Anti-Aging Effect and Mechanism of Proanthocyanidins Extracted from Sea buckthorn on Hydrogen Peroxide-Induced Aging Human Skin Fibroblasts

Abstract

Oxidative stress is the leading cause of skin aging damage. Excessive accumulation of reactive oxygen species (ROS) in cells induced by hydrogen peroxide (H2O2) triggers a decrease in collagen synthesis and an increase in collagen degradation, which are biomarkers of skin aging. We evaluated the potential protective mechanism of Sea buckthorn proanthocyanidins (SBP) against the oxidative stress-induced skin aging process from multiple aspects. We treated human skin fibroblasts (HSFs) with 300 µmoL/L of H2O2 for 24 h, followed by 25, 50, and 100 µg/mL of SBP for 24 h. The results showed that SBP could enhance the activities of superoxide dismutase (SOD) and glutathione (GSH), effectively remove excess ROS, and significantly improve the changes in cell morphology and viability caused by excessive ROS in skin cells. In addition, SBP could promote the synthesis of Col I in aging HSFs through the TGF-β1/Smads pathway and inhibit the degradation of Col I by regulating the MMPs/TIMPs system, thereby maintaining the stability of the ECM structure to achieve anti-aging purposes. Finally, we studied the migration ability of SBP, and the results showed that 100 µg/mL of SBP was most conducive to the cell migration of senescent cells, laying a foundation for follow-up animal experiments. These results will increase the application value of SBP in the cosmetic and antioxidative functional food industries.

Anti‐skin aging effect of sea buckthorn proanthocyanidins in D‐galactose‐induced aging mice

“…More and more studies have focused on the external supplementation of purely natural antioxidants to effectively resist oxidative stress damage and achieve the purpose of delaying aging. From the previous study by our group, we can find that SBP, an oligomeric proanthocyanidin with good free radical scavenging ability, acts as an all‐natural antioxidant and exerts anti‐aging effects by increasing the relative content of Col I in H 2 O 2 ‐induced senescence human skin fibroblasts (Liu et al., 2022 ; Zhu et al., 2021 ). In this study, we used these findings as the basis to start from the most basic aspects of delaying skin aging, such as the total antioxidant capacity of the skin, the thickness of the skin, the water content of the skin dermis, the content of HA, collagen, and elastin, and the structure of collagen fibers and elastic fibers.…”

“…P0013B). Following the method described by Liu et al., 2022 , the BCA protein assay kit (Beyotime, Shanghai, China, cat. no.…”

“…In our previous studies, we completed the isolation and identification of Sea buckthorn proanthocyanidins (SBP) and found that it is a source of low‐molecular‐weight proanthocyanidins with good free radical scavenging ability (Zhu et al., 2021 ). In order to investigate the possible application of SBP in skin aging, we pre‐investigated and found through cellular experiments that SBP could exert the anti‐cellular senescence effect by increasing the relative content of type I collagen (Col I) in H 2 O 2 ‐induced senescent cells of human dermal fibroblasts (Liu et al., 2022 ). To further examine its feasibility in preventing skin aging and further increase the market application value of SBP, we established a senescence model by subcutaneously injecting D‐galactose into mice and then gavage with different doses of SBP to explore the effects of SBP on the skin tissues of senescent mice and to elucidate the related mechanism of action.…”

Preventive Effect of Nuciferine on H2O2-Induced Fibroblast Senescence and Pro-Inflammatory Cytokine Gene Expression

“…The early onset of cellular senescence induced by oxidative stress is termed stress-induced premature senescence [ 5 ]. Senescent fibroblast cells have a specifically enlarged cytoplasm, poor response to growth factors, and β-galactosidase activity [ 4 , 23 , 24 ]. The H 2 O 2 , when being exposed to cultured fibroblasts, induces premature senescence by imposing oxidative stress and sustained accumulation of oxidative DNA damage [ 10 , 11 ].…”

Extracellular vesicles derived from mesenchymal stem cells: the wine in Hebe's hands to treat skin aging

“…However, when present in high concentrations, ROS trigger oxidative stress damage, culminating in cell necrosis and apoptosis [ 126 ]. The cellular ROS level is intricately tied to the regulation of collagen metabolism; elevated ROS levels activate MMP-1, MMP-3, and MMP-9, initiating collagen degradation and, consequently, affecting the assembly and turnover of the ECM [ 127 ]. Under normal physiological conditions, the antioxidant defense system, composed of glutathione peroxidase (GPx), superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), is activated to control ROS accumulation, thereby averting excessive ROS production, which could otherwise lead to extensive lipid peroxidation damaging cell membranes and causing cell death.…”