Pleiotropic effects of simvastatin are associated with mitigation of apoptotic component of cell death upon lethal myocardial reperfusion-induced injury

Title:

Pleiotropic effects of simvastatin are associated with mitigation of apoptotic component of cell death upon lethal myocardial reperfusion-induced injury

Creator:

Rajtík, T., Slávka Čarnická, Szobi, A., Mesárošová, L., Máťuš, M., Pavel Švec, Ravingerová, T., and Adriana Adameová

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:215e1b29-ca54-461a-8170-0230f6f0f8f3
uuid:215e1b29-ca54-461a-8170-0230f6f0f8f3

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, cell death, apoptosis, myocardial ischemia-reperfusion injury, statins, STAT3, 14, and 612

Type:

article, články, model:article, and TEXT

Description:

Although statins exert non-lipid cardioprotective effects, their influence on cell death is not fully elucidated. For this purpose, we investigated whether simvastatin treatment (S, 10 mg/kg, 5 days) is capable of mitigating ischemia/reperfusion-induced (IR) apoptosis in the isolated rat hearts, which was examined using immunoblotting analysis. In addition, the content of signal transducer and activator of transcription 3 (STAT3) and its active form, phosphorylated STAT3 (pSTAT3-Thr705), was analyzed. Simvastatin induced neither variations in the plasma lipid levels nor alterations in the baseline content of analysed proteins with the exception of upregulation of cytochrome C. Furthermore, simvastatin significantly increased the baseline levels of pSTAT3 in contrast to the control group. In the IR hearts, simvastatin reduced the expression of Bax and non-cleaved caspase-3. In these hearts, phosphorylation of STAT3 did not differ in comparison to the non-treated IR group, however total STAT3 content was slightly increased. The improved recovery of left ventricular developed pressure co-existed with the increased Bcl- 2/Bax ratio. In conclusion, pleiotropic action of statins may ameliorate viability of cardiomyocytes by favouring the expression of anti-apoptotic Bcl-2 and downregulating the proapoptotic markers; however STAT3 does not seem to be a dominant regulator of this anti-apoptotic action of simvastatin., T. Rajtík, ... [et al.]., and Obsahuje seznam literatury

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2012 Volume:61 | Number:Suppl 2

Harvested from:

CDK

Metadata only:

false