Effect of carvacrol on various cytokines genes expression in splenocytes of asthmatic mice
Publish place: Iranian Journal of Basic Medical Sciences، Vol: 19، Issue: 4
Publish Year: 1395
نوع سند: مقاله ژورنالی
زبان: English
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شناسه ملی سند علمی:
JR_IJBMS-19-4_009
تاریخ نمایه سازی: 30 مهر 1400
Abstract:
Objective(s):With regard to pharmacological effects of carvacrol on the respiratory system, its effect on cytokines genes expression in splenocytes of asthmatic mice was examined in this study. Materials and Methods:Splenocytes were isolated from non-sensitized (control group), sensitized mice to ovalbumin (OVA) (group S), and S animals treated with dexamethasone, and three concentrations of carvacrol. IL-۴, IFN-γ, TGF-β, FOXP۳, and IL-۱۷ genes expression were carried out in cultured splenocytes using the real-time PCR method. Results:Compared to the control group, IFN-γ and FOXP۳ genes expression were significantly decreased (P<۰.۰۰۱ for both cases), but IL-۴ and IL-۱۷ genes expression were significantly increased in the S group (P<۰.۰۰۱ and P<۰.۰۵, respectively). IL-۴ gene expression due to treatment of all concentrations of carvacrol, TGF-β gene expression due to its two higher concentrations, and IL-۱۷ gene expression due to its high concentration were significantly decreased compared to group S (P<۰.۰۱ to P<۰.۰۰۱). IFN-γ gene expression was significantly increased due to last carvacrol concentration (۳۰۰ µg/ml, P<۰.۰۱), and FOXP۳ due to its two last concentrations (۱۵۰ and ۳۰۰ µg/ml, P<۰.۰۵ and P<۰.۰۰۱, respectively) in treated S splenocytes. Dexamethasone treatment of sensitized splenocytes only showed significant inhibitory effect on IL-۴ and TGF-β genes expression (P<۰.۰۰۱ for both cases). Conclusion: These results showed the immunomodulatory effect of carvacrol indicating increased IFN-γ and FOXP۳ but decreased IL-۴, TGF-β, and IL-۱۷ genes expression, which was more selective than the effect of dexamethasone in sensitized mice splenocytes, which indicates its possible therapeutic value in allergy, autoimmunity, and infectious diseases.
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Authors
Majid Kianmehr
Neurogenic Inflammation Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Abdolrahim Rezaei
Inflammation and Inflammatory Diseases Research Center, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
Mohammad Hossein Boskabady
Neurogenic Inflammation Research Center and Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
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