Protective effects of Da-cheng-qi decoction in rats with intracerebral hemorrhage.


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:
Sep 2021
Historique:
received: 30 01 2021
revised: 15 05 2021
accepted: 10 06 2021
pubmed: 5 7 2021
medline: 30 9 2021
entrez: 4 7 2021
Statut: ppublish

Résumé

Intracerebral hemorrhage (ICH), the most fatal subtype of stroke, has no disease-modifying treatment. Da-cheng-qi decoction (DCQ), composed of rhubarb, is one of the most commonly used Chinese traditional decoctions in ICH treatment. But the mechanism is not clear. Emodin is an active compound found in rhubarb. To study the protective effects of DCQ on ICH and its possible mechanisms of action. The ICH model was reproduced by injecting collagenase-VII into the left caudate putamen (CPu) of rats. DCQ and emodin were used to treat the ICH rats for 7 days. Behavior tests, proteomic analysis, morphological studies, and western blotting were performed. The neurological deficits in the ICH rats recovered with DCQ and emodin on the 14 The protective effects of DCQ on ICH were confirmed in this study, and its mechanism may be related to the inhibition of MAPK and activation of M2 microglia. These results are beneficial to the development of ICH therapeutic targets.

Sections du résumé

BACKGROUND BACKGROUND
Intracerebral hemorrhage (ICH), the most fatal subtype of stroke, has no disease-modifying treatment. Da-cheng-qi decoction (DCQ), composed of rhubarb, is one of the most commonly used Chinese traditional decoctions in ICH treatment. But the mechanism is not clear. Emodin is an active compound found in rhubarb.
PURPOSE OBJECTIVE
To study the protective effects of DCQ on ICH and its possible mechanisms of action.
METHODS METHODS
The ICH model was reproduced by injecting collagenase-VII into the left caudate putamen (CPu) of rats. DCQ and emodin were used to treat the ICH rats for 7 days. Behavior tests, proteomic analysis, morphological studies, and western blotting were performed.
RESULTS RESULTS
The neurological deficits in the ICH rats recovered with DCQ and emodin on the 14
CONCLUSION CONCLUSIONS
The protective effects of DCQ on ICH were confirmed in this study, and its mechanism may be related to the inhibition of MAPK and activation of M2 microglia. These results are beneficial to the development of ICH therapeutic targets.

Identifiants

pubmed: 34217968
pii: S0944-7113(21)00173-2
doi: 10.1016/j.phymed.2021.153630
pii:
doi:

Substances chimiques

Da-Cheng-Qi 0
Drugs, Chinese Herbal 0
p38 Mitogen-Activated Protein Kinases EC 2.7.11.24
Emodin KA46RNI6HN

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

153630

Informations de copyright

Copyright © 2021. Published by Elsevier GmbH.

Auteurs

Peng Zeng (P)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China.

Xiao-Ming Wang (XM)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China.

Hong-Fei Su (HF)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China.

Teng Zhang (T)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China.

Lin-Na Ning (LN)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China.

Yan Shi (Y)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China.

Shu-Sheng Yang (SS)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China; Department of Traditional Chinese Medicine, Wuhan Red Cross Hospital, Wuhan 430015, China. Electronic address: elibaba1972@163.com.

Li Lin (L)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China; Laboratory of Medical Molecular and Cellular Biology, College of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan 430065, China. Electronic address: linli@hbtcm.edu.cn.

Qing Tian (Q)

Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Key Laboratory of Neurological Disease of National Education Ministry and Hubei Province, Huazhong University of Science and Technology, Wuhan 430030, China. Electronic address: tianq@hust.edu.cn.

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