Rapamycin Attenuates H2O2-Induced Oxidative Stress-Related Senescence in Human Skin Fibroblasts.

Aug 2, 2024Tissue engineering and regenerative medicine

Rapamycin reduces hydrogen peroxide-related aging in human skin cells

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Abstract

Rapamycin (0.1 nmol/L for 48 h) significantly improved the proliferation and migration of HO-treated human skin fibroblasts.

Decreased senescent characteristics were observed in skin cells, as indicated by reduced SA-β-gal staining and lower levels of P53 and MMP-1 proteins.
An increase in COL1A-1 expression was noted, suggesting enhanced collagen production.
Rapamycin treatment enhanced the activity of antioxidant enzymes SOD and HO-1, leading to reduced levels of harmful substances like ROS and MDA.
Elevations in autophagy-related proteins and genes were significant after rapamycin pretreatment.
The protective effects of rapamycin are associated with its ability to reduce oxidative damage and activate the autophagy pathway.

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BACKGROUND: Oxidative stress plays an important role in the skin aging process. Rapamycin has been shown to have anti-aging effects, but its role in oxidative senescence of skin cells remains unclear. The aim of this study was to explore the effect of rapamycin on oxidative stress-induced skin cell senescence and to illustrate the mechanism.

METHODS: Primary human skin fibroblasts (HSFs) were extracted and a model of HO-induced oxidative senescence was constructed, and the effects of rapamycin on their value-added and migratory capacities were detected by CCK-8 and scratch assays. SA-β-gal was utilized to detect senescence, oxidatively closely related factors were also assessed. Gene and protein expressions of senescence, oxidative, and autophagy were detected by western blotting and quantitative-PCR. The data were analyzed by one-way analysis of variance. 2 2

RESULTS: Rapamycin (0.1 nmol/L for 48 h) promoted the proliferative and migration of HO-treated HSFs (p < 0.05), decreased senescent phenotypes SA-β-gal staining and the expression of P53, and MMP-1 proteins, and increased the expression level of COL1A-1 (p < 0.001). Rapamycin also enhanced the activities of SOD and HO-1, and effectively removed intracellular ROS, MDA levels (p < 0.05), in addition, autophagy-related proteins and genes were significantly elevated after rapamycin pretreatment (p < 0.001). Rapamycin upregulated the autophagy pathway to exert its protective effects. 2 2

CONCLUSION: Our findings indicate that rapamycin shields HSFs from HO-induced oxidative damage, the mechanism is related to the reduction of intracellular peroxidation and upregulation of autophagy pathway. Therefore, rapamycin has the potential to be useful in the investigation and prevention of signs of aging and oxidative stress. 2 2

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