Abstract
Autophagy is an evolutionarily conserved process that degrades damaged organelles and recycles macromolecules to support cell survival. However, in certain disease states, dysregulated autophagy can play an important role in cell death. In pancreatitis, the accumulation of autophagic vacuoles and damaged mitochondria and premature activation of trypsinogen are shown in pancreatic acinar cells (PACs), which are the hallmarks of impaired autophagy. Oxidative stress mediates inflammatory signaling and cytokine expression in PACs, and it also causes mitochondrial dysfunction and dysregulated autophagy. Thus, oxidative stress may be a mediator for autophagic impairment in pancreatitis. Lycopene is a natural pigment that contributes to the red color of fruits and vegetables. Due to its antioxidant activity, it inhibited oxidative stress-induced expression of cytokines in experimental models of acute pancreatitis. Lycopene reduces cell death through the activation of 5′-AMP-activated protein kinase-dependent autophagy in certain cells. Therefore, lycopene may ameliorate pancreatitis by preventing oxidative stress-induced impairment of autophagy and/or by directly activating autophagy in PACs.
Highlights
Pancreatitis is a gastrointestinal disorder with considerable morbidity and mortality [1]
Because autophagic dysfunction is commonly observed in neurodegenerative diseases, the autophagy pathway is viewed as a promising therapeutic target
It has been suggested that lycopene may protect advanced glycation end products (AGEs)-induced oxidative autophagy in endothelial progenitor cells from patients with diabetes mellitus (DM) and offers a new therapy for DM vascular complications
Summary
Pancreatitis is a gastrointestinal disorder with considerable morbidity and mortality [1]. The major form of autophagy is macroautophagy It involves the sequestration of cytosolic components, such as long-lived proteins, lipids, and organelles, by double-membrane vacuoles known as autophagosomes [6,7,8]. Autophagy is impaired in pancreatitis, with a lower degradation rate of long-lived proteins, premature activation of trypsinogen, and accumulation of autophagic vacuoles in PACs. reducing oxidative stress may protect PACs against autophagic impairment. Lycopene has the potential to prevent autophagy impairment, which is shown in pancreatitis by reducing ROS-mediated Ca overload, mitochondrial dysfunction, premature activation of trypsinogen, and by preventing cell death of PACs. Here, the role of autophagy in pancreatitis and the possible mechanisms by which lycopene prevents pancreatitis via the regulation of oxidative stress-associated autophagy impairment are discussed
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