title: Beneficial effect of methylprednisolone on cardiac myocytes in a rat model of severe brain injury.
abstract: Cardiac injury, occurred after traumatic brain injury (TBI), has been recognized for more than a century. Bcl-2 is a key regulatory component of the mitochondrial cell death pathway, and its overexpression is cytoprotective in many cell types. The therapeutic agents, which induce the expression of bcl-2 protein, might provide a new therapy to prevent cardiac myocyte damage following TBI. In this study, we investigated whether methylprednisolone sodium succinate (MPSS) influences the expression of bcl-2 in the heart. Wistar-Albino female rats underwent TBI (300 g/cm) generated by the weight-drop method, and were left untreated (n = 6) or treated with either MPSS (30 mg/kg) (n = 6) or vehicle (albumin solution) (n = 6). The heart was isolated from each animal with TBI. For comparison, the hearts were isolated from sham-operated (n = 6) and control rats (n = 6). The relative expression of bcl-2 mRNA in the heart was quantitated by real-time polymerase chain reaction. We also assessed lipid peroxidation in the heart tissue by determining the concentration of thiobarbituric acid-reactive substances (TBARs) as an indicator of tissue damage. The bcl-2 expression level was significantly higher in the hearts of MPSS-treated rats compared to that of other TBI groups (p < 0.0001). Moreover, TBI increased the lipid peroxidation in the heart, which was significantly reduced by the treatment with MPSS (p < 0.0001). These findings provide evidence for the efficacy of MPSS in protection of cardiac myocytes to achieve optimal heart donation after TBI in heart transplantation.
authors.affiliation: Department of Cardiovascular Surgery, TYIH, Ankara, Turkey.
authors.forename: Mustafa
authors.initials: M
authors.lastname: Emir
authors.forename: Kanat
authors.initials: K
authors.lastname: Ozisik
authors.forename: Kerim
authors.initials: K
authors.lastname: Cagli
authors.forename: Pinar
authors.initials: P
authors.lastname: Ozisik
authors.forename: Serdar
authors.initials: S
authors.lastname: Tuncer
authors.forename: Vedat
authors.initials: V
authors.lastname: Bakuy
authors.forename: Erkan
authors.initials: E
authors.lastname: Yildirim
authors.forename: Kamer
authors.initials: K
authors.lastname: Kilinc
authors.forename: Kamil
authors.initials: K
authors.lastname: Gol
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001930:Brain Injuries / Q000503:physiopathology*; D004195:Disease Models, Animal; D005260:Female; D015227:Lipid Peroxidation / Q000187:drug effects; D008776:Methylprednisolone Hemisuccinate / Q000627:therapeutic use*; D032383:Myocytes, Cardiac / Q000187:drug effects*; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis / Q000378:metabolism
chemical_list: D018696:Neuroprotective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D012333:RNA, Messenger; D017392:Thiobarbituric Acid Reactive Substances; D008776:Methylprednisolone Hemisuccinate