重症肌无力
医学
蛋白激酶B
PI3K/AKT/mTOR通路
炎症
骨骼肌
车站3
肌肉无力
药理学
信号转导
癌症研究
免疫学
内科学
细胞生物学
生物
作者
Yuanfeng Zeng,Haihua Zeng,Xinghua Liu,Tingting Fan
出处
期刊:Allergologia et immunopathologia
[Codon Publications]
日期:2024-09-01
卷期号:52 (5): 59-64
标识
DOI:10.15586/aei.v52i5.1147
摘要
Acquired myasthenia (AM), a debilitating autoimmune disease, is typically characterized by skeletal muscle fatigue and weakness. Despite advances in myasthenia gravis treatment, current approaches remain unsatisfactory and many result in unexpected side effects. Traditional Chinese medicine has shown great potential in the treatment of myasthenia gravis, including relieving myasthenic symptoms, improving patients' quality of life, and reducing Western medicine side effects. This study investigates the protective effects and mechanism of BZYQD in mice with acquired myasthenia. BZYQD alleviates the reduced grip strength and increased expression of MAFbx and MuRF-1 in mice with acquired myasthenia. It also reduces levels of pro-inflammatory factors IL-1β, IL-6, and TNF-α in the mouse serum. In addition, BZYQD reduces ROS accumulation and the mitochondrial ROS production rate, while increasing ATP levels and mitochondrial membrane potential in mice with acquired myasthenia. Moreover, BZYQD decreases the expression of p-JAK2, p-STAT3, and p-AKT in the skeletal muscle of mice with acquired myasthenia. In summary, BZYQD reduces inflammation, enhances mitochondrial function, and regulates the JAK2/STAT3/AKT signaling pathway to treat acquired myasthenia.
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