Protective effects of Lizhong decoction on ulcerative colitis in mice by suppressing inflammation and ameliorating gut barrier.
Animals
Anti-Inflammatory Agents
/ pharmacology
Colitis, Ulcerative
/ chemically induced
Colon
/ drug effects
Cytokines
/ metabolism
Dextran Sulfate
Drugs, Chinese Herbal
/ pharmacology
Inflammation
/ drug therapy
Intestinal Mucosa
/ metabolism
Male
Mice
Mice, Inbred C57BL
NF-kappa B
/ metabolism
Tight Junction Proteins
/ metabolism
Tight Junctions
/ metabolism
Toll-Like Receptor 4
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
Cytokines
LZD
Tight junction proteins
Ulcerative colitis
Journal
Journal of ethnopharmacology
ISSN: 1872-7573
Titre abrégé: J Ethnopharmacol
Pays: Ireland
ID NLM: 7903310
Informations de publication
Date de publication:
15 Sep 2020
15 Sep 2020
Historique:
received:
06
08
2019
revised:
21
04
2020
accepted:
25
04
2020
pubmed:
4
5
2020
medline:
26
2
2021
entrez:
4
5
2020
Statut:
ppublish
Résumé
Lizhong Decoction (LZD) is a classical prescription firstly recorded in "Shanghan Lun". It has been used to clinically treat ulcerative colitis (UC) for thousands of years. However, its mechanism is not clear up to now. The goal of this study was to assess the amelioration of LZD on dextran sodium sulfate (DSS)-induced colitis in mice and further clarify its mechanism. The ulcerative colitis model induced by DSS was successfully established and applied to evaluate the intervention effect after oral administration of LZD. Furthermore, the expression of key targets in inflammatory signaling pathways and intestinal tight junction proteins were investigated by enzyme-linked immunosorbent assay (ELISA) and quantitative real time polymerase chain reaction (qPCR) analysis. The results showed that all doses of LZD could notably improve DSS-induced colon lesions, reduce histological scores, prolong colon length and increase body weight. Colonic inflammation in UC mice was significantly alleviated by inhibiting the activities of myeloperoxidase (MPO) and superoxide dismutase (SOD), reducing the yield of nitric oxide (NO) and inflammatory cytokines such as interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6), and along with promoting the production of anti-inflammatory cytokines such as interleukin-4 (IL-4) and interleukin-10 (IL-10) after LZD treatment. Furthermore, LZD remarkably down-regulated the level of toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) mRNA and up-regulated the expression of tight junction proteins (zonula occluden-1, occludin and claudin-1) in UC mice. In summary, this study indicated that LZD could notably improve UC symptoms by suppressing inflammation and ameliorating gut barrier, which provided scientific basis for its clinical application in the future.
Identifiants
pubmed: 32360800
pii: S0378-8741(19)33136-8
doi: 10.1016/j.jep.2020.112919
pii:
doi:
Substances chimiques
Anti-Inflammatory Agents
0
Cytokines
0
Drugs, Chinese Herbal
0
NF-kappa B
0
Tight Junction Proteins
0
Toll-Like Receptor 4
0
Tumor Necrosis Factor-alpha
0
yijung-tang
0
Dextran Sulfate
9042-14-2
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
112919Informations de copyright
Copyright © 2020 Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors declare that they have no conflicts of interest.