Myocardial Expression of the Proautophagic Marker Beclin-1 after Experimental Cardiac Contusion: Dependence on Stress Resistance

Introduction. Individual resistance to everyday and life-threatening stressors may influence the severity of post-traumatic cellular responses, but its role in myocardial autophagy after blunt cardiac injury remains poorly understood. Beclin‑1 is a key proautophagic protein, and its expression level reflects the activation of autophagy.

Objective. To compare the expression of Beclin‑1 in the myocardium of high-resistance and low-resistance male rats at 24 and 72 hours after experimental cardiac contusion.

Methods. The study was performed on 110 outbred male rats. Based on Open Field and Porsolt forced swim tests, animals were divided into high-resistance and low-resistance subgroups. Cardiac contusion was modeled under anesthesia. Myocardial samples were taken from the interventricular septum and ventricular walls. Beclin‑1 expression was assessed by immunohistochemistry and quantified using a semi-automatic image analysis method (ImageJ/Fiji) with calculation of an expression index. Statistical analysis included the Mann–Whitney U test, Kruskal–Wallis test, and Bonferroni correction.

Results. In high-resistance animals, the median expression index increased from 0.5 in controls to 2.0 at 24 hours after contusion (p<0.0001) and remained elevated at 1.5 at 72 hours (p=0.0027). In low-resistance rats, the index rose to 1.5 at 24 hours (p=0.0115) but returned to the control level (0.5) by 72 hours (p=0.0358, non‑significant after correction). Between‑group comparison showed significantly higher Beclin‑1 expression in high-resistance rats at 24 hours (2.0 vs. 1.5, p<0.0001) and at 72 hours (1.5 vs. 0.5, p=0.0096). Qualitatively, high-resistance animals displayed diffuse moderate‑to‑strong cytoplasmic staining, whereas low-resistance rats showed only isolated foci of weak‑to‑moderate staining.

Conclusion. Cardiac contusion induces Beclin‑1 expression in both groups, but high resistance to everyday and life‑threatening stressors is associated with a more pronounced and sustained autophagic response. Low stress resistance leads to a weaker and transient increase in the proautophagic marker, suggesting impaired autophagic activation after mechanical heart injury.