PUBLICATION
            Rifampicin decreases neuroinflammation to maintain mitochondrial function and calcium homeostasis in rotenone-treated zebrafish
- Authors
 - Yurtsever, İ., Üstündağ, Ü.V., Ünal, İ., Ateş, P.S., Emekli-Alturfan, E.
 - ID
 - ZDB-PUB-201120-121
 - Date
 - 2020
 - Source
 - Drug and chemical toxicology 45(4): 1544-1551 (Journal)
 - Registered Authors
 - Emekli-Alturfan, Ebru, Üstündağ, Ünsal Veli
 - Keywords
 - Parkinson’s disease, Rifampicin, calcium, neuroinflammation, zebrafish
 - MeSH Terms
 - 
    
        
        
            
                
- Mitochondria
 - Inflammation/chemically induced
 - Inflammation/drug therapy
 - Oxidative Stress
 - Calcium/metabolism
 - Zebrafish/metabolism
 - Animals
 - Rifampin/toxicity
 - Neurodegenerative Diseases*/metabolism
 - Homeostasis
 - Rotenone*/toxicity
 - Neuroinflammatory Diseases
 
 - PubMed
 - 33187454 Full text @ Drug Chem. Toxicol.
 
            Citation
        
        
            Yurtsever, İ., Üstündağ, Ü.V., Ünal, İ., Ateş, P.S., Emekli-Alturfan, E. (2020) Rifampicin decreases neuroinflammation to maintain mitochondrial function and calcium homeostasis in rotenone-treated zebrafish. Drug and chemical toxicology. 45(4):1544-1551.
        
    
                
                    
                        Abstract
                    
                    
                
                
            
        
        
    
        
            
            
 
    
    
        
    
    
    
        
                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.
            
    
        
        
    
    
    
                
                    
                        Genes / Markers
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Expression
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Phenotype
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mutations / Transgenics
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Human Disease / Model
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Sequence Targeting Reagents
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Fish
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Orthology
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Engineered Foreign Genes
                    
                    
                
                
            
        
        
    
        
            
            
        
        
    
    
    
                
                    
                        Mapping