Xerosis cutis represents one of the most common dermatological diagnoses, which, when untreated, can be the trigger for open wounds, infections, and other skin diseases. Plant extracts are a valuable option for long-term treatments for xerosis due to their phytocompounds, especially polyphenols, flavonoids, triterpenes, and polysaccharides, with antioxidant, anti-inflammatory, antimicrobial, moisturizing, and reparatory effects. Active substances have different mechanisms; therefore, evaluating the effects on the cells can be a key indicator, providing valuable information in terms of both cytotoxicity and efficacy. The in vitro and in vivo toxicity tests performed for Betulae extractum, Liquiritiae extractum, and Avenae extractum highlighted potential toxic effects at higher concentrations in a dose-dependent relationship, but at lower levels they can be considered safe (12.5 µg/mL for birch and licorice extracts, 50 µg/mL for oat extract). Concerning the re-epithelialization process, the results revealed that all three dry extracts effectively stimulate skin cell migration, highlighting a potential anti-inflammatory effect by increasing the cell migration rate in conditions of induced inflammation associated with oxidative stress. Among the tested concentrations with a potential contribution to wound healing, the following standout: are birch bark extract 3 μg/mL, licorice root extract 7.5 µg/mL, and oat herb (harvested before flowering) extract 7.5 µg/mL.

UVA radiation induces multiple and complex changes in the skin, affecting epidermal cell behavior. This study reports the effects of UVA exposure on normal (HaCaT) and dysplastic (DOK) keratinocytes. The adherence, spreading and proliferation were investigated by time-lapse measurement of cell layer impedance on different matrix proteins. Prior to UVA exposure, the time required for adherence and spreading did not differ significantly for HaCaT and DOK cells, while spreading areas were larger for HaCaT cells. Under UVA exposure, HaCaT and DOK cells behavior differed in terms of movement and proliferation. The cells’ ability to cover the denuded surface and individual cell trajectories were recorded by time-lapse videomicroscopy, during wound healing experiments. Dysplastic keratinocytes showed more sensitivity to UVA, exhibiting transient deficiencies in directionality of movement and a delay in re-coating the denuded area. The actin cytoskeleton displayed a cortical organization immediately after irradiation, in both cell lines, similar to mock-irradiated cells. Post-irradiation, DOK cells displayed a better organization of stress fibers, persistent filopodia, and new, stronger focal contacts. In conclusion, after UVA exposure HaCaT and DOK cells showed a different behavior in terms of adherence, spreading, motility, proliferation, and actin cytoskeleton dynamics, with the dyplastic keratinocytes being more sensitive.

UVA affects epidermal cell physiology in a complex manner, but the harmful effects have been studied mainly in terms of DNA damage, mutagenesis and carcinogenesis. We investigated UVA effects on membrane integrity and antioxidant defense of dysplastic keratinocytes after one and two hours of irradiation, both immediately after exposure, and 24 h post-irradiation. To determine the UVA oxidative stress on cell membrane, lipid peroxidation was correlated with changes in fatty acid levels. Membrane permeability and integrity were assessed by propidium iodide staining and lactate dehydrogenase release. The effects on keratinocyte antioxidant protection were investigated in terms of catalase activity and expression. Lipid peroxidation increased in an exposure time-dependent manner. UVA exposure decreased the level of polyunsaturated fatty acids, which gradually returned to its initial value. Lactate dehydrogenase release showed a dramatic loss in membrane integrity after 2 h minimum of exposure. The cell ability to restore membrane permeability was noted at 24 h post-irradiation (for one hour exposure). Catalase activity decreased in an exposure time-dependent manner. UVA-irradiated dysplastic keratinocytes developed mechanisms leading to cell protection and survival, following a non-lethal exposure. The surviving cells gained an increased resistance to apoptosis, suggesting that their pre-malignant status harbors an abnormal ability to control their fate.