| Autor: |
Parfenova EV; National Medical Research Center of Cardiology, Moscow, Russia., Zubkova ES; National Medical Research Center of Cardiology, Moscow, Russia., Boldyreva MA; National Medical Research Center of Cardiology, Moscow, Russia., Tsokolaeva ZI; National Medical Research Center of Cardiology, Moscow, Russia., Olefir YV; Scientific Centre for Expert Evaluation of Medicinal Products, Moscow, Russia., Romanov BK; Scientific Centre for Expert Evaluation of Medicinal Products, Moscow, Russia., Prokofiev AB; Scientific Centre for Expert Evaluation of Medicinal Products, Moscow, Russia; I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia., Kukes VG; Scientific Centre for Expert Evaluation of Medicinal Products, Moscow, Russia; I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia., Goroshko OA; Scientific Centre for Expert Evaluation of Medicinal Products, Moscow, Russia., Aleksandrova TV; Scientific Centre for Expert Evaluation of Medicinal Products, Moscow, Russia., Gazdanova AA; I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia., Parfenova OK; I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia., Sidorov NG; I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia., Andreev AD; I.M. Sechenov First Moscow State Medical University (Sechenov University), Moscow, Russia. |
| Abstrakt: |
In heart attack, FSTL-1 is actively secreted by cardiomyocytes, accelerates growth of heart myofibrils and stimulates of vascular endothelial growth factor expression. The aim of this work was to investigate the effect of Etoxidol on synthesis of FSTL-1 in rats after myocardial infarction. The experiments were performed on Wistar rats weighing 250-350 g with simulated myocardial infarction or intact (group 5). Animals of control groups (groups 1, 2) were treated with saline for 7 and 14 days; Ethoxidol (24 mg/kg) was injected to animals of experimental groups (group 3, 4) (the daily dose was 6.36 mg/animal) for 6 or 14 days. The injection volume was 0.2 ml. At the beginning and at the end of the study plasma concentrations of FSTL-1 were determined by the ELISA method. Myocardial FSTL-1 gene expression was determined by real-time PCR. At the end of the experiments, the hearts were also used for histochemical analysis. To determine the size of the scar formed after the modeled heart attack, we used the classic Mallory staining method. The results show that the development of experimental acute myocardial infarction is accompanied by a significant increase in FSTL-1 expression in the heart, which was detected on the 7th day and stored increased by 14 days after a heart attack. After therapy with Ethoxidol, a tendency to a decrease in the expression of FSTL-1 by the 14th day was observed; it coincided with the dynamics of the plasma protein FSTL-1 level. It can be assumed that the downregulation trend in the FSTL-1 expression is associated with a more effective repair process after a heart attack, since FSTL-1 increases precisely in response to myocardial damage and decreases when the incentives for its expression from damaged heart tissue are reduced. Indirectly, this assumption is confirmed by the detected tendency to reduce the size of post-infarction fibrosis in the treatment with Ethoxidol. The results indicate the ability of Ethoxidol to influence FSTL-1 synthesis of in rats after myocardial infarction. |
