Cannabis sativa L. extract reduces inflammatory markers in human fibroblasts and keratinocytes

Dermatitis and psoriasis are inflammatory skin diseases in which keratinocytes and fibroblasts play a key role in the release of pro-inflammatory mediators (e.g. IL-8, MMP9, VEGF, and NF-κB). The flowered tops of Cannabis sativa L. (hemp) contain the highest concentration of cannabinoids including cannabidiol (CBD), the second major cannabinoid without psychotropic activity.

The aim of the present study was to investigate the potential effect of a Cannabis sativa L. ethanolic extract (CSE), standardized in CBD, as anti-inflammatory agent in human keratinocytes and fibroblasts.

CSE and CBD (99.5% HPLC purity) were prepared by LINNEA SA (Riazzino, Switzerland) and assayed in fibroblasts (HDF) and keratinocytes (HaCaT), stimulated by TNFα or UVB.

CSE reduced TNFα-induced IL-8 secretion (HDF, IC₅₀ 15.13 µg/ml), VEGF (HaCaT, IC₅₀ 26.8 µg/ml) and MMP-9 (IC₅₀ 18.0 and 7.21, for HaCaT and HDF, respectively), while CBD showed low or no inhibitory effect, but reduced the NF-κB driven transcription.

CSE (25 μg/mL) and CBD (4 μM) were tested on the expression of 84 genes involved in inflammation and wound healing. CSE decreased the mRNA levels of the TNFα-up-regulated genes, whereas CBD was not able to fully explain the activity of the extract.

These results suggest that CSE inhibits the release of pro-inflammatory mediators in human fibroblasts and keratinocytes, acting on the NF-κB pathway. The down-regulation of genes involved in wound healing and skin inflammation, were not strictly associated to the presence of CBD, suggesting that other unknown compounds occurring in the extract my exert anti-inflammatory effects.