Photoprotective Effects of Cannabidiol against Ultraviolet-B-Induced DNA Damage and Autophagy in Human Keratinocyte Cells and Mouse Skin Tissue.
Yanmei LiDan HaoDanfeng WeiYue XiaoLiang LiuXiaoxue LiLian WangYu GanWei YanBowen KeJiang XianPublished in: Molecules (Basel, Switzerland) (2022)
Cannabidiol (CBD) has emerged as a phytocannabinoid with various beneficial effects for the skin, including anti-photoaging effects, but its mechanisms of action are not fully elucidated. The study assessed CBD's photoprotective effects against acute ultraviolet B (UVB)-induced damage in HaCaT human keratinocyte cells and murine skin tissue. CBD (8 μM) alleviated UVB-induced cytotoxicity, apoptosis, and G2/M cell cycle arrest in HaCaT cells. The contents of γH2AX and cyclobutane pyrimidine dimers were decreased after CBD treatment. CBD reduced the production of reactive oxygen species and modulated the expression of antioxidant-related proteins such as nuclear factor erythroid 2-related factor 2 in UVB-stimulated HaCaT cells. Furthermore, CBD mitigated the UVB-induced cytotoxicity by activating autophagy. In addition, a cream containing 5% CBD showed effectiveness against UVB-induced photodamage in a murine model. The CBD cream improved the skin's condition by lowering the photodamage scores, reducing abnormal skin proliferation, and decreasing expression of the inflammation-related protein cyclooxygenase-2 in UVB-irradiated skin tissue. These findings indicate that CBD might be beneficial in alleviating UVB-induced skin damage in humans. The photoprotective effects of CBD might be attributed to its modulatory effects on redox homeostasis and autophagy.
Keyphrases
- cell cycle arrest
- cell death
- oxidative stress
- induced apoptosis
- diabetic rats
- high glucose
- endoplasmic reticulum stress
- signaling pathway
- pi k akt
- endothelial cells
- drug induced
- dna damage
- soft tissue
- wound healing
- reactive oxygen species
- nuclear factor
- systematic review
- poor prognosis
- nitric oxide
- liver failure
- cell proliferation
- dna repair
- hepatitis b virus
- replacement therapy
- combination therapy