title: Ischemic preconditioning attenuates lipid peroxidation and apoptosis in the cecal ligation and puncture model of sepsis.
abstract: Sepsis and septic shock are are among the major causes of mortality in intensive care units. The lung and kidney are the organs most affected by sepsis. Evidence exists that lipid peroxidation and apoptosis may be responsible for the high mortality due to sepsis. Ischemic preconditioning (IP) is a method for the protection of tissues and organs against ischemia/reperfusion injury by reducing reactive oxygen species levels, lipid peroxidation and apoptosis. In the present study, the effects of IP were investigated in cecal ligation and puncture (CLP)-induced sepsis in rats. The three groups of animals used in the present controlled study were the sham-operated group (sham, n=7), which only underwent a laparotomy; the sepsis group (sepsis, n=7), which underwent cecal ligation and perforation; and the IP + sepsis group (IP+sepsis, n=7), which underwent CLP immediately prior to the application of three cycles of IP to the hind limb. The study was terminated at 6 h after the induction of CLP. Blood, kidney and lung tissue samples were collected for the determination of serum creatinine, blood urea nitrogen (BUN), neutrophil gelatinase-associated lipocalin (NGAL) and lung tissue malondialdehyde (MDA) levels, as well as histological examination. The serum creatinine, plasma NGAL and lung tissue MDA levels in the sepsis group were significantly increased compared with those in the sham and the IP+sepsis groups (P<0.05). Alveolar macrophage counts, histological kidney and lung injury scores, kidney (caspase 3) and lung tissue immuonreactivity (M30) scores in the sepsis group were also significantly increased compared with those in the sham and IP+sepsis groups (P<0.05). The alveolar macrophage count in the IP+sepsis group was increased compared with that in the sham group (P<0.05). In conclusion, IP inhibits lipid peroxidation and attenuates histological injury and apoptosis in the lung and kidney during sepsis.
authors.affiliation: Departments of Anaesthesiology and Reanimation, School of Medicine, Dokuz Eylül University, İzmir 35340;
authors.forename: Cimen Gülben
authors.initials: CG
authors.lastname: Olguner
authors.forename: Uğur
authors.initials: U
authors.lastname: Koca
authors.forename: Emel
authors.initials: E
authors.lastname: Altekin
authors.forename: Bekir Uğur
authors.initials: BU
authors.lastname: Ergür
authors.forename: Seden
authors.initials: S
authors.lastname: Duru
authors.forename: Pelin
authors.initials: P
authors.lastname: Girgin
authors.forename: Aydin
authors.initials: A
authors.lastname: Taşdöğen
authors.forename: Kerim
authors.initials: K
authors.lastname: Gündüz
authors.forename: Seda
authors.initials: S
authors.lastname: Güzeldağ
authors.forename: Muhammed
authors.initials: M
authors.lastname: Akkuş
authors.forename: Serap Cilaker
authors.initials: SC
authors.lastname: Micili
keywords: apoptosis; ischemic preconditioning; kidney; lipid peroxidation; lung; sepsis