ARE/Nrf2 Transcription System Involved in Carotenoid, Polyphenol, and Estradiol Protection from Rotenone‐Induced Mitochondrial Oxidative Stress in Dermal Fibroblasts

Published: July 18, 2024

Cell aging is associated with the increased production of mitochondrial reactive oxygen species (mtROS) due to dysfunction, and various phytonutrients estrogens have been shown improve skin health. Thus, aim current study was examine damage dermal fibroblasts by chemically-induced dysfunction mechanism protective effects carotenoids, polyphenols, estradiol. Rotenone, a Complex I inhibitor, caused in human fibroblasts, substantially reducing respiration ATP levels, followed cytosolic ROS, which resulted apoptotic cell death, matrix metalloproteinase-1 (MMP1) secretion, decreased collagen secretion. Pre-treatment carotenoid-rich tomato extracts, rosemary extract, estradiol reversed these effects. These can be partially explained cooperative activation antioxidant response element (ARE/Nrf2) transcriptional activity compounds rotenone, led upregulation proteins such as NQO1. To determine if ARE/Nrf2 crucial for protection, we inhibited it using Nrf2 inhibitors ML385 ochratoxin A. This inhibition markedly reduced test diminishing their effect reduce ROS. Our results indicate that protect cells from mitochondria-generated ROS and, thus, may delay

Language: Английский

ARE/Nrf2 Transcription System Involved in Carotenoid, Polyphenol, and Estradiol Protection from Rotenone-Induced Mitochondrial Oxidative Stress in Dermal Fibroblasts

Antioxidants, Journal Year: 2024, Volume and Issue: 13(8), P. 1019 - 1019

Published: Aug. 21, 2024

Skin aging is associated with the increased production of mitochondrial reactive oxygen species (mtROS) due to dysfunction, and various phytonutrients estrogens have been shown improve skin health. Thus, aim current study was examine damage dermal fibroblasts by chemically induced dysfunction mechanism protective effects carotenoids, polyphenols, estradiol. Rotenone, a Complex I inhibitor, caused in human fibroblasts, substantially reducing respiration ATP levels, followed cytosolic ROS, which resulted apoptotic cell death, an number senescent cells, matrix metalloproteinase-1 (MMP1) secretion, decreased collagen secretion. Pre-treatment carotenoid-rich tomato extracts, rosemary extract, estradiol reversed these effects. These can be partially explained cooperative activation antioxidant response element (ARE/Nrf2) transcriptional activity compounds rotenone, led upregulation proteins such as NQO1. To determine if ARE/Nrf2 crucial for protection, we inhibited it using Nrf2 inhibitors ML385 ochratoxin A. This inhibition markedly reduced test diminishing their effect reduce ROS. Our results indicate that protect cells from mtROS, thus may delay senescence

Language: Английский

Topical nanoencapsulated cannabidiol cream as an innovative strategy combating UV-A–induced nuclear and mitochondrial DNA injury: A pilot randomized clinical study

Journal of the American Academy of Dermatology, Journal Year: 2024, Volume and Issue: 91(5), P. 855 - 862

Published: July 25, 2024

BackgroundUV-A radiation contributes to photoaging/photocarcinogenesis by generating inflammation and oxidative damage. Current photoprotective strategies are limited the availability/utilization of UV-A filters, highlighting an unmet need. Cannabidiol (CBD), having anti-inflammatory/antioxidant properties via regulation nuclear erythroid 2–related factor, heme oxygenase 1, peroxisome proliferator-activated receptor gamma, could potentially mitigate damage from exposure.Objective/MethodsThis is a prospective, single-center, pilot clinical trial (NCT05279495). Nineteen participants applied nano-CBD (nCBD) or vehicle (VC) cream randomized, blinded buttock sites twice daily for 14 days; then, treated were irradiated with ≤3× minimal erythema dose. After 24 hours, punch biopsies obtained histology, immunohistochemistry, real-time polymerase chain reaction.ResultsAt 21% had less observed on CBD-treated skin than VC skin. Histologically, nCBD-treated reduced UV-A–induced epidermal hyperplasia (P = .01). Immunohistochemistry detected cytoplasmic/nuclear 8-oxoguanine glycosylase 1 staining in compared < Quantitative mtDNA reaction demonstrated that deletion ND4 (proxy:4977 bp deletion; P .003) ND1 (proxy:3895 .002) was significantly vivo nCBD treatment VC.LimitationsSmall sample size this study's limitation.ConclusionTopically formation frequent mutagenic DNA base lesion protected against mutations associated aging. To our knowledge, first identify UV-protective capacity CBD-containing topicals humans. exposure. This reaction. At VC. Small limitation. Topically

Language: Английский