Abstract
Cerebral ischemia reperfusion (I/R) injury is associated with a high incidence of neurological morbidity and mortality worldwide. Higenamine has anti-inflammatory, anti-oxidative and anti-apoptotic capacities and has been successfully used in myocardial and intestinal ischemia reperfusion. We hypothesized that higenamine might serve the same effects in cerebral I/R. In a rat model of cerebral I/R, higenamine improved functional state of nerves, significantly inhibited the I/R-induced increase in the serum level of tumor necrosis factor α (TNF-alpha) and interleukins (ILs) such as IL-1, IL-6 and IL-18, and CD14+ cells, while decreasing the axonal nerve degeneration. Together, the data demonstrate that higenamine has therapeutic effect in cerebral I/R injury.
MeSH terms
-
Alkaloids / pharmacology*
-
Animals
-
Anti-Inflammatory Agents, Non-Steroidal / pharmacology
-
Antioxidants / therapeutic use
-
Apoptosis / drug effects
-
Axons / pathology
-
Brain / pathology
-
Brain Ischemia / blood*
-
Caspase 3 / metabolism
-
Cerebrovascular Circulation
-
Enzyme-Linked Immunosorbent Assay
-
Flow Cytometry
-
Inflammation
-
Lipopolysaccharide Receptors / metabolism
-
Male
-
Nerve Regeneration
-
Oxidation-Reduction
-
Oxidative Stress / drug effects
-
Rats
-
Rats, Sprague-Dawley
-
Reperfusion Injury / drug therapy*
-
Signal Transduction
-
Tetrahydroisoquinolines / pharmacology*
-
Tumor Necrosis Factor-alpha / metabolism
Substances
-
Alkaloids
-
Anti-Inflammatory Agents, Non-Steroidal
-
Antioxidants
-
Lipopolysaccharide Receptors
-
Tetrahydroisoquinolines
-
Tumor Necrosis Factor-alpha
-
Casp3 protein, rat
-
Caspase 3
-
higenamine