ArticleExperimental and therapeutic medicine2013
Ischemic preconditioning attenuates lipid peroxidation and apoptosis in the cecal ligation and puncture model of sepsis.
Article in Experimental and therapeutic medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 28 citations in OpenAlex.
- Septic acute kidney injury: a review of basic research.Clinical and experimental nephrology · 2020Review
- Remote ischemic preconditioning ameliorates indirect acute lung injury by modulating phosphorylation of IκBα in mice.The Journal of international medical research · 2019Article
- Resveratrol enhances vascular reactivity in mice following lipopolysaccharide challenge via the RhoA-ROCK-MLCP pathway.Experimental and therapeutic medicine · 2017Article
- Subcellular Energetics and Metabolism: Potential Therapeutic Applications.Anesthesia and analgesia · 2017Review
- Subcellular Energetics and Metabolism: A Cross-Species Framework.Anesthesia and analgesia · 2017Review
- Urinary neutrophil gelatinase-associated lipocalin is an early predictor of acute kidney injury in premature infants.Experimental and therapeutic medicine · 2016Article
- Alpha-Lipoic Acid Attenuates Oxidative Damage in Organs After Sepsis.Inflammation · 2016Article
- Effects of ghrelin on sepsis-induced acute kidney injury: one step forward.Clinical and experimental nephrology · 2015Article
- Adjuvant potential of selegiline in attenuating organ dysfunction in septic rats with peritonitis.PloS one · 2014Article
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11 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
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.
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