Affiliation:
1. Omsk State Medical University
Abstract
Aim. To evaluate the activity of autophagy and apoptosis in the myocardium of rats with differentstress resistance after the modeling of myocardial contusion.Materials and Methods. The study was performed on 106 white male rats weighing 250-300 g. The rats were ranked according to stress tolerance, and medium-resistant individuals (n = 42) were excluded from the experiment. Control (n = 16) and experimental (n = 48) groups were formed from the remaining animals; the control group included subgroups with high and low stress resistance, and the experimental group included 6 subgroups (rats with high and low stress resistance; 6, 12, and 24-hour time points). Each of the subgroups included 8 animals. Myocardial contusion was modeled in the experimental group. At 6-, 12- and 24-hour time point, rat hearts have been excised and 5×5 mm myocardial fragments were dissected from the areas with the most prominent traumatic effects (interventricular septum, anterior walls of the left and right ventricles). Tissues were then sectioned and stained with antibodies to Beclin-1 and caspase-3.Results. We have documented a significant expression of Beclin-1 and Caspase 3 expression in rat hearts after myocardial contusion. From 6 to 24 hours upon the myocardial contusion, Beclin-1 expression has been increased in rats with high stress resistance but was reduced in rats with low stress resistance. Expression of caspase-3 expression was registered exclusively at 24-hour time point in rats with high stress resistant but increased along the time points in rats with low stress resistance.Conclusion. Expression of Beclin-1 and caspase-3 in rat myocardium indicated autophagy and apoptosis upon the myocardial contusion. Temporal patterns of Beclin-1 and caspase-3 expression were opposite in rats with high and low stress resistance.
Publisher
Kemerovo State Medical University
Reference29 articles.
1. Weber B, Lackner I, Gebhard F, Miclau T, Kalbitz M. Trauma, a Matter of the Heart-Molecular Mechanism of Post-Traumatic Cardiac Dysfunction. Int J Mol Sci. 2021;22(2):737. https://doi.org/10.3390/ijms22020737
2. Klyuchnikova EI, Korpacheva OV, Mozgovoy SI, Zolotov AN, Kononov AV. Influence of Stress Resistance on Myocardial Expression of the ProAutophagic Protein Beclin-1 After Cardiac Contusion in Experimental Setting. General Reanimatology. 2023;19(6):54-61. (In Russ.). https://doi.org/10.15360/1813-9779-2023-6-54-61
3. Tao L, Liu HR, Gao F, Qu Y, Christopher TA, Lopez BL, Ma XL. Mechanical traumatic injury without circulatory shock causes cardiomyocyte apoptosis: role of reactive nitrogen and reactive oxygen species. Am J Physiol Heart Circ Physiol. 2005;288(6):2811-2818. https://doi.org/10.1152/ajpheart.01252.2004
4. Yan Z, He JL, Guo L, Zhang HJ, Zhang SL, Zhang J, Wen YJ, Cao CZ, Wang J, Wang J, Zhang MS, Liang F. Activation of caspase-12 at early stage contributes to cardiomyocyte apoptosis in trauma-induced secondary cardiac injury. Sheng Li Xue Bao. 2017;69(4):367-377.
5. Kalbitz M, Amann EM, Bosch B, Palmer A, Schultze A, Pressmar J, Weber B, Wepler M, Gebhard F, Schrezenmeier H, Brenner R, Huber-Lang M. Experimental blunt chest trauma-induced myocardial inflammation and alteration of gap-junction protein connexin 43. PLoS One. 2017;12(11). https://doi.org/10.1371/journal.pone.0187270