Journal of Exercise & Organ Cross Talk

Abstract NAFLD is one of the chronic liver diseases closely related to metabolic disorders. Borage and physical activity improves oxidative indices. Also, Beclin-1 is a key gene in the autophagy process, and Parkin acts as a protective mechanism against liver damage. So, this study aims to investigate the effect of aerobic training and borage extract on the expression of Beclin-1 and Parkin genes in the liver cells in NAFLD. In this experimental study,40male Wistar rats weighing were divided into 4groups. (control, supplement, training), and training+supplement. The data were analyzed using SPSS 25 software. Training and borage extract had no significant effect on Beclin-1 expression (P=0.267), with fold changes of 1.05±0.07 for training, 1.07±0.06 for borage extract, and 1.12±0.08 for training+borage extract, compared to the control. However, Parkin expression increased significantly (P=0.006), with fold changes of 1.15±0.08 for Training, 1.18±0.09 for borage extract, and 1.20±0.10 for training+borage extract. Post hoc confirmed a significant increase in Parkin expression in the training+borage extract group compared to the control (P=0.035). This study showed that it is possible that the consumption of borage extract and aerobic training together and alone have an increasing the expression of Parkin. So, both borage extract and aerobic training have individual benefits for improving liver health by targeting Beclin-1 and PARKIN pathways, and their combination could provide a more robust approach to managing NAFLD by promoting effective autophagy, mitophagy, and mitochondrial function. This dual intervention could reduce liver damage, inflammation, and fibrosis, ultimately improving metabolic outcomes in individuals suffering from NAFLD.

Abstract Most of the intracellular and extracellular factors that play a vital role in regulating energy metabolism and determining cell fate converge in the mitochondria. To promote or hinder cell survival through regulating the function and maintaining the mitochondrial structure. The decline of mitochondrial function and homeostasis with aging is the basis of the pathogenesis of aging-related diseases, especially in skeletal muscles. One of the important components of mitochondrial quality control that helps maintain the homeostasis of myocytes is autophagy, which is an important biological and evolutionary process, and its vital function is the removal of defective organelles. Although it has been proven that regular sports activities act as autophagy stimulators and play a role in maintaining the cellular homeostasis of skeletal muscle fibers and regulating intracellular metabolism. However, cellular autophagic responses to exercise in skeletal muscle appear to be different in different exercise protocols and disease models. How exercise activity modulates autophagy in skeletal muscle and how the effect of exercise is regulated by the autophagy signaling pathway are still poorly understood. The importance of understanding the obscure angles of this process can be an important goal in preventing the pathology of age-related diseases in skeletal muscle.