The study results revealed the neuroprotective effects of ischemic preconditioning, supported with the upregulated pro-survival miRNAs in MCA infarcts.
BackgroundRemote ischemic preconditioning (IPreC) could provide tissue-protective
effect at a remote site by anti-inflammatory, neuronal, and humoral
signaling pathways.ObjectivesThe aim of the study was to investigate the possible protective effects of
remote IPreC on myocardium after transient middle cerebral artery occlusion
(MCAo) in streptozotocin- induced diabetic (STZ) and non-diabetic rats.Methods48 male Spraque Dawley rats were divided into eight groups: Sham, STZ, IPreC,
MCAo, IPreC+MCAo, STZ+IPreC, STZ+MCAo and STZ+IPreC+MCAo groups. We induced
transient MCAo seven days after STZ-induced diabetes, and performed IPreC 72
hours before transient MCAo. Remote myocardial injury was investigated
histopathologically. Bax, Bcl2 and caspase-3 protein levels were measured by
Western blot analysis. Total antioxidant status (TAS), total oxidant status
(TOS) of myocardial tissue were measured by colorimetric assay. Oxidative
stress index(OSI) was calculated as TOS-to-TAS ratio. For all statistical
analysis, p values < 0.05 were considered significant.ResultsWe observed serious damage including necrosis, congestion and mononuclear
cell infiltration in myocardial tissue of the diabetic and ischemic groups.
In these groups TOS and OSI levels were significantly higher; TAS levels
were lower than those of IPreC related groups (p < 0.05). IPreC had
markedly improved histopathological alterations and increased TAS levels in
IPreC+MCAo and STZ+IPreC+MCAo compared to MCAo and STZ+MCAo groups (p <
0.05). In non-diabetic rats, MCAo activated apoptotic cell death via
increasing Bax/Bcl2 ratio and caspase-3 levels. IPreC reduced apoptotic cell
death by suppressing pro-apoptotic proteins. Diabetes markedly increased
apoptotic protein levels and the effect did not reversed by IPreC.ConclusionsWe could suggest that IPreC attenuates myocardial injury via ameliorating
histological findings, activating antioxidant mechanisms, and inducing
antiapoptotic activity in diabetic rats.
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