JAX2, an ethanol extract of Hyssopus cuspidatus Boriss, can prevent bronchial asthma by inhibiting MAPK/NF-κB inflammatory signaling.


Journal

Phytomedicine : international journal of phytotherapy and phytopharmacology
ISSN: 1618-095X
Titre abrégé: Phytomedicine
Pays: Germany
ID NLM: 9438794

Informations de publication

Date de publication:
Apr 2019
Historique:
received: 07 08 2018
revised: 18 12 2018
accepted: 29 12 2018
pubmed: 27 2 2019
medline: 25 6 2019
entrez: 27 2 2019
Statut: ppublish

Résumé

Hyssopus cuspidatus Boriss has been used to treat bronchial asthma for many years in Uighur medicine. JAX2, an ethanol extract from this plant, has effectiveness against bronchial asthma. However, the molecular basis for the anti-inflammatory effects of JAX2 remains unclear. This study aimed to evaluate the mechanism of JAX2 against bronchial asthma. We established an asthma model in rats using ovalbumin (OVA), and an inflammatory model in RAW264.7 cells using lipopolysaccharide (LPS) stimulation. To evaluate the anti-inflammatory effects of JAX2, the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-4, IL-6, IL-17, eotaxin and immunoglobulin (Ig)E were measured by enzyme-linked immunosorbent assay (ELISA). Cell viability was investigated by the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)2H-tetrazolium, inner salt (MTS) assay. Further, nitric oxide (NO) and reactive oxygen species (ROS) were determined using Griess reagent and 2,7-dichlorofluorescein diacetate. The phosphorylation of p-extracellular signal-regulated kinase (ERK), p-Jun-NH2-terminal kinase (JNK), p38 kinases (p38) and p-inhibitor of nuclear factor kappa-B kinase (IKK), and nuclear translocation of p-p65 kinases (p-p65) were determined by immunofluorescence to uncover the effects of JAX2 on the Mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways. After JAX2 administration to rats, Interferon (IFN)-γ concentrations in BALF increased significantly. Further, the concentrations of TNF-α, IL-4, IL-6, IL-17 and eotaxin in BALF, and IgE in serum decreased. JAX2 decreased TNF-α, IL-6 and NO in cell supernatant, and reduced ROS intracellularly. Concurrently, IFN-γ concentrations increased in cell supernatant significantly. In LPS-induced RAW264.7 cells, JAX2 inhibited phosphorylation of p-ERK, p-JNK and p-38 MAPK. The subsequent phosphorylation of p-IKK and nuclear translocation of the p-p65 subunit of NF-κB were also suppressed. Based on these findings, we believe that JAX2 has both preventive and treatment effects in bronchial asthma. Furthermore, in the RAW264.7 cell inflammatory model, JAX2 also inhibited NF-κB and MAPK signaling pathways.

Sections du résumé

BACKGROUND BACKGROUND
Hyssopus cuspidatus Boriss has been used to treat bronchial asthma for many years in Uighur medicine. JAX2, an ethanol extract from this plant, has effectiveness against bronchial asthma. However, the molecular basis for the anti-inflammatory effects of JAX2 remains unclear.
PURPOSE OBJECTIVE
This study aimed to evaluate the mechanism of JAX2 against bronchial asthma.
METHODS METHODS
We established an asthma model in rats using ovalbumin (OVA), and an inflammatory model in RAW264.7 cells using lipopolysaccharide (LPS) stimulation. To evaluate the anti-inflammatory effects of JAX2, the concentrations of tumor necrosis factor (TNF)-α, interleukin (IL)-4, IL-6, IL-17, eotaxin and immunoglobulin (Ig)E were measured by enzyme-linked immunosorbent assay (ELISA). Cell viability was investigated by the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)2H-tetrazolium, inner salt (MTS) assay. Further, nitric oxide (NO) and reactive oxygen species (ROS) were determined using Griess reagent and 2,7-dichlorofluorescein diacetate. The phosphorylation of p-extracellular signal-regulated kinase (ERK), p-Jun-NH2-terminal kinase (JNK), p38 kinases (p38) and p-inhibitor of nuclear factor kappa-B kinase (IKK), and nuclear translocation of p-p65 kinases (p-p65) were determined by immunofluorescence to uncover the effects of JAX2 on the Mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways.
RESULTS RESULTS
After JAX2 administration to rats, Interferon (IFN)-γ concentrations in BALF increased significantly. Further, the concentrations of TNF-α, IL-4, IL-6, IL-17 and eotaxin in BALF, and IgE in serum decreased. JAX2 decreased TNF-α, IL-6 and NO in cell supernatant, and reduced ROS intracellularly. Concurrently, IFN-γ concentrations increased in cell supernatant significantly. In LPS-induced RAW264.7 cells, JAX2 inhibited phosphorylation of p-ERK, p-JNK and p-38 MAPK. The subsequent phosphorylation of p-IKK and nuclear translocation of the p-p65 subunit of NF-κB were also suppressed.
CONCLUSION CONCLUSIONS
Based on these findings, we believe that JAX2 has both preventive and treatment effects in bronchial asthma. Furthermore, in the RAW264.7 cell inflammatory model, JAX2 also inhibited NF-κB and MAPK signaling pathways.

Identifiants

pubmed: 30807985
pii: S0944-7113(18)30635-4
doi: 10.1016/j.phymed.2018.12.043
pii:
doi:

Substances chimiques

Anti-Asthmatic Agents 0
Lipopolysaccharides 0
NF-kappa B 0
Plant Extracts 0
Nitric Oxide 31C4KY9ESH
Ethanol 3K9958V90M

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

305-314

Informations de copyright

Copyright © 2019 Elsevier GmbH. All rights reserved.

Auteurs

Fengjuan Yuan (F)

Xinjiang Institute of Materia Medica, Urumqi 830004, China; Xinjiang Uygur Autonomous Region for Food and Drug Control, Urumqi 830002, China.

Rui Liu (R)

Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050,China.

Mengying Hu (M)

Xinjiang Institute of Materia Medica, Urumqi 830004, China.

Xiaojuan Rong (X)

Xinjiang Institute of Materia Medica, Urumqi 830004, China.

Liping Bai (L)

Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050,China.

Lei Xu (L)

Xinjiang Institute of Materia Medica, Urumqi 830004, China.

Yan Mao (Y)

Xinjiang Institute of Materia Medica, Urumqi 830004, China.

Hamulati Hasimu (H)

Xinjiang Institute of Materia Medica, Urumqi 830004, China.

Yuhua Sun (Y)

Xinjiang Institute of Materia Medica, Urumqi 830004, China. Electronic address: 1641636482@qq.com.

Jinhua He (J)

Xinjiang Institute of Materia Medica, Urumqi 830004, China. Electronic address: hejh1216@163.com.

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Classifications MeSH