Higenamine alleviates cerebral ischemia-reperfusion injury in rats

Front Biosci (Landmark Ed). 2019 Mar 1;24(5):859-869. doi: 10.2741/4756.

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