Table 2.
Summary of studies investigating the cosmetic properties of CBD
| Evidence | Model/setting | Concentration/dose | Result | Biological context | References |
|---|---|---|---|---|---|
| In vitro | Human keratinocytes (PCS 200-013) and melanocytes (PCS-200-011), exposed to UVB (60 mJ/cm2) | 4 µM | ↑ Cell viability in a dose-dependent manner in both keratinocytes and melanocytes; CBD did not show absorption in the UVB spectra | Oxidative stress (UV) | [59] |
| In vitro | Human keratinocytes, exposed to UVA (30 J/cm2) and UVB (60 mJ/cm2) | 4 µM | ↓ ROS; ↑ thioredoxin-dependent system, vitamins A and E | Oxidative stress (UV) | [60] |
| In vitro | Human keratinocytes (CDD 1102 KERTr), exposed to UVB (60 mJ/cm2) and H2O2 (200 µM) | 4 µM | ↓ Lipid peroxidation, LDH release; ↑ PUFA; CBD penetrated keratinocytes and accumulated within the cellular membrane | Oxidative stress (UV, H2O2) | [61] |
| In vitro | Human keratinocytes (CDD 1102 KERTr), exposed to UVA (30 J/cm2) and UVB (60 mJ/cm2) | 1 µM | ↑ NRF-2 and HOMX1 expression; ↓ NF-κB pathway | Oxidative stress (UV) | [62] |
| In vitro/in vivo | NHEK, HaCaT cells in vitro; BALB/cByJRj mice in vivo | 10 µM in vitro; 0.1–10% in vivo (topically, 1/day for 5 days) | ↑ HOMX1 expression through ↓ BACH1 in vitro; ↑ HOMX1 in vivo | Oxidative stress (endogenous peroxidase) | [63] |
| In vitro | 2D and 3D culture models of fibroblasts (CCD-25Sk), exposed to UVA (30 J/cm2) and UVB (60 mJ/cm2) | 4 µM | ↓ NF-κB pathway; ↑ PPARγ expression; CBD reduced the collagen degradation in both 2D and 3D fibroblast models | Oxidant stress (UV) | [64] |
| In vitro | HaCaT and HDF cells (PCS-201-012), treated with TNF-α (10 ng/mL) | 0.05–5 µM in HaCaT cells; 0.1–2.5 µM in HDF cells | In HaCaT cells: ↓ NF-κB, MMP-9; CBD down-regulated 15 out of 26 TNF-α-induced genes. In HDF cells: CBD down-regulated 11 out of 16 TNF-α-induced genes with no inhibition of NF-κB. | Inflammation (TNF-α) | [66] |
| In vitro | HaCaT cells, stimulated with poly-(I:C) [100 µg/mL] | 1–20 µM | ↑ AEA; ↓ MCP-2, IL-6, IL-8, and TNF-α in a CB2R-dependent and TRPV1-dependent manner | Inflammation (poly-[I:C]) | [67] |
| In vivo | Sprague-Dawley rats, carrageenan induction (0.1 mL, 1% w/v in saline, injected into the plantar of the right hind paw) | 1% gel | ↓ Paw edema, lymphocytic inflammation | Inflammation (carrageenan) | [68] |
| In vivo | CD1 nude mice, carrageenan induction | Ethosomal formulation (3% w/w CBD and 40% w/w EtOH in a carbomer gel) | ↓ Paw edema; transdermal absorption; detection in the plasma | Inflammation (carrageenan) | [69] |
| Clinical | Psoriasis (n = 5), atopic dermatitis (n = 5), and resulting scars (n = 10) | CBD-containing ointment (2/day for 3 months) | ↓ PASI in patients with psoriasis; ↓ number of papules and pustules in dermatological patients; CBD improved TEWL, hydration, and elasticity in all patients | Inflammation (psoriasis, atopic dermatitis); dry skin | [11] |
| Clinical | Mild-to-moderate scalp psoriasis (n = 22) and seborrheic dermatitis (n = 28) | 0.075% CBD in shampoo (2/day for 2 weeks) | ↓ Scores for arborizing vessels, twisted capillaries, and scales; ↓ scores for erythema and scaling; ↓ scores for itching and burning | Inflammation (psoriasis, seborrheic dermatitis) | [13] |
| Clinical | Atopic dermatitis (n = 16) | 1% CBD-infused gel (2/day for 2 weeks) | ↓ EASI score, VAS-Pruritus and 5-D Pruritus scales | Inflammation (atopic dermatitis) | [75] |
| In vivo | HR-1 mice | 1% CBD solution (2/day for 14 days) | ↑ Dermal water contents, AQP3 expression; CBD did not affect the expression levels of loricrin, filaggrin, and other moisturizing factors | Dry skin | [78] |
| In vitro | Human sebocytes (SZ95) | 1–10 µM | ↓ Lipogenic actions of arachidonic acid and a mixture of linoleic acid and testosterone; ↓ proliferation of sebocytes via TRPV4 activation, ERK1/2 MAPK pathway, and down-regulation of NRIP1; ↓ inflammation via the A2A adenosine receptor-dependent up-regulation of TRIB3 and inhibition of NF-κB | Acne | [154] |
| In vitro | NHEK, stimulated with Cutibacterium acnes-derived extracellular vesicles | 0.5–2 µM | ↓ IL-6, IL-8, and TNF-α expression via CB2R activation; ↓ MAPK and NF-κB signaling pathway | Acne | [85] |
| Clinical | Moderate-to-severe acne (n = 23) | 5% CBD formulation (2/day for 28 days) | Safe and well tolerated; the results have not been published | Acne | [90] |
| In vitro | Normal fibroblasts and SIPS fibroblasts (CCD-1064Sk and-1135Sk) | 2 µM | ↑ Wound healing in both healthy and SIPS fibroblasts; inhibits the change in nuclear architecture in both healthy and SIPS fibroblasts; ↓ β-galactosidase activity in SIPS fibroblasts but not in normal fibroblasts; ↓ cyclin D1 expression in normal fibroblast exposed to H2O2 |
Wound healing Aging |
[92] |
| In vitro/in vivo | HUVECs, mouse embryonic fibroblast cells of NIH 3T3 (in vivo); skin defect model for acute wound using Sprague Dawley rats (male, 8–10 weeks old) | Hydrogel dressing (CBD/Alg@Zn) | Scavenged DPPH (2,2-diphenyl-1-picrylhydrazyl) free radicals, ↓ inflammatory response (in vitro); facilitates the wound-healing process by ↓ inflammatory infiltration, ↑ collagen deposition, ↑ granulation tissue, and ↑ blood vessel formation (in vivo) | Wound healing; anti-oxidant stress | [148] |
| Clinical | Epidermolysis bullosa (n = 3) | Topical CBD | ↑ Wound healing | Wound healing | [14] |
| In vitro | SIPS fibroblasts (CCD-1064Sk) | 2 µM with or without rapamycin, metformin, or TRSV | CBD combined with TRSV up-regulated the viability of skin fibroblasts, wound-healing functional activity; ↓ metabolic dysfunction and nuclear eccentricity | Aging (oxidative stress) | [97] |
| In vitro/ex vivo/clinical | HaCaT, UVB exposure (60 mJ/cm2, in vitro); human skin organ culture, UVB exposure (350 mJ/cm2, ex vivo); female aged 45–65 years, n = 34 (clinical) | 10 µg/mL (in vitro); 0.1% (ex vivo and clinical) | CBD inhibited the secretion of PGE2 and IL-8 following UV exposure; PEA potentiated the inhibitory activity of CBD on PGE2 and IL-8 secretion (in vitro); ↑ ECM remodeling following UV exposure (ex vivo); ↓ crow’s feet wrinkle area and volume, fine line wrinkle volume, and age-dependent subepidermal low-echogenic band (clinical) | Aging (UV) | [98] |
2D two-dimensional, 3D three-dimensional, BACH1 BTB And CNC Homology 1, CBD cannabidiol, EASI Eczema Area and Severity Index, ECM extracellular matrix, HDF human dermal fibroblasts, HMOX1 heme oxygenase 1 gene, HUVEC human umbilical vein endothelial cell, LDH lactate dehydrogenase, NF-κB nuclear factor-kappa B, NHEK normal human epidermal keratinocytes, NRF-2 nuclear factor erythroid 2-like 2, NRIP1 nuclear receptor interacting protein-1, PASI Psoriasis Area and Severity Index, PUFA polyunsaturated fatty acid, PGE2 prostaglandin E2, ROS reactive oxygen species, SIPS stress-induced premature senescence, TEWL transepidermal water loss, TRIB3 tribbles homolog 3, TRSV triacetylresveratrol, UVA ultraviolet A, UVB ultraviolet B, VAS visual analog scale, ↑ increased, ↓ decreased