Effect of cold atmospheric plasma on some molecular markers in rats with experimentally induced atopic dermatitis

Objective: The aim of this study is to investigate the effect of cold atmospheric plasma (SAP) treatment on some molecular markers in rats with experimentally induced Atopic Dermatitis (AD). Materials and Methods: In this study, 24 newborn rats were used. Eight newborn rats were determined as the control group, the remaining 16 newborn rats were treated with Kapsaisin immediately after birth and housed under normal care and feeding conditions for 6 weeks to develop AD. 8 of the rats with AD were determined as the AD group without SAP application and their care and feeding continued under normal care and feeding conditions, while eight were determined as the SAP group and SAP treatment was applied to two lesion areas on them for a total of 3 minutes 5 times. At the end of the applications, blood and skin samples were collected from all 3 groups under general anesthesia. Serums were separated from the blood samples and IgE, IL-13 and IL-4 analyses were performed using the ELISA method. Additionally, one of the skin samples was subjected to histopathological examination. Furthermore, the expression levels of antimicrobial peptides Defensin 1, Defensin-2, and cathelicidin (LL-37), which play an important role in the pathogenesis of Atopic Dermatitis, as well as the Aryl Hydrocarbon Receptor (AHR) and Peroxisome Proliferator-Activated Receptor PPARα genes, which control the genes responsible for lipid oxidation, were determined using the qRT-PCR method. Results: When evaluated histopathologically, it was determined that AD occurred in all of the AD and SAP groups. When the analyzed parameters of keratin increase, spongiosis degeneration in the epithelium, atrophy in the hair follicles, deepening of the rete and eosinophil leukocyte scores were compared, findings very similar to the control group were obtained in the SAP group. When the parameters were evaluated as a result of the ELISA tests we performed on blood samples, it was seen that the SAP and control group findings were parallel. In gene-level studies, no statistical difference was detected between groups when examining the expression levels of LL-37 (KAMP) and Defensin-1 genes in AD, SAP, and control groups. It was determined that the AHR gene expression decreased significantly in the AD group and was expressed lower than the control group. Defensin-2 gene expression was found to be lower in the AD group than the control and SAP treatment groups. It was determined that the PPARα gene was expressed lower in the SAP treatment group than in the other groups. It was observed that the PPARα gene expression in the AD group was higher compared to the other groups. Conclusion: SAP treatment caused changes in the IgE, IL-13 and IL-4 levels in rats in the experimentally created AD model. It was confirmed macroscopically and microscopically that both biochemical and histopathological improvements were observed after SAP treatment. In this respect, the effectiveness of SAP application in the treatment of AD was demonstrated. It was concluded that more detailed studies should be conducted on the effect of SAP on gene expression. It has been observed that it has effects on AHR, Defensin-2 and PPARα gene expressions, which are genes that play an important role in AD pathogenesis. In light of the information obtained as a result of this study, it has been revealed that SAP, an innovative approach in the treatment of AD, which is an important problem in animals and humans, has the potential to be recommended as a supportive treatment in clinical applications. Keywords: dermatitis, Atopic; Cold atmospheric plasma; IgE; IL-4; IL-13; beta-Defensin; Cathelicidin LL-37; Aryl Hydrocarbon Receptor; PPARalpha; Rats