인간 피부각질세포 HaCaT Cell에서 TNF-α/IFN-γ로 유도된 염증 반응에 대한 펄스형 전자기장 (PEMF) 자극의 염증 인자 완화 효과
Effect of Pulsed Electromagnetic Field Stimulation on TNF-α/IFN-γ induced inflammatory response in human skin keratinocytes HaCaT Cell to reduce inflammatory factors
0
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
The purpose of this study was to observe cell death in human keratinocytes stimulated against the infec- tious cytokines TNF-α and IFN-γ, and to observe the expression of Phospho-NF-κB due to phosphorylation of IkB to confirm the mechanism of inhibiting the expression of inflammatory cytokines. As a result of cell viability analysis, differences in PEMF stimulation time were observed little by little after 1 hour, 3 hours, 6 hours, 12 hours, 24 hours, and 48 hours, but there was no statistical significance according to PEMF stimulation time for each time (p>0.05). No significant difference was observed in the total amount of NF-κB present in the cytoplasm and nucleus, but a sig- nificant decrease in the expression of phosphorylated NF-κB was observed in the group exposed to PEMF stimulation for 24 hours (*p<0.05). The expression of IL-1β was observed in all inflammation-induced groups, and the con- centration of IL-1β compared to α-Tubulin expression was reduced by about 54% in the PEMF-stimulated group for 24 hours compared to the control group (***p<0.001). As a result of the study, it is shown that PEMF stimulation does not negatively affect HaCaT cells from 0 to 48 hours and can inhibit the expression of inflammatory cytokines by inhibiting the pathway of NF-κB.
Abstract
The purpose of this study was to observe cell death in human keratinocytes stimulated against the infec- tious cytokines TNF-α and IFN-γ, and to observe the expression of Phospho-NF-κB due to phosphorylation of IkB to confirm the mechanism of inhibiting the expression of inflammatory cytokines. As a result of cell viability analysis, differences in PEMF stimulation time were observed little by little after 1 hour, 3 hours, 6 hours, 12 hours, 24 hours, and 48 hours, but there was no statistical significance according to PEMF stimulation time for each time (p>0.05). No significant difference was observed in the total amount of NF-κB present in the cytoplasm and nucleus, but a sig- nificant decrease in the expression of phosphorylated NF-κB was observed in the group exposed to PEMF stimulation for 24 hours (*p<0.05). The expression of IL-1β was observed in all inflammation-induced groups, and the con- centration of IL-1β compared to α-Tubulin expression was reduced by about 54% in the PEMF-stimulated group for 24 hours compared to the control group (***p<0.001). As a result of the study, it is shown that PEMF stimulation does not negatively affect HaCaT cells from 0 to 48 hours and can inhibit the expression of inflammatory cytokines by inhibiting the pathway of NF-κB.
참고문헌 (40)
- Kashem SW, "Antigen-presenting cells in the skin", Annual review of immunology, 35, pp.469~499 (2017)
- Mathers AR, "Professional antigen-presenting cells of the skin", Immunologic research, 36, pp.127~136 (2006)
- Ariotti S, "Tissue-resident memory CD8+ T cells continuously patrol skin epithelia to quickly recognize local antigen", Proceedings of the National Academy of Sciences, 109(48), pp.19739~19744 (2012)
- Schroder JM, "Cytokine networks in the skin", Journal of investigative dermatology, 105(1), pp.S20~S24 (1995)
- Hanel KH, "Cytokines and the skin barrier", International journal of molecular sciences, 14(4), pp.6720~6745 (2013)
- Sebastiani S, "The role of chemokines in allergic contact dermatitis", Archives of dermatological research, 293, pp.552~559 (2002)
- Nedoszytko B, "Chemokines and cytokines network in the pathogenesis of the inflammatory skin diseases : atopic dermatitis, psoriasis and skin mastocytosis", Advances in Dermatology and Allergology, 2014, pp.31(2), 84~91
- Campo GM, "TNF-α, IFN-γ, and IL-1β modulate hyaluronan synthase expression in human skin fibroblasts : Synergistic effect by concomital treatment with FeSO4 plus ascorbate", Molecular and cellular biochemistry, 292, pp.169~178 (2006)
- Skurkovich B, "Inhibition of IFN-γ as a method of treatment of various autoimmune diseases, including skin diseases", Cytokines as Potential Therapeutic Targets for Inflammatory Skin Diseases, pp.1~27 (2006)
- Van der ZH, "Elevated levels of tumour necrosis factor(TNF)-α, interleukin(IL)-1β and IL-10 in hidradenitis suppurativa skin : a rationale for targeting TNF-α and IL-1β", British Journal of Dermatology, 164(6), pp.1292~1298 (2011)
- Ishida Y, "The essential involvement of cross-talk between IFN-γ and TGF-β in the skin wound-healing process", The Journal of Immunology, 172(3), pp.1848~1855 (2004)
- Hijnen D, "CD8+ T cells in the lesional skin of atopic dermatitis and psoriasis patients are an important source of IFN-γ, IL-13, IL-17, and IL-22", Journal of Investigative Dermatology, 133(4), pp.973~979 (2013)
- Boguniewicz M, "Atopic dermatitis : a disease of altered skin barrier and immune dysregulation", Immunological reviews, 242(1), pp.233~246 (2011)
- Evers A, "Common burden of chronic skin diseases? Contributors to psychological distress in adults with psoriasis and atopic dermatitis", British Journal of Dermatology, 152(6), pp.1275~1281 (2005)
- Leung DY, "Atopic dermatitis : the skin as a window into the pathogenesis of chronic allergic diseases", Journal of allergy and clinical immunology, 96(3), pp.302~319 (1995)
- Moynagh PN, "The NF-κB pathway", Journal of cell science, 118(20), pp.4589~4592 (2005)
- Yamamoto Y, "Role of the NF-kB pathway in the pathogenesis of human disease states", Current molecular medicine, 1(3), pp.287~296 (2001)
- Senftleben U, "The Ikk", nf-κb pathway, 2002, pp.30(1), S18~S26
- Lawrence T, "The nuclear factor NF-κB pathway in inflammation", Cold Spring Harbor perspectives in biology, 1(6), pp.a001651~ (2009)
- Yamamoto Y, "IκB kinases : key regulators of the NF-κB pathway", Trends in biochemical sciences, 29(2), pp.72~79 (2004)
- Zhou D, "Effects of NF-κB1(p50)targeted gene disruption on ionizing radiation-induced NF-κB activation and TNFα, IL-1α, IL-1β and IL-6 mRNA expression in vivo", International journal of radiation biology, 77(7), pp.763~772 (2001)
- Hiscott J, "Characterization of a functional NF-κB site in the human interleukin 1β promoter : evidence for a positive autoregulatory loop", Molecular and cellular biology, 13(10), pp.6231~6240 (1993)
- Flodströma M, "Cytokines activate the nuclear factor κB(NF-κB)and induce nitric oxide production in human pancreatic islets", FEBS letters, 385, pp.4~6 (1996)
- Meier Kriesche HU, "Immunosuppression : evolution in practice and trends, 1994-2004", American Journal of Transplantation, 6(5), pp.1111~1131 (2006)
- Khurana A, "Current concepts of immunosuppression and side effects. Pathology of solid organ transplantation", pp.11~30 (2010)
- Kim JY, "Evaluation of Atopic Dermatitis Improvement Caused by Low-Level, Low-Frequency Pulsed Electromagnetic Fields", Bioelectromagnetics, 43(4), pp.268~277 (2022)
- Ross CL, "The use of pulsed electromagnetic field to modulate inflammation and improve tissue regeneration : A review", Bioelectricity, 1(4), pp.247~259 (2019)
- Vincenzi F, "Pulsed electromagnetic fields increased the anti-inflammatory effect of A2A and A3 adenosine receptors in human T", C-28a2 chondrocytes and hFOB 1.19 osteoblasts, 2013, pp.8(5), e65561~
- Vincenzi F, "Pulsed electromagnetic field exposure reduces hypoxia and inflammation damage in neuron-like and microglial cells", Journal of Cellular Physiology, 232(5), pp.1200~1208 (2017)
- Li S, "CCK-8 inhibits LPS-induced IL-1β production in pulmonary interstitial macrophages by modulating PKA, p38, and NF-κB pathway", Shock, 27(6), pp.678~686 (2007)
- Viatour P, "Phosphorylation of NF-κB and IκB proteins : implications in cancer and inflammation", Trends in biochemical sciences, 30(1), pp.43~52 (2005)
- Christian F, "The regulation of NF-κB subunits by phosphorylation", Cells, 5(1), pp.12~ (2016)
- Yasuda T, "Hyaluronan inhibits cytokine production by lipopolysaccharide-stimulated U937 macrophages through downregulation of NF-κB via ICAM-1", Inflammation Research, 56, pp.246~253 (2007)
- Colombo I, "HaCaT cells as a reliable in vitro differentiation model to dissect the inflammatory", repair response of human keratinocytes, 2017, pp.2017, ~
- Wilson VG, "Growth and differentiation of HaCaT keratinocytes", Epidermal Cells: Methods and Protocols, pp.33~41 (2014)
- Cai L, "Comparison of cytotoxicity evaluation of anticancer drugs between real-time cell analysis and CCK-8 method", ACS omega, 4(7), pp.12036~12042 (2019)
- Kim H, "Anti-inflammatory activity of a water extract of Acorus calamus L. leaves on keratinocyte HaCaT cells", Journal of ethnopharmacology, 122(1), pp.149~156 (2009)
- Zandi E, "The IkB kinase complex(IKK)contains two kinase subunits, IKKa and IKKb, necessary for IkB phosphorylation and NFkB activation", Cell, 91(2), pp.243~252 (1997)
- Magnani M, "The ubiquitin-dependent proteolytic system and other potential targets for the modulation of nuclear factor-kB(NF-kB)", Current drug targets, 1(4), pp.387~399 (2000)
- Gilmore TD, "The Rel", NF-κB signal transduction pathway : introduction, 1999, pp.18(49), 6842~6844