Drug Design Development and Therapy
·
2026
·
IF 6.1
Liwei Feng,Linjie Tian,Jing Guo,Lingling Zhang,Peng Wang,Xiaolin Bu
Introduction Ultraviolet B (UVB) irradiation is a key exogenous factor contributing to skin photoaging. Idebenone (IDE), a structural analog of coenzyme Q10 (CoQ10), exhibits potent free radical scavenging capacity and is mainly employed in the treatment of neurodegenerative disorders, and in anti-aging products. However, the molecular mechanisms underlying its photoprotective effects in skin cells remain poorly understood.Purpose This study aims to investigate the protective effects of IDE against UVB-induced photoaging in human immortalized epidermal keratinocytes (HaCaT cells).Methods We applied IDE to a UVB-induced HaCaT cell photoaging model and found that it significantly ameliorated the photoaging damage caused by UVB irradiation.Results Specifically, cell morphology recovered from a shrinkage state toward normal, the positivity rate of senescence-associated β-galactosidase (SA-β-gal) decreased, and enhanced the impaired cell migration and proliferation capacities. Additionally, oxidative stress imbalance was alleviated, as evidenced by a significant reduction in reactive oxygen species (ROS) and malondialdehyde (MDA) levels, along with an increase in superoxide dismutase (SOD) activity. Impaired mitochondrial function was restored, reflected by the repolarization of mitochondrial membrane potential (MMP) and an increase in adenosine triphosphate (ATP) synthesis. Furthermore, the elevated secretion levels of pro-inflammatory factors such as tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-8 (IL-8) were significantly reduced. Transcriptomic analysis and protein validation revealed that IDE significantly downregulated the expression of IL-3RA and effectively restored the expression of TUBA8.Conclusion IDE significantly improved UVB-induced photoaging damage in HaCaT cells through multiple pathways, including restoring cell viability, alleviating oxidative stress damage, reducing pro-inflammatory factor infiltration, and protecting mitochondrial function. Its mechanism of action may involve the regulation of targets such as IL-3RA and TUBA8.
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高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2021
·
IF 9.776
Yuying Huang,Minchao Ma,Xiaolei Zhu,Mo Li,Mengran Guo,Peng Liu,Zhonggui He,Qiang Fu
Idebenone (IDB) has demonstrated the potential to treat mitochondrial and neurodegenerative diseases , including Alzheimer's disease (AD). However, its therapeutic effects are compromised by poor compliance due to low bioavailability. The objective of this study is to fabricate IDB nanorods (IDBNRs) to improve oral bioavailability and increase concentrations in the brain in order to enhance therapeutic effects of IDB in the treatment of AD. IDBNRs showed desired sizes and rod-shaped morphologies. The release rate and the antioxidant activity of IDBNRs were improved relative to other delivery routes. The plasma and brain concentrations were enhanced due to rapid release into the systemic circulation . In behavioral tests, mice treated orally with IDBNRs showed amelioration of AD-induced impairment of learning and memory. Thus, because of improved efficiency of drug delivery, doses can be reduced, and the compliance and therapeutic experience of patients can be improved. IDBNRs may provide effective and convenient treatments for AD patients in the future.
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高影响因子
Biomedicines
·
2023
·Vol. 11
·期 6
·1649
·
IF 4.7
Yuan Xie,Jingping Ye,Yaqi Ouyang,Jianing Gong,Chujie Li,Yang Deng,Yang Mai,Yang Liu,Wenbin Deng
Ultraviolet (UV) radiation can penetrate the basal layer of the skin and induce profound alterations in the underlying dermal tissues, including skin pigmentation, oxidative stress, photoaging, glycation, and skin cancer. Idebenone (IDB), an effective antioxidant that suppresses melanin biosynthesis and glycation, can protect the skin from UV-induced damage, accounting for its use in commercial anti-aging formulations. Ideally, IDB formulations should retain IDB inside the skin for a sufficient period, despite disturbances such as sweating or swimming. Herein, we present an IDB topical formulation based on Tris (tris(hydroxymethyl)-aminomethane)-modified bioadhesive nanoparticles (Tris-BNPs) and microneedle-assisted delivery. We found that Tris-BNPs loaded with IDB (IDB/Tris-BNPs) effectively reached the basal layer of the skin and were retained for at least 4 days with a slow and continuous drug release profile, unlike non-bioadhesive nanoparticles (NNPs) and bioadhesive nanoparticles (BNPs) of similar sizes (ranging from 120–142 nm) and zeta-potentials (above −20 mV), which experienced a significant reduction in concentration within 24 h. Notably, IDB/Tris-BNPs showed superior performance against UV-induced damage relative to IDB/NNPs and IDB/BNPs. This effect was demonstrated by lower levels of reactive oxygen species and advanced glycation end-products in skin tissues, as well as suppressed melanogenesis. Therefore, the proposed IDB delivery strategy provided long-term protective effects against UV-induced skin damage.Keywords:UV-induced skin damage;idebenone;bioadhesive nanoparticles;microneedle
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高影响因子
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