PMID- 38163133
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240103
IS  - 2405-8440 (Print)
IS  - 2405-8440 (Electronic)
IS  - 2405-8440 (Linking)
VI  - 10
IP  - 1
DP  - 2024 Jan 15
TI  - Jianpi Yangxue Qufeng compound alleviates atopic dermatitis via TLR4/MyD88/NF-kappaB 
      signaling pathway.
PG  - e23278
LID - 10.1016/j.heliyon.2023.e23278 [doi]
LID - e23278
AB  - BACKGROUND: Jianpi Yangxue Qufeng Compound (JPYXQFC) is a Chinese medicine widely 
      used in the clinical treatment of atopic dermatitis (AD) and has a significantly 
      therapeutic effect. However, the mechanism of JPYXQFC in AD has been not 
      understood clearly. OBJECTIVE: This study aimed to explore the effect of JPYXQFC 
      on AD model cells and rats by regulating TLR4/MyD88/NF-kappaB signaling pathway. 
      METHODS: The rats (n > 5) were given JPYXQFC decoction orally twice a day for 
      three days, and their abdominal aortic blood was collected. HaCaT cell 
      proliferation rate was tested by cell counting kit-8 (CCK-8) assays. We induced 
      AD rat model through 2, 4-dinitrofluorobenzene (DNFB). AD rats were given oral 
      JPYXQFC decoction and cetirizine (positive control). HaCaT cells were pretreated 
      with JPYXQFC drug serum or cetirizine for 0.5 h and then stimulated with 
      TNF-alpha/IFN-gamma for 1 h. The mRNA levels of TLR4, MyD88, NF-kappaB, IL-4, IL-13, MCP1, 
      TNF-alpha and TSLP were detected by quantitative real-time PCR (Q-RT-PCR), and 
      TLR4/MyD88/NF-kappaB pathway protein expression was tested by Western blot. The total 
      serum levels of immunoglobulin E (IgE), thymus and activation regulated 
      chemokine/chemokine (C-C motif) ligand 17 (TARC/CCL17) were detected by 
      enzyme-linked immunosorbent assay (ELISA). The epidermal thickness was detected 
      by hematoxylin and eosin (HE) staining. The dermatitis area and score were 
      measured by a ruler and a four-point scoring method, respectively. RESULTS: 
      JPYXQFC significantly inhibited mRNA and protein expression of the 
      TLR4/MyD88/NF-kappaB pathway and Histone H3 in TNF-alpha/IFN-gamma-induced HaCaT cells and 
      DNFB-induced rats, decreased the mRNA of IL-4, IL-13, MCP1, CCL22, TSLP and the 
      level of AD-related genes IgE and TAEC/CCL17 of TNF-alpha/IFN-gamma-induced HaCaT cells. 
      Meanwhile, JPYXQFC significantly reduced the dermatitis area and dermatitis score 
      in DNFB-induced rats, inhibited the levels of pro-inflammatory cytokines IL-6 and 
      TNF-alpha, and upregulated FLG, as well as inhibited the levels of IgE and TARC/CCL17 
      in the serum of AD rats. CONCLUSION: JPYXQFC alleviates AD by inhibiting the 
      activation of TLR4/MyD88/NF-kappaB pathway.
CI  - (c) 2023 The Authors.
FAU - Yang, Xuesong
AU  - Yang X
AD  - Department of Dermatology, First Affiliated Hospital of Yunnan University of 
      Chinese Medicine, Kunming 650032, Yunnan, China.
FAU - Wang, Zhimin
AU  - Wang Z
AD  - Department of Dermatology, First Affiliated Hospital of Yunnan University of 
      Chinese Medicine, Kunming 650032, Yunnan, China.
FAU - Huang, Hong
AU  - Huang H
AD  - Department of Dermatology, First Affiliated Hospital of Yunnan University of 
      Chinese Medicine, Kunming 650032, Yunnan, China.
FAU - Luo, Guangyun
AU  - Luo G
AD  - College of Basic Medicine, Yunnan University of Chinese Medicine, Kunming 650500, 
      Yunnan, China.
FAU - Cong, Lin
AU  - Cong L
AD  - Department of Dermatology, First Affiliated Hospital of Yunnan University of 
      Chinese Medicine, Kunming 650032, Yunnan, China.
FAU - Yang, Jianting
AU  - Yang J
AD  - Department of Dermatology, First Affiliated Hospital of Yunnan University of 
      Chinese Medicine, Kunming 650032, Yunnan, China.
FAU - Ye, Jianzhou
AU  - Ye J
AD  - Department of Dermatology, First Affiliated Hospital of Yunnan University of 
      Chinese Medicine, Kunming 650032, Yunnan, China.
LA  - eng
PT  - Journal Article
DEP - 20231203
PL  - England
TA  - Heliyon
JT  - Heliyon
JID - 101672560
PMC - PMC10757010
OTO - NOTNLM
OT  - Atopic dermatitis
OT  - Inflammation
OT  - TLR4/MyD88/NF-kappaB signaling pathway
COIS- The authors declare that they have no known competing financial interests or 
      personal relationships that could have appeared to influence the work reported in 
      this paper.
EDAT- 2024/01/02 11:43
MHDA- 2024/01/02 11:44
PMCR- 2023/12/03
CRDT- 2024/01/01 04:36
PHST- 2023/07/19 00:00 [received]
PHST- 2023/11/23 00:00 [revised]
PHST- 2023/11/30 00:00 [accepted]
PHST- 2024/01/02 11:44 [medline]
PHST- 2024/01/02 11:43 [pubmed]
PHST- 2024/01/01 04:36 [entrez]
PHST- 2023/12/03 00:00 [pmc-release]
AID - S2405-8440(23)10486-5 [pii]
AID - e23278 [pii]
AID - 10.1016/j.heliyon.2023.e23278 [doi]
PST - epublish
SO  - Heliyon. 2023 Dec 3;10(1):e23278. doi: 10.1016/j.heliyon.2023.e23278. eCollection 
      2024 Jan 15.