神经炎症
斑马鱼
氧化应激
线粒体
钙代谢
鱼藤酮
平衡
钙
兴奋毒性
药理学
生物
炎症
神经毒性
细胞生物学
神经退行性变
内科学
内分泌学
谷氨酸受体
免疫学
医学
生物化学
受体
疾病
毒性
基因
作者
İlknur Yurtsever,Ünsal Veli Üstündağ,İsmail Ünal,Perihan Seda Ateş,Ebru Emekli-Alturfan
标识
DOI:10.1080/01480545.2020.1846549
摘要
Among the mechanisms underlying Parkinson's disease, many pathogenic mechanisms are suggested to be effective such as oxidative stress, mitochondrial dysfunction, disruption of the ubiquitin-proteasome system, and neuroinflammation. Calcium is very important for neuronal and glial cells, neurodegenerative disease mechanisms are closely related to disturbed calcium homeostasis. Recent studies strongly support the role of inflammation in nigrostriatal degeneration in PD. In recent years, Rifampicin, a macrocyclic antibiotic has been shown to have a protective effect on neurons. This study aims to evaluate the effects of rifampicin in the experimental PD model induced by rotenone in zebrafish focusing on the relationship between calcium-dependent mitochondrial dysfunction and inflammation. Adult zebrafish were exposed to rotenone and rifampicin for 3 weeks. Locomotor activity was determined as the total distance that the zebrafish traveled for 5 min. Neuroinflammation and PD-related gene expressions were determined by RT-PCR. Mitochondrial calcium levels were determined using inductively coupled plasma-optical emission spectrometry (ICP-OES). Gamma synuclein, Park 7, Sigma-1 receptor expressions were determined by Western Blot. Our results show that rifampicin may be effective in reducing neuroinflammation, which may be an effective strategy to reduce mitochondrial dysfunction due to impaired calcium homeostasis in PD.
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