Homeostasis maintenance is crucial to AbMole Simetryn ensure the function of body organs, and homeostatic dysregulation may cause multiple organ dysfunctions. There is compelling evidence that autophagy is important for the maintenance of homeostasis under basal conditions. Autophagy is an important cellular function that enables the recycling of long-lived proteins or damaged organelles. Autolysosomal degradation of membrane lipids and proteins generates free fatty acids and amino acids, which can be reused to maintain mitochondrial ATP production and protein synthesis and promote cell survival. Disruption of this pathway prevents cell survival in diverse organisms. Studies have shown that autophagy is involved in various physiological processes, such as neurodegenerative diseases, cancer, heart disease, aging, and infections. Although substantial evidence exists that autophagy plays a critical role in homeostasis maintenance and organ function, whether or not autophagy is changed and contributes to delayed cardiac injury after mechanical trauma remains largely unknown. To determine how autophagic activity is altered after nonlethal mechanical trauma, the heart was removed at different time points after trauma and the protein levels of Beclin 1 and LC3 were first determined. During the formation of autophagosomal membranes, LC3-I is recruited to the autophagosome where LC3II is generated by 
proteolysis and lipidation. Thus, the levels of LC3-II serve as a good indicator of autophagy, and the amount of LC3 II is correlated with the extent of autophagosome formation. Similar trends were revealed in the expression of the LC3 II protein, which was decreased shortly after trauma, then reached a minimal level at 6 h after trauma, and nearly recovered at 24 h after trauma compared to sham group rats. To determine whether the mRNA level changed, the mRNA expression of Beclin-1 and LC3 II were evaluated at different time points after trauma. Beclin 1 and LC3 II were decreased at the beginning of the completion of trauma and reached a minimal level at 6 h after trauma versus sham group rats. Rapamycin, a macrolide antibiotic, is a widely used inducer of autophagy. To confirm the ability of rapamycin to induce autophagy, rapamycin was intraperitoneally injected 30 min before trauma, and the expression of Beclin 1 and LC3 II were detected 6 h after trauma. Pretreatment with rapamycin significantly induced the mRNA expression of Beclin 1 and LC3 II in the injured myocardium, although administration of this compound had no homodynamic effect in sham animals. By immunofluorescence staining technology, the Beclin 1 and LC3 II punctate dots were significantly reduced 6 h after trauma, and treatment with rapamycin 30 min before trauma partially prevented trauma-induced alterations in Beclin 1 and LC3 immunoreactivity at 6 h after nonlethal mechanical trauma. It is well known that mitochondria play an especially important role in cardiomyocytes.