title: Ischemic preconditioning and postconditioning alleviates hippocampal tissue damage through abrogation of apoptosis modulated by oxidative stress and inflammation during transient global cerebral ischemia-reperfusion in rats.
abstract: BACKGROUND
  It has been argued recently that ischemic preconditioning (IPre) and postconditioning (IPost) have beneficial effects in many ischemic disorders however; their effects on global ischemia/reperfusion (I/R) are poorly understood. Thus, the present work aimed to study the possible mechanisms underlying the neuroprotective effects of IPre and IPost.
  
  
  METHODS
  Animals were randomly allocated into 4 groups (n = 30): (1) Sham operated (SO); (2) I/R group, animals were subjected to 15 min global ischemia followed by 60 min reperfusion; (3) IPre, animals were subjected to 3 episodes of 5 min ischemia followed by 10 min reperfusion before I/R; (4) IPost, animals were subjected to three episodes of 10s of ischemia and 10s of reperfusion after the period of ischemia followed by a 60 min reperfusion period. Lactate dehydrogenase activity, oxidative stress, inflammatory and apoptotic biomarkers, as well as neurotransmitters, infarct size and histopathological examination were assessed.
  
  
  RESULTS
  I/R induced hippocampal damage through increasing oxidative stress, inflammatory, excitotoxic and apoptotic markers as well as lactate dehydrogenase activity and infarct size. Both, IPre and IPost attenuated most markers induced by I/R.
  
  
  CONCLUSIONS
  IPre and IPost neuroprotective effects can be explained through their anti-oxidant, anti-inflammatory and anti-apoptotic mechanisms.
authors: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. Electronic address: muhammed.abdullatif@gmail.com.
authors: M A
authors: MA
authors: Saad
authors: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
authors: R M
authors: RM
authors: Abdelsalam
authors: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
authors: S A
authors: SA
authors: Kenawy
authors: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
authors: A S
authors: AS
authors: Attia
mesh_terms: D000818:Animals; D017209:Apoptosis; D015415:Biomarkers / Q000378:metabolism; D002545:Brain Ischemia / Q000473:pathology*; D004660:Encephalitis / Q000378:metabolism / Q000473:pathology; D018698:Glutamic Acid / Q000378:metabolism; D006624:Hippocampus / Q000098:blood supply* / Q000378:metabolism / Q000473:pathology*; D057775:Ischemic Postconditioning; D019194:Ischemic Preconditioning; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000473:pathology* / Q000628:therapy; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D015415:Biomarkers; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D007770:L-Lactate Dehydrogenase
keywords: Apoptosis; Inflammation; Ischemia/reperfusion; Oxidative stress; Postconditioning; Preconditioning