Effects of Kumaizasa (


Journal

Anticancer research
ISSN: 1791-7530
Titre abrégé: Anticancer Res
Pays: Greece
ID NLM: 8102988

Informations de publication

Date de publication:
Aug 2021
Historique:
received: 22 05 2021
revised: 22 06 2021
accepted: 28 06 2021
entrez: 20 7 2021
pubmed: 21 7 2021
medline: 30 7 2021
Statut: ppublish

Résumé

We investigated the effect of Kumaizasa leaf extract (KLE) on innate immunity using the HEK293 and RAW 264.7 cell lines. KLE, lipopolysaccharides (LPS), or KLE with LPS were added to RAW 264.7 cells. The TNF-α and IL-1β mRNA expression was then quantified. The expression of MAPKs, NFĸB, TNF-α and IL-1β proteins was also quantified. In addition, KLE was added to HEK293 cells and the IL-8 concentration was measured. In RAW 264.7 cells, KLE increased the levels of TNF-α and IL-1β mRNA. By contrast, when KLE and LPS were added to RAW 264.7 cells, the increase in TNF-α and IL-1β mRNA was ameliorated. Similarly, the expression of JNK and ERK proteins was reduced. The addition of KLE to HEK293 cells induced IL-8 production. Based on these results, a KLE-mediated mechanism may regulate immunity by suppressing the expression of JNK and ERK, which are involved in inflammatory signal transduction.

Sections du résumé

BACKGROUND/AIM OBJECTIVE
We investigated the effect of Kumaizasa leaf extract (KLE) on innate immunity using the HEK293 and RAW 264.7 cell lines.
MATERIALS AND METHODS METHODS
KLE, lipopolysaccharides (LPS), or KLE with LPS were added to RAW 264.7 cells. The TNF-α and IL-1β mRNA expression was then quantified. The expression of MAPKs, NFĸB, TNF-α and IL-1β proteins was also quantified. In addition, KLE was added to HEK293 cells and the IL-8 concentration was measured.
RESULTS RESULTS
In RAW 264.7 cells, KLE increased the levels of TNF-α and IL-1β mRNA. By contrast, when KLE and LPS were added to RAW 264.7 cells, the increase in TNF-α and IL-1β mRNA was ameliorated. Similarly, the expression of JNK and ERK proteins was reduced. The addition of KLE to HEK293 cells induced IL-8 production.
CONCLUSION CONCLUSIONS
Based on these results, a KLE-mediated mechanism may regulate immunity by suppressing the expression of JNK and ERK, which are involved in inflammatory signal transduction.

Identifiants

pubmed: 34281880
pii: 41/8/4093
doi: 10.21873/anticanres.15212
doi:

Substances chimiques

Cytokines 0
Lipopolysaccharides 0
Plant Extracts 0
Extracellular Signal-Regulated MAP Kinases EC 2.7.11.24
JNK Mitogen-Activated Protein Kinases EC 2.7.11.24

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

4093-4100

Informations de copyright

Copyright © 2021 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved.

Auteurs

Keisuke Sato (K)

Faculty of Pharmaceutical Sciences, Hokkaido University of Science, Sapporo, Japan.

Ryosuke Tatsunami (R)

Faculty of Pharmaceutical Sciences, Hokkaido University of Science, Sapporo, Japan.

Akifumi Nakata (A)

Faculty of Pharmaceutical Sciences, Hokkaido University of Science, Sapporo, Japan.

Ken-Ichi Komatsu (KI)

Faculty of Pharmaceutical Sciences, Hokkaido University of Science, Sapporo, Japan.

Shinji Harakawa (S)

Bio-Self Regulating Science Laboratory, Obihiro University of Agriculture and Veterinary Medicine, Obihiro, Japan.
Hakuju Institute for Health Science Co. Ltd., Tokyo, Japan.

Takaki Nedachi (T)

Hakuju Institute for Health Science Co. Ltd., Tokyo, Japan.

Kaoru Haketa (K)

Hakuju Institute for Health Science Co. Ltd., Tokyo, Japan.

Hiroyuki Inagawa (H)

Control of Innate Immunity, Technology Research Association, Takamatsu, Japan.
Research Institute for Healthy Living, Niigata University of Pharmacy and Applied Life Sciences, Niigata, Japan.

Koji Wakame (K)

Faculty of Pharmaceutical Sciences, Hokkaido University of Science, Sapporo, Japan wakame-k@hus.ac.jp.

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Classifications MeSH