大黄素
MMP3型
关节炎
化学
软骨
炎症
基质金属蛋白酶
类风湿性关节炎
时间1
脚踝
医学
内科学
内分泌学
药理学
病理
解剖
生物化学
基因表达
基因
作者
Shuai Zhou,Wen‐Song Yang,Li Zeng,C Cao,Shiyun Yuan,X Rong
出处
期刊:PubMed
[National Institutes of Health]
日期:2023-10-20
卷期号:43 (10): 1776-1781
被引量:8
标识
DOI:10.12122/j.issn.1673-4254.2023.10.16
摘要
OBJECTIVE: To investigate the osteoprotective mechanism of emodin in light of the ferroptosis signaling pathway in a rat model of rheumatoid arthritis. METHODS: SD rat models of collagen-induced arthritis (CIA) were treated with methotrexate or low or high doses of emodin, and the changes in arthritis scores and toe volume were recorded. model of CIA rats. Malondialdehyde (MDA) content in the joint cartilage was determined, and ankle joint tissue pathologies were observed using caffein solid green staining and hematoxylin-spermine red staining. MMP3 and MMP13 expressions in the ankle joint tissues were detected using immunohistochemistry, and Western blotting was used to detect the protein expressions of ACSL4, SLC7A11, GPX4, and FTH1. RESULTS: <0.05). CONCLUSION: Emodin can effectively control joint inflammation and improve joint bone erosion in CIA rats possibly by inhibiting the ferroptosis signaling pathways and reducing the expressions of MMP3 and MMP13.
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