PMID- 38356236 OWN - NLM STAT- MEDLINE DCOM- 20240417 LR - 20240417 IS - 1522-7278 (Electronic) IS - 1520-4081 (Linking) VI - 39 IP - 5 DP - 2024 May TI - Supercritical CO(2) fluid extract from Stellariae Radix ameliorates 2,4-dinitrochlorobenzene-induced atopic dermatitis by inhibit M1 macrophages polarization via AMPK activation. PG - 3188-3197 LID - 10.1002/tox.24145 [doi] AB - Yin chai hu (Radix Stellariae) is a root medicine that is frequently used in Chinese traditional medicine to treat fever and malnutrition. In modern medicine, it has been discovered to have anti-inflammatory, anti-allergic, and anticancer properties. In a previous study, we were able to extract lipids from Stellariae Radix using supercritical CO(2) extraction (SRE), and these sterol lipids accounted for up to 88.29% of the extract. However, the impact of SRE on the development of atopic dermatitis (AD) has not yet been investigated. This study investigates the inhibitory effects of SRE on AD development using a 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model. Treatment with SRE significantly reduced the dermatitis score and histopathological changes compared with the DNCB group. The study found that treatment with SRE resulted in a decrease of pro-inflammatory cytokines TNF-alpha, CXC-10, IL-12, and IL-1beta in skin lesions. Additionally, immunohistochemical analysis revealed that SRE effectively suppressed M1 macrophage infiltration into the AD lesion. Furthermore, the anti-inflammatory effect of SRE was evaluated in LPS + INF-gamma induced bone marrow-derived macrophages (BMDMs) M1 polarization, SRE inhibited the production of TNF-alpha, CXC-10, IL-12, and IL-1beta and decreased the expression of NLRP3. Additionally, SRE was found to increase p-AMPK(T172), but had no effect on total AMPK expression, after administration of the AMPK inhibitor Compound C, the inhibitory effect of SRE on M1 macrophages was partially reversed. The results indicate that SRE has an inhibitory effect on AD, making it a potential therapeutic agent for this atopic disorder. CI - (c) 2024 Wiley Periodicals LLC. FAU - Wu, Wei AU - Wu W AUID- ORCID: 0000-0001-6710-6211 AD - School of Life Sciences, Ningxia University, Yinchuan, China. FAU - Song, Le AU - Song L AD - School of Life Sciences, Ningxia University, Yinchuan, China. FAU - Wang, Hong AU - Wang H AD - School of Life Sciences, Ningxia University, Yinchuan, China. FAU - Feng, Lu AU - Feng L AD - School of Life Sciences, Ningxia University, Yinchuan, China. FAU - Li, Zhenkai AU - Li Z AD - School of Life Sciences, Ningxia University, Yinchuan, China. FAU - Li, Yanqing AU - Li Y AD - School of Life Sciences, Ningxia University, Yinchuan, China. FAU - Li, Le AU - Li L AD - School of Life Sciences, Ningxia University, Yinchuan, China. FAU - Peng, Li AU - Peng L AD - School of Life Sciences, Ningxia University, Yinchuan, China. LA - eng GR - 2021FRD05024/Central Government Guided Local Special Basic Research Program/ GR - 2020AAC02013/Ningxia Natural Science Foundation of China/ GR - 2021BEG02042/Ningxia Provincial Key Research and Development Project/ PT - Journal Article DEP - 20240214 PL - United States TA - Environ Toxicol JT - Environmental toxicology JID - 100885357 RN - 0 (Dinitrochlorobenzene) RN - EC 2.7.11.31 (AMP-Activated Protein Kinases) RN - 142M471B3J (Carbon Dioxide) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (Cytokines) RN - 0 (Anti-Inflammatory Agents) RN - 187348-17-0 (Interleukin-12) RN - 0 (Lipids) SB - IM MH - Animals MH - Mice MH - *Dermatitis, Atopic/chemically induced/drug therapy/metabolism MH - Dinitrochlorobenzene/toxicity/therapeutic use MH - AMP-Activated Protein Kinases MH - Carbon Dioxide/toxicity/therapeutic use MH - Tumor Necrosis Factor-alpha MH - Cytokines/metabolism MH - Macrophages/metabolism MH - Anti-Inflammatory Agents/therapeutic use MH - Interleukin-12/toxicity/therapeutic use MH - Lipids MH - Mice, Inbred BALB C MH - Skin OTO - NOTNLM OT - AMPK activation OT - NLRP3 OT - Stellariae Radix supercritical CO2 fluid extract OT - atopic dermatitis OT - macrophages polarization EDAT- 2024/02/15 06:42 MHDA- 2024/04/17 06:42 CRDT- 2024/02/15 01:04 PHST- 2023/12/29 00:00 [revised] PHST- 2023/10/05 00:00 [received] PHST- 2024/01/06 00:00 [accepted] PHST- 2024/04/17 06:42 [medline] PHST- 2024/02/15 06:42 [pubmed] PHST- 2024/02/15 01:04 [entrez] AID - 10.1002/tox.24145 [doi] PST - ppublish SO - Environ Toxicol. 2024 May;39(5):3188-3197. doi: 10.1002/tox.24145. Epub 2024 Feb 14.