Abstract
The aim of this study was to compare the chemical composition, as well as antioxidant, anti-inflammatory, antiacne, and cytotoxic activites of various extracts of Cephalaria gigantea and C. uralensis. It is worth underlining that we are the first to characterize the composition and evaluate the biological properties of extracts from Cephalaria gigantea and C. uralensis. Thus, the LC-DAD-MS3 analysis revealed the presence of 41 natural products in studied extracts. The 5-O-caffeoylquinic acid, isoorinetin, and swertiajaponin were the main detected compounds. Among the tested samples, ethanol extract of the aerial parts of C. uralensis (CUE) possessed the most suitable biological properties. It exhibited moderate ability to scavenge free radicals and good capacity to inhibit cyclooxygenase-1, as well as cyclooxygenase-2. Moreover, CUE possessed moderate antibacterial activity against all tested bacterial strains (S. aureus, S. epidermidis, and P. acnes), and importantly, it was non-toxic towards normal skin fibroblasts. Taking into account the value of calculated therapeutic index (>10), it is worth noting that CUE can be subjected to in vivo study. Thus, CUE constitutes a very promising antiacne agent.
Highlights
Among all skin diseases that are marked by an abnormal function of the sebaceous glands in the skin, acne vulgaris is the most common, accounting for 99% of acne cases [1]
The phytochemical analysis of extracts of C. uralensis and C. gigantea revealed the presence of forty-one constituents, which were characterized based on UV-Vis spectrum and MS/MS spectra
We identified the main compounds presenting in extracts as well as we determined antioxidant, anti-inflammatory, antimicrobial, and cytotoxic properties of such extracts
Summary
Among all skin diseases that are marked by an abnormal function (usually hyperactivity) of the sebaceous glands in the skin, acne vulgaris is the most common, accounting for 99% of acne cases [1]. The prevalence of acne vulgaris globally was 681.2 million in 2016, which was an increase of 10% from 612 million in 2006. There are four key processes in its pathogenesis: increased sebum production, follicular hyperkeratinization, which leads to follicular obstruction, colonization by the causative agent, Cutibacterium acnes (=Propionibacterium acnes), and host inflammatory responses triggered as a result of bacterial infection [2,3]. As a result of the increased sebum production due to high androgen levels, C. acnes produces various hydrolytic enzymes that act on the sebum to release free fatty acids. These free fatty acids act as chemokines and increase the release of pro-inflammatory cytokines like interleukins 8 (IL-8) and tumor necrosis factors (TNF-α), which attract macrophages, and lead to severe inflammation. Follicular wall ruptures due to the action of hydrolytic enzymes cause oxidative damage with the release of free radicals [2,3]
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