<p>Resveratrol attenuates hydrogen peroxide-induced aging through upregulation of autophagy in human umbilical vein endothelial cells</p>

Abstract

Purpose Resveratrol (RESV; trans-3,5,4′-trihydroxystilbene) has emerged as a potential new therapeutic for age-related atherosclerotic diseases. However, the effect of RESV on cellular aging and its underlying mechanisms remain unknown. Therefore, the aim of this study was to examine whether RESV can delay cellular aging through upregulation of autophagy. Materials and methods Human umbilical endothelial vein cells (HUVECs) were divided into four groups: the control group, and the hydrogen peroxide (H 2 O 2 ) alone, H 2 O 2 + RESV pretreatment, and H 2 O 2 + 3-methyladenine (3-MA) + RESV pretreatment intervention groups. The cell viability was evaluated by a cell counting kit-8 assay. Superoxide dismutase (SOD) activity and intracellular reactive oxygen species (ROS) levels were tested using commercial kits. Senescence-related β-galactosidase activities were detected by immunohistochemical staining. The expression levels of aging-related and autophagy-related markers, including phosphorylated Rb (p-Rb), LC3, and p62, with or without RESV were measured by Western blotting. Results Pretreatment with 10 µM RESV increased the cell viability and SOD levels. The remarkably higher positive rate of senescence-associated β-galactosidase and increased intracellular ROS levels in the H 2 O 2 treatment group were reversed by treatment with 10 µM RESV. As compared to the H 2 O 2 treatment group, 10 µM RESV could upregulate autophagy through the regulation of p-Rb, LC3, and p62 levels. The anti-aging effect of RESV via an autophagy regulation mechanism was further confirmed by the suppression of these effects with 3-MA treatment. Conclusion RESV may reverse and delay the aging process of HUVECs via upregulation of autophagy and could be a candidate therapeutic for age-related atherosclerotic diseases.

Resveratrol attenuates cigarette smoke induced endothelial apoptosis by activating Notch1 signaling mediated autophagy

“…Emerging evidence indicates that RESV attenuates endothelial oxidative injury in HUVECs by inducing autophagy [11,23]. Here, in the present study we found that blocking autophagy with 3-MA aggravated the apoptosis by upregulating caspase3 expression, while inducing autophagy with rapamycin relieved the apoptosis, indicating that autophagy confers the ability to protect endothelial cells from CSE-induced apoptosis.…”

Piwi-interacting RNAs play a role in vitamin C-mediated effects on endothelial aging

“…Herein, we investigated the effect of VC on H2O2-induced senescence in endothelial cells and whether piRNA is involved in VC-mediated antiaging effects. (15)(16)(17). After 2 h, some of these cells were then cultured in medium containing VC (200 μM; Sigma-Aldrich, St. Louis, MO, USA) to investigate the effect of VC on aging endothelial cells (VC group).…”

Resveratrol attenuates cigarette smoke induced endothelial apoptosis by activating Notch1 signaling mediated autophagy

“…Autophagy is an essential intracellular process responsible for the selective degradation of pathogens, damaged organelles and proteins that cannot be degraded by the proteasome, to support protein and organellar homeostasis, as well as recycling of biomolecular resources, to maintain energy homeostasis and cell survival [23]. Emerging evidence indicates that RESV attenuates endothelial oxidative injury in HUVECs by inducing autophagy [13,24]. Here, in the present study we found that blocking autophagy with 3-MA aggravated the apoptosis by upregulating caspase3 expression, while inducing autophagy with rapamycin relieved the apoptosis, indicating that autophagy confers the ability to protect endothelial cells from CSE-induced apoptosis.…”

“…Autophagy is a fundamental intracellular process, which can degrade microorganisms (viruses, bacteria, fungi and protists/protozoa) and damaged organelles and proteins that cannot be degraded by the proteasome, providing raw materials for cell reconstruction, regeneration, and repair, thereby ensuring the metabolic balance of cells. Furthermore, RESV has been found to exert a protective effect via regulating autophagy [13]. However, no study has focused on the role of RESV-induced autophagy in CSrelated endothelial apoptosis.…”