Penehyclidine hydrochloride ameliorates renal ischemia-reperfusion injury in rats

J Surg Res. 2014 Jan;186(1):390-7. doi: 10.1016/j.jss.2013.07.041. Epub 2013 Aug 12.

Abstract

Background: Renal ischemia-reperfusion (I/R) injury is a major cause of acute kidney failure by mechanisms that involve oxidative stress, inflammation, and apoptosis. Penehyclidine hydrochloride (PHC), a selective anticholinergic agent, possesses anti-inflammatory, antioxidative stress, and antiapoptotic effects. Therefore, we investigated the ability of PHC to ameliorate renal I/R injury in Sprague-Dawley rats.

Materials and methods: Rats were randomly assigned to three groups (35 rats per group): sham operated, saline-treated I/R, and PHC-treated I/R. After removing the right kidney, renal I/R injury was induced by clamping the left renal artery for 45 min followed by reperfusion. The rats were administered PHC (0.45 mg/kg, intravenously) or saline 30 min before renal ischemia. The blood and kidneys were harvested at 1, 3, 6, 12, or 24 h after reperfusion. Renal function and histologic changes were assessed. Markers of oxidative stress, inflammation, and apoptosis in the kidneys were also measured.

Results: PHC treatment significantly attenuated renal dysfunction and histologic damage caused by I/R injury. The treatment also decreased malondialdehyde level and attenuated the reduction in superoxide dismutase activity in the kidney. Moreover, the levels of activated p38 mitogen-activated protein kinase, nuclear factor kappa B, and caspase 3 were lower in the PHC-treated animals.

Conclusions: PHC protected rat kidneys from I/R injury by attenuating oxidative stress, inflammatory response, and apoptosis. Thus, PHC may represent a novel practical strategy for the treatment of renal I/R injury.

Keywords: Apoptosis; Inflammation; Ischemia–reperfusion injury; Kidney; Oxidative stress; Penehyclidine hydrochloride.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caspase 3 / analysis
  • Cholinergic Antagonists / therapeutic use*
  • Kidney / blood supply*
  • Male
  • Malondialdehyde / analysis
  • Oxidative Stress
  • Quinuclidines / therapeutic use*
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / drug therapy*
  • Reperfusion Injury / metabolism
  • Superoxide Dismutase / metabolism
  • Transcription Factor RelA / analysis
  • p38 Mitogen-Activated Protein Kinases / metabolism

Substances

  • Cholinergic Antagonists
  • Quinuclidines
  • Transcription Factor RelA
  • penehyclidine
  • Malondialdehyde
  • Superoxide Dismutase
  • p38 Mitogen-Activated Protein Kinases
  • Caspase 3