) protects against cerebral ischemia; however, whether eNOS is required for LPS preconditioning-induced protection in neonatal rats is unknown. We hypothesized that Akt activation, which upregulates eNOS in neurons and endothelial cells, is required for LPS preconditioning-induced tolerance against HI in the neonatal brain.

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