@article{BetzSchneiderKressetal.2012,
  author    = {Betz, Boris and Schneider, Reinhard and Kress, Tobias and Schick, Martin Alexander and Wanner, Christoph and Sauvant, Christoph},
  title     = {Rosiglitazone Affects Nitric Oxide Synthases and Improves Renal Outcome in a Rat Model of Severe Ischemia/Reperfusion Injury},
  series = {PPAR Research},
  volume    = {2012},
  journal   = {PPAR Research},
  number    = {Article ID 219319},
  doi       = {10.1155/2012/219319},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-130872},
  pages     = {12},
  year      = {2012},
  abstract  = {Background. Nitric oxide (NO)-signal transduction plays an important role in renal ischemia/reperfusion (I/R) injury. NO produced by endothelial NO-synthase (eNOS) has protective functions whereas NO from inducible NO-synthase (iNOS) induces impairment. Rosiglitazone (RGZ), a peroxisome proliferator-activated receptor (PPAR)-gamma agonist exerted beneficial effects after renal I/R injury, so we investigated whether this might be causally linked with NOS imbalance. Methods. RGZ (5 mg/kg) was administered i.p. to SD-rats (f) subjected to bilateral renal ischemia (60 min). Following 24 h of reperfusion, inulin-and PAH-clearance as well as PAH-net secretion were determined. Morphological alterations were graded by histopathological scoring. Plasma NOx-production was measured. eNOS and iNOS expression was analyzed by qPCR. Cleaved caspase 3 (CC3) was determined as an apoptosis indicator and ED1 as a marker of macrophage infiltration in renal tissue. Results. RGZ improves renal function after renal I/R injury (PAH-/inulin-clearance, PAH-net secretion) and reduces histomorphological injury. Additionally, RGZ reduces NOx plasma levels, ED-1 positive cell infiltration and CC3 expression. iNOS-mRNA is reduced whereas eNOS-mRNA is increased by RGZ. Conclusion. RGZ has protective properties after severe renal I/R injury. Alterations of the NO pathway regarding eNOS and iNOS could be an explanation of the underlying mechanism of RGZ protection in renal I/R injury.},
  language  = {en}
}
@article{ChenLotzRoeweretal.2018,
  author    = {Chen, Shasha and Lotz, Christopher and Roewer, Norbert and Broscheit, Jens-Albert},
  title     = {Comparison of volatile anesthetic-induced preconditioning in cardiac and cerebral system: molecular mechanisms and clinical aspects},
  series = {European Journal of Medical Research},
  volume    = {23},
  journal   = {European Journal of Medical Research},
  number    = {10},
  doi       = {10.1186/s40001-018-0308-y},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-175509},
  year      = {2018},
  abstract  = {Volatile anesthetic-induced preconditioning ( APC) has shown to have cardiac and cerebral protective properties in both pre-clinical models and clinical trials. Interestingly, accumulating evidences demonstrate that, except from some specific characters, the underlying molecular mechanisms of APC-induced protective effects in myocytes and neurons are very similar; they share several major intracellular signaling pathways, including mediating mitochondrial function, release of inflammatory cytokines and cell apoptosis. Among all the experimental results, cortical spreading depolarization is a relative newly discovered cellular mechanism of APC, which, however, just exists in central nervous system. Applying volatile anesthetic preconditioning to clinical practice seems to be a promising cardio- and neuroprotective strategy. In this review, we also summarized and discussed the results of recent clinical research of APC. Despite all the positive experimental evidences, large-scale, long-term, more precisely controlled clinical trials focusing on the perioperative use of volatile anesthetics for organ protection are still needed.},
  language  = {en}
}