Inflammatory Response and Oxidative Stress in the Degeneration of Dopamine Neurons in Parkinson's Disease

2001 ◽  
Author(s):  
Catherine Mytilineou
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Inflammatory Response ◽  
Dopamine Neurons ◽  
And Oxidative Stress

Explore the Effects of Fe3O4 Nanoparticles and Oxidative Stress and Neuroinflammatory Responses on the Intestinal Flora Based on a Parkinson Rat Model

2021 ◽  
Vol 21 (2) ◽  
pp. 1176-1183
Author(s):  
Li Xu ◽  
Tuexun Mayila ◽  
Jie Wang
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Inflammatory Response ◽  
Rat Model ◽  
Clinical Symptoms ◽  
Synergistic Effects ◽  
Intestinal Flora ◽  
And Oxidative Stress

Parkinson’s disease is a degenerative disease of the central nervous system, and it occurs in middle-aged and elderly people. Studies have shown that both the clinical symptoms and neuropathological evidence of Parkinson’s disease suggest that Parkinson’s disease may originate in the gut. Intestinal flora homeostasis plays an important role in maintaining normal functions of the brain and nervous system. It participates in changes in cellular flora through oxidative stress, inflammatory response, and immune response during metabolism. Intestinal flora disorders are closely related to the onset of neurological diseases such as Parkinson’s disease (PD). In order to better understand the relationship between intestinal flora and Parkinson’s disease, this article studies the correlation between PD rat models and intestinal flora, and analyzes the possible relationship between them. The 6-OHDA PD rat model is currently a better model preparation method, which is widely used in PD research. The experimental results show that using Fe3O4 nanoparticle technology to detect intestinal flora disorders in PD patients, and the role of intestinal flora disorders in Parkinson’s disease may include affecting inflammatory response and oxidative stress, α-synuclein Protein (α-syn), these modes of action are not independent, there are complex and synergistic effects, and the molecular simulation mechanism may play a key role in these effects. There is a certain relationship between intestinal flora and Parkinson’s disease, but the specific mechanism is not clear, and further research is needed to provide more directions for the early diagnosis and early treatment of PD.

scholarly journals Inhibition of Microglia-Derived Oxidative Stress by Ciliary Neurotrophic Factor Protects Dopamine Neurons In Vivo from MPP+ Neurotoxicity

2018 ◽  
Vol 19 (11) ◽  
pp. 3543 ◽  
Author(s):  
Jeong Baek ◽  
Jae Jeong ◽  
Kyoung Kim ◽  
So-Yoon Won ◽  
Young Chung ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurotrophic Factor ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Ciliary Neurotrophic Factor ◽  
Dopamine Neurons ◽  
Transient Receptor Potential Vanilloid

We demonstrated that capsaicin (CAP), an agonist of transient receptor potential vanilloid subtype 1 (TRPV1), inhibits microglia activation and microglia-derived oxidative stress in the substantia nigra (SN) of MPP+-lesioned rat. However, the detailed mechanisms how microglia-derived oxidative stress is regulated by CAP remain to be determined. Here we report that ciliary neurotrophic factor (CNTF) endogenously produced by CAP-activated astrocytes through TRPV1, but not microglia, inhibits microglial activation and microglia-derived oxidative stress, as assessed by OX-6 and OX-42 immunostaining and hydroethidine staining, respectively, resulting in neuroprotection. The significant increase in levels of CNTF receptor alpha (CNTFRα) expression was evident on microglia in the MPP+-lesioned rat SN and the observed beneficial effects of CNTF was abolished by treatment with CNTF receptor neutralizing antibody. It is therefore likely that CNTF can exert its effect via CNTFRα on microglia, which rescues dopamine neurons in the SN of MPP+-lesioned rats and ameliorates amphetamine-induced rotations. Immunohistochemical analysis revealed also a significantly increased expression of CNTFRα on microglia in the SN from human Parkinson’s disease patients compared with age-matched controls, indicating that these findings may have relevance to the disease. These data suggest that CNTF originated from TRPV1 activated astrocytes may be beneficial to treat neurodegenerative disease associated with neuro-inflammation such as Parkinson’s disease.

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