PMID- 35676724 OWN - NLM STAT- PubMed-not-MEDLINE LR - 20230916 IS - 1749-8546 (Print) IS - 1749-8546 (Electronic) IS - 1749-8546 (Linking) VI - 17 IP - 1 DP - 2022 Jun 8 TI - Inhibitory effect of Isatis tinctoria L. water extract on DNCB-induced atopic dermatitis in BALB/c mice and HaCaT cells. PG - 66 LID - 10.1186/s13020-022-00624-5 [doi] LID - 66 AB - 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-kappaB 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-kappaB signaling pathway were decreased in serum and dorsal skin tissues. Furthermore, PLG inhibited inflammatory chemokine production and blocked the nuclear translocation of NF-kappaB 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. CI - (c) 2022. The Author(s). FAU - Min, Ga-Yul AU - Min GY AD - Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 41062, Republic of Korea. FAU - Kim, Tae In AU - Kim TI AD - Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 41062, Republic of Korea. FAU - Kim, Ji-Hye AU - Kim JH AD - Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 41062, Republic of Korea. FAU - Cho, Won-Kyung AU - Cho WK AD - Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 41062, Republic of Korea. FAU - Yang, Ju-Hye AU - Yang JH AD - Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 41062, Republic of Korea. jjuhye@kiom.re.kr. FAU - Ma, Jin-Yeul AU - Ma JY AD - Korean Medicine (KM) Application Center, Korea Institute of Oriental Medicine, 70 Cheomdan-ro, Dong-gu, Daegu, 41062, Republic of Korea. jyma@kiom.re.kr. LA - eng GR - KSN1812101/Korea Institute of Oriental Medicine/ GR - KSN2021230/Korea Institute of Oriental Medicine/ PT - Journal Article DEP - 20220608 PL - England TA - Chin Med JT - Chinese medicine JID - 101265109 PMC - PMC9175348 OTO - NOTNLM OT - Atopic dermatitis OT - BALB/c mice OT - HaCaT cells OT - Isatis tinctoria L COIS- The authors declare that they have no competing interests. EDAT- 2022/06/09 06:00 MHDA- 2022/06/09 06:01 PMCR- 2022/06/08 CRDT- 2022/06/08 23:42 PHST- 2022/01/05 00:00 [received] PHST- 2022/05/28 00:00 [accepted] PHST- 2022/06/08 23:42 [entrez] PHST- 2022/06/09 06:00 [pubmed] PHST- 2022/06/09 06:01 [medline] PHST- 2022/06/08 00:00 [pmc-release] AID - 10.1186/s13020-022-00624-5 [pii] AID - 624 [pii] AID - 10.1186/s13020-022-00624-5 [doi] PST - epublish SO - Chin Med. 2022 Jun 8;17(1):66. doi: 10.1186/s13020-022-00624-5.