Comparison of the in vitro Anti-Inflammatory Effect of Cannabidiol to Dexamethasone

Abstract

Background Cannabidiol (CBD) is a non-psychoactive phytocannabinoid constituent of Cannabis sativa with pain-relieving and anti-inflammatory properties. With the emphasis on natural ingredients in cosmetics, CBD has become a new cosmetic ingredient due to its ability to alleviate inflammation. However, in-depth studies that directly compare the effective mechanism and the therapeutic potential of CBD are still needed. Purpose The aim of the present study was to investigate the anti-inflammatory effect of CBD in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages and compare it to dexamethasone (DEX). Methods RAW264.7 macrophages in the logarithmic growth phase were incubated in the presence or absence of LPS. After that, the production of nitric oxide (NO), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were measured. A luciferase reporter assay for nuclear factor kappa B (NF-κB) was performed, and the phosphorylation levels of the mitogen-activated protein kinase (MAPK) and NF-κB signaling pathways were measured. Results The present study indicated that CBD had a similar anti-inflammatory effect to DEX by attenuating the LPS-induced production of NO, IL-6, and TNF-α. However, only CBD attenuated JNK phosphorylation levels, and only DEX attenuated IKK phosphorylation levels. Conclusion These results suggested that CBD and DEX exhibit similar anti-inflammatory effects on LPS-induced RAW264.7 macrophages mainly through suppressing the MAPK and NF-κB signaling pathways, but with different intracellular mechanisms. These findings suggested that CBD may be considered a natural anti-inflammatory agent for protecting skin from immune disorders.

Cannabidiol-Loaded Nanostructured Lipid Carriers (NLCs) for Dermal Delivery: Enhancement of Photostability, Cell Viability, and Anti-Inflammatory Activity

“…When macrophages are exposed to LPS, inflammatory mediators such as IL-6 are released [ 52 ]. Recently, it was reported that treatment with CBD (0.02 mg/mL) significantly inhibited the LPS-induced levels of IL-6 and TNF-α produced in RAW264.7 cell macrophages [ 53 ]. In this study, the ability of CBD extract and CBD-NLCs to inhibit or reduce the production of IL-6 was studied in RAW264.7 cell macrophages by evaluating the concentrations of IL-6 in the culture supernatants.…”

Cannabidiol as a Promising Therapeutic Option in IC/BPS: In Vitro Evaluation of Its Protective Effects against Inflammation and Oxidative Stress

“…The suppressive in vitro inhibitory effects of CBD on the production and release of IL1, IL8, and CXCL1 have also been previously shown in other pre-clinical in vitro inflammatory models using various cell types, including monocytes [70], macrophages [71], epithelial cells, and fibroblasts [72,73], stimulated with LPS or TNFα. A previous study showed that CBD has a similar anti-inflammatory effect to dexamethasone in macrophages by attenuating the LPS-induced production of NO, IL6, and TNFα through inhibition of NFκB p65 phosphorylation [74]. Since the molecular mechanism underlying the observed anti-inflammatory effects of CBD in urothelial cells has never been studied before, we next investigated the activation of the transcription factor NFκB, which plays a central role in chronic inflammatory diseases characterized mainly by an inflammatory and innate immune response, including IC/BPS [75][76][77][78].…”

Effects of combined cannabidiol (CBD) and hops (Humulus lupulus) terpene extract treatment on RAW 264.7 macrophage viability and inflammatory markers

“…Numerous publications have demonstrated the potent anti-inflammatory effect of CBD both in-vitro and in-vivo [ 13 , 57 , 58 ]. The underlying mechanisms involve direct suppression of the activation of different types of immune cells, induction of apoptosis, and promotion of regulatory cells, which in turn control other immune cell targets.…”

“…Several in vitro and ex vivo studies have demonstrated that CBD possesses anti-inflammatory properties. Mechanistically, this is due to its modulation of the TLR4 signal transduction cascade and altered activation of the transcription factors NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells) or AP-1 (activating protein-1), leading to lower levels of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α [ 13 – 16 ].…”