Atopic dermatitis (AD), characterized by rashes, itching, and pruritus, is a chronic inflammatory condition of the skin with a marked infiltration of inflammatory cells into the lesion. It usually commences in early childhood and coexists with other atopic diseases such as allergic rhinitis, bronchial asthma, allergic conjunctivitis, etc. With a prevalence rate of 1–20% in adults and children worldwide, AD is gradually becoming a major health concern. Immunological aspects have been frequently focused on in the pathogenesis of AD, including the role of the epidermal barrier and the consequent abnormal cytokine expressions. Disrupted epidermal barriers, as well as allergic triggers (food allergy), contact allergens, irritants, microbes, aggravating factors, and ultraviolet light directly initiate the inflammatory response by inducing epidermal keratinocytes, resulting in the abnormal release of various pro-inflammatory mediators, inflammatory cytokines, and chemokines from keratinocytes. In addition, abnormal proteinases, gene mutations, or single nucleotide polymorphisms (SNP) affecting the function of the epidermal barrier can also contribute towards disease pathophysiology. Apart from this, imbalances in cholinergic or adrenergic responses in the epidermis or the role played by immune cells in the epidermis such as Langerhans cells or antigen-presenting cells can also aggravate pathophysiology. The dearth of specific biomarkers for proper diagnosis and the lack of a permanent cure for AD necessitate investigation in this area. In this context, the widespread role played by keratinocytes in the pathogenesis of AD will be reviewed in this article to facilitate the opening up of new avenues of treatment for AD.
The compound methyl cinnamoyl catalpol (DAM-1) was isolated from the methanol extract of Dolichandrone atrovirens. Studies have already reported the antioxidant activity of Dolichandrone atrovirens bark extract, but till date the antioxidant activity of the isolated compound DAM-1, remains unexplored. The endogenous process of reactive oxygen species generation which leads to various degenerative diseases, can be broken down using these exogenous moieties from plant origin, herein this study we sought to evaluate the antioxidant potential of the DAM-1 compound using Caenorhabditis elegans (C. elegans), which is the primary model to study the antioxidant activity of compounds. Cytotoxicity assay results showed that DAM-1 treatment in the concentration of 10, 25 and 50 μg/ml has shown 100%, 91%, and 50% survival respectively with overall p<0.0001 (treatment v/s control group). 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide–Formazan (MTT) assay results showed that treatment had better survival rates than the control group at different time intervals i.e. 48 h, and 72 h with p<0.01. Mechanosensation (behavioral study) as well as in vivo study results showed that at 0 h, 10 μg/ml of DAM-1 treatment showed a better anti-oxidative activity than the control group, 25 and 50 μg/ml of DAM-1 treated groups with p<0.001 but at 2.5 h incubation with 10, 25, 50 μg/ml of DAM-1 showed an increased anti-oxidative activity than the control group with p<0.001. Thermoresistance assay confirmed that the treatment group had more survival than control group with p<0.001. Absorption study of DAM-1 in C. elegans has shown that the absorption of the drug increases up to 180 mins with a slight decrease after 360 mins and then constant absorption up to 1440 mins. This study paves the way towards the initiative to explore the pharmacological role of DAM-1 in various oxidative stress mediated diseases at molecular levels and the absorption study points out its potential role which could be utilized in the metabolomics and proteomics analysis of this compound in other studies.
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