4.7 Article

Inhibitory effect of Isatis tinctoria L. water extract on DNCB-induced atopic dermatitis in BALB/c mice and HaCaT cells

期刊

CHINESE MEDICINE
卷 17, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s13020-022-00624-5

关键词

Isatis tinctoria L; Atopic dermatitis; BALB; c mice; HaCaT cells

资金

  1. Korea Institute of Oriental Medicine (KIOM)
  2. Ministry of Science and ICT, Republic of Korea [KSN1812101, KSN2021230]
  3. National Research Council of Science & Technology (NST), Republic of Korea [KSN2021230, KSN1812101] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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The study demonstrates that PLG is a potent therapeutic agent for attenuating symptoms of atopic dermatitis by inhibiting inflammatory chemokine production and blocking the nuclear translocation of NF-kappa B p65.
Background Isatis tinctoria L (PLG) is a medicinal herb from the roots of Isatis indigotica Fort (Family Cruciferae). Previous studies have shown that PLG has anti-inflammatory and therapeutic effects against conditions such as acute and chronic hepatitis, various respiratory inflammations, and cancer. The purpose of this study was to define the pharmacological effects of PLG on inflammatory reactions and skin hyperkeratosis, which are the main symptoms of atopic dermatitis (AD), in vivo and in vitro. Methods For the AD in vivo experiment, 2,4-dinitrochlorobenzene (DNCB) induction and oral administration of PLG were performed on male BALB/c mice for four weeks. For in vitro experiments, keratinocytes were activated using TNF-alpha/IFN-gamma in cultured human keratinocyte (HaCaT) cells. PLG inhibited inflammatory chemokine production and blocked the nuclear translocation of NF-kappa B p65 in activated keratinocytes. Results As a result of oral administration of PLG, dermis and epidermis thickening, as well as eosinophil and mast cell infiltration, were attenuated in AD skin lesions. In addition, the levels of immunoglobulin E (IgE), pro-inflammatory cytokines, and the MAPK/NF-kappa B signaling pathway were decreased in serum and dorsal skin tissues. Furthermore, PLG inhibited inflammatory chemokine production and blocked the nuclear translocation of NF-kappa B p65 in activated keratinocytes. In addition, epigoitrin and adenosine, the standard compounds of PLG, were identified as candidate AD compounds. Conclusions These results indicate that PLG is a potent therapeutic agent for attenuating symptoms of AD.

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