Lycopene protects against apoptosis in hypoxia/reoxygenationinduced H9C2 myocardioblast cells through increased autophagy

Abstract

Lycopene (Ly), the most common type of antioxidant in the majority of diet types, provides tolerance to ischemia/reperfusion injury. However, the underlying mechanism of the protective effects observed following Ly administration remains poorly investigated. The aim of the current study was to investigate whether Ly prevents damage to hypoxia/reoxygenation (HR)induced H9C2 myocardioblasts in an autophagydependent manner. The levels of autophagic markers were detected using western blotting, the level of apoptosis was detected using western blotting and flow cytometry. The activation of autophagy was impaired via knockdown of the expression of 'microtubuleassociated protein 1light chain 3β (MAP1LC3B)' and 'Beclin 1'. After 16 h hypoxia, followed by 2 h reoxygenation, the expression levels of the microtubuleassociated protein 1A/1Blight chain 3 (LC3) and βeclin 1 autophagic biomarkers, and cell viability were reduced, whereas the percentage of apoptotic cells, and the expression levels of the Bax/Bcell lymphoma 2 (Bcl2) and active caspase3 apoptotic biomarkers were increased. Preincubation of the cells with different Ly concentrations reversed the HRinduced inhibition of autophagy and cell viability, and the HRinduced elevation in apoptotic levels. The induction of autophagy was accompanied by reduced apoptosis, and decreased expression levels of Bax/Bcl2 and active caspase3. In addition, the impairment of autophagy by silencing the expression of MAP1LC3B and Beclin 1 accelerated HRinduced H9C2 cell apoptosis and the Lymediated protective effects disappeared. Furthermore, Bax/Bcl2 and active caspase3 expression levels were increased. Moreover, Lyinduced autophagy was associated with increased adenosine monophosphate kinase (AMPK) phosphorylation. Suppressed AMPK phosphorylation using compound C terminates Lymediated cytoprotective effects. Ly treatment improves cell viability and reduces apoptosis as a result of the activation of the adaptive autophagic response on HRinduced H9C2 myocardioblasts. AMPK phosphorylation may be involved in the progression.