The Modulation of Blue-Light-Induced Inflammation, Intracellular Lipid Secretion, and Oxidative Stress in Sebocytes with Cannabidiol.
Yanran WeiTan TangJitao LiuSiyi YuHuo TongPeipei ZhangPublished in: Photochemistry and photobiology (2022)
Light-induced skin damage leads to cellular or molecular dysfunction, thus potentially causing different skin issues (e.g., skin aging, seborrheic dermatitis and pigmentation). Blue light, a potent visible light that was previously adopted for promoting skin regeneration, draws considerable concerns in the past several years due to their potential damage to the skins. In this work, we investigated the roles of blue light in skewing the functions of sebocytes - the major cells that compose the sebaceous gland - an important "active" neuro-immuno-endocrine organ in maintaining skin functions. For therapeutically purposes, we employed cannabidiol (CBD), a clinically used non-psychotropic phytocannabinoid, to revert blue-light-induced sebocytes dysfunctions, including intracellular lipid secretion, inflammation, reactive oxygen species (ROS) secretion, and cell cycles. At the cellular level, CBD reduced the blue-light-enhanced intracellular lipid secretion, decreased inflammation, down-regulated intracellular ROS production, and restored the skewed cell cycles in the sebocytes. In the intracellular mechanism, CBD inhibited the blue-light-induced pro-apoptotic activity through rebalance BCL-2/BAX expression and down-regulated the NF-κB p65 pathway. Collectively, this study demonstrated that CBD was a potent therapeutic agent for maintaining normal sebocytes functions, thus is a promising drug for skincare purposes, especially considering its effectiveness in restoring the twisted sebocytes behaviors.
Keyphrases
- oxidative stress
- reactive oxygen species
- induced apoptosis
- dna damage
- soft tissue
- wound healing
- cell death
- light emitting
- diabetic rats
- single cell
- ischemia reperfusion injury
- anti inflammatory
- stem cells
- fatty acid
- randomized controlled trial
- cell therapy
- systematic review
- cell cycle arrest
- atopic dermatitis
- pi k akt
- long non coding rna
- binding protein
- lps induced
- high speed
- adverse drug