The Anti-Atopic Dermatitis Effects of Mentha arvensis Essential Oil Are Involved in the Inhibition of the NLRP3 Inflammasome in DNCB-Challenged Atopic Dermatitis BALB/c Mice

Abstract

The NLRP3 inflammasome is upregulated by various agents, such as nuclear factor-kappa B (NF-κB), lipopolysaccharide (LPS), and adenosine triphosphate (ATP). The NLRP3 inflammasome facilitations the maturation of interleukin (IL)-1β, a proinflammatory cytokine that is critically involved in the pathogenesis of atopic dermatitis (AD). Although the NLRP3 inflammasome clearly exacerbates AD symptoms such as erythema and pruritus, drugs for AD patients targeting the NLRP3 inflammasome are still lacking. Based on the previous findings that Mentha arvensis essential oil (MAEO) possesses strong anti-inflammatory and anti-AD properties through its inhibition of the ERK/NF-κB signaling pathway, we postulated that MAEO might be capable of modulating the NLRP3 inflammasome in AD. The aim of this research was to investigate whether MAEO affects the inhibition of NLRP3 inflammasome activation in murine bone marrow-derived macrophages (BMDMs) stimulated with LPS + ATP in vitro and in a murine model displaying AD-like symptoms induced by 2,4-dinitrochlorobenzene (DNCB) in vivo. We found that MAEO inhibited the expression of NLRP3 and caspase-1, leading to the suppression of NLRP3 inflammasome activation and IL-1β production in BMDMs stimulated with LPS + ATP. In addition, MAEO exhibited efficacy in ameliorating AD symptoms in a murine model induced by DNCB, as indicated by the reduction in dermatitis score, ear thickness, transepidermal water loss (TEWL), epidermal thickness, and immunoglobulin E (IgE) levels. Furthermore, MAEO attenuated the recruitment of NLRP3-expressing macrophages and NLRP3 inflammasome activation in murine dorsal skin lesions induced by DNCB. Overall, we provide evidence for the anti-AD effects of MAEO via inhibition of NLRP3 inflammasome activation.

Multiplicative Effects of Essential Oils and Other Active Components on Skin Tissue and Skin Cancers

“…Moreover, infiltration of mast cell and epidermal layer thickness are attenuated by treatment with MA-EO in a DNCB-induced AD mouse model [80]. Furthermore, the formation of the nucleotide-binding oligomerization-domain-like receptor (NLR) family pyrin-domain-containing 3 (NLRP3) inflammasome is attenuated by treatment with MA-EO in the macrophage of a DNCB-induced AD mouse [83].…”

Special Issue “Molecular and Cellular Advances in Atopic Diseases”

“…Moreover, the NLR family pyrin domain containing 3 (NLRP3) inflammasome is a critical element of the innate immune system, playing a key role in inflammation. Its altered expression has been linked to the exacerbation of AD, making it an important target for therapeutic intervention, which is an aspect addressed in one of the articles of this Special Issue [42].…”