Involvement of protein kinase C in the nitric oxide-mediated peripheral nerve disturbance in endotoxemic rats

Neurosci Lett. 1999 Jan 8;259(2):99-102. doi: 10.1016/s0304-3940(98)00910-0.

Abstract

The role of protein kinase C (PKC) in nitric oxide (NO)-mediated peripheral nerve disturbance in lipopolysaccharide (endotoxin, LPS)-treated rat was studied. The impaired Na+,K+ -ATPase activities in sciatic nerves from LPS-treated rats were prevented by aminoguanidine (NO synthase inhibitor) and corrected by PKC agonist in vitro. Using Western blot to determine PKC isoforms alpha and beta polypeptide levels in LPS-treated rat sciatic nerves, we found that alpha isoform was markedly reduced in the particulate fraction, but the beta isoform was unaffected. The alpha and beta isoforms in the cytosolic fractions were not significantly different as compared with control. This diminished particulate PKC alpha isoform was prevented by the treatment of aminoguanidine. Moreover, the motor nerve conduction velocity was significantly reduced in endotoxemic rats and corrected by aminoguanidine. These results indicate that the alteration of PKC alpha isoform in Na+,K+ -ATPase-enriched fraction of sciatic nerve may be related to the NO-mediated peripheral nerve disturbance in endotoxemic rats.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Endotoxemia / pathology
  • Lipopolysaccharides / pharmacology
  • Male
  • Nitric Oxide / physiology*
  • Protein Kinase C / metabolism
  • Protein Kinase C / physiology*
  • Rats
  • Rats, Wistar
  • Sciatic Nerve / drug effects
  • Sciatic Nerve / physiology*
  • Sodium-Potassium-Exchanging ATPase / antagonists & inhibitors

Substances

  • Lipopolysaccharides
  • Nitric Oxide
  • Protein Kinase C
  • Sodium-Potassium-Exchanging ATPase