Lycopene protects against apoptosis in hypoxia/reoxygenation-induced 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 autophagy‑dependent 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 'microtubule‑associated protein 1‑light chain 3β (MAP1LC3B)' and 'Beclin 1'. After 16 h hypoxia, followed by 2 h reoxygenation, the expression levels of the microtubule‑associated protein 1A/1B‑light 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/B‑cell lymphoma 2 (Bcl‑2) and active caspase‑3 apoptotic biomarkers were increased. Pre‑incubation of the cells with different Ly concentrations reversed the HR‑induced inhibition of autophagy and cell viability, and the HR‑induced elevation in apoptotic levels. The induction of autophagy was accompanied by reduced apoptosis, and decreased expression levels of Bax/Bcl‑2 and active caspase‑3. In addition, the impairment of autophagy by silencing the expression of MAP1LC3B and Beclin 1 accelerated HR‑induced H9C2 cell apoptosis and the Ly‑mediated protective effects disappeared. Furthermore, Bax/Bcl‑2 and active caspase‑3 expression levels were increased. Moreover, Ly‑induced autophagy was associated with increased adenosine monophosphate kinase (AMPK) phosphorylation. Suppressed AMPK phosphorylation using compound C terminates Ly‑mediated cytoprotective effects. Ly treatment improves cell viability and reduces apoptosis as a result of the activation of the adaptive autophagic response on HR‑induced H9C2 myocardioblasts. AMPK phosphorylation may be involved in the progression.

Antagonistic effects of lycopene on cadmium-induced hippocampal dysfunctions in autophagy, calcium homeostatis and redox

“…In addition, previous studies showed that Ca 2+ concentration, autophagy, and redox regulation are linked to neurotoxicity as stated elsewhere. LYC treatment improves cell viability and reduces apoptosis as a result of the activation of the adaptive autophagic response on HR induced H9C2 myocardioblasts [ 64 ]. In the future study, we will focus on unveiling the inherent associations of Cd-induced Ca 2+ homeostatic change, redox stress and autophagy activation to Cd-triggered hippocampal neurotoxicity; also, we will further optimize the LYC dietary treatment in order to initiate the clinical based study.…”

Recent trends in the development of nanophytobioactive compounds and delivery systems for their possible role in reducing oxidative stress in Parkinson’s disease models

“…54,56,57,[202][203][204] Lycopene has a protective effect against neurological disorders including Alzheimer's and PD by reducing oxidative stress. [205][206][207][208][209][210][211] Lycopene supplementation of a rotenone-induced rat model of PD enhances the protective effect against oxidative stress and reduces neurobehavioral abnormalities.…”

Neuroprotective effects of lycopene pretreatment on transient global cerebral ischemia-reperfusion in rats: The role of the Nrf2/HO-1 signaling pathway

“…Lycopene, a member of the carotenoid family, is found predominantly in tomatoes and other red colored fruits (8). It has been reported that lycopene protects against apoptosis in hypoxia/reoxygenation-induced H9C2 myocardioblast cells (34). In addition, He et al (35) reported that lycopene attenuates inflammation and apoptosis in postmyocardial infarction remodeling.…”