Cytisine is neuroprotective in female but not male 6‐hydroxydopamine lesioned parkinsonian mice and acts in combination with 17‐β‐estradiol to inhibit apoptotic endoplasmic reticulum stress in dopaminergic neurons

2020 ◽  
Author(s):  
Sara M. Zarate ◽  
Gauri Pandey ◽  
Sunanda Chilukuri ◽  
Jose A. Garcia ◽  
Brittany Cude ◽  
...  
2018 ◽  
Vol 56 (6) ◽  
pp. 3865-3881 ◽  
Author(s):  
Govindhasamy Pushpavathi Selvakumar ◽  
Shankar S Iyer ◽  
Duraisamy Kempuraj ◽  
Mohammad Ejaz Ahmed ◽  
Ramasamy Thangavel ◽  
...  

2022 ◽  
Vol 145 ◽  
pp. 112389
Author(s):  
Sora Kang ◽  
Ying Piao ◽  
Young Cheol Kang ◽  
Suyeol Lim ◽  
Youngmi Kim Pak

2007 ◽  
Vol 293 (6) ◽  
pp. C1884-C1894 ◽  
Author(s):  
Katsura Takano ◽  
Yasuko Kitao ◽  
Yoshiyuki Tabata ◽  
Hikari Miura ◽  
Kosuke Sato ◽  
...  

The enhancement of intracellular stresses such as oxidative stress and endoplasmic reticulum (ER) stress has been implicated in several neurodegenerative disorders including Parkinson's disease (PD). During a search for compounds that regulate ER stress, a dibenzoylmethane (DBM) derivative 14-26 (2,2′-dimethoxydibenzoylmethane) was identified as a novel neuroprotective agent. Analysis in SH-SY5Y cells and in PC12 cells revealed that the regulation of ER stress by 14-26 was associated with its anti-oxidative property. 14-26 prevented the production of reactive oxygen species (ROS) when the cells were exposed to oxidants such as hydrogen peroxide and 6-hydroxydopamine (6-OHDA) or an ER stressor brefeldin A (BFA). 14-26 also prevented ROS-induced damage in both the ER and the mitochondria, including the protein carbonylation in the microsome and the reduction of the mitochondrial membrane potential. Further examination disclosed the presence of the iron-chelating activity in 14-26. In vivo, 14-26 suppressed both oxidative stress and ER stress and prevented neuronal death in the substantia nigra pars compacta (SNpc) after injection of 6-OHDA in mice. These results suggest that 14-26 is an antioxidant that protects dopaminergic neurons against both oxidative stress and ER stress and could be a therapeutic candidate for the treatment of PD.


2009 ◽  
Vol 459 (1) ◽  
pp. 7-10 ◽  
Author(s):  
Yun-Mi Oh ◽  
Eun-Hee Jang ◽  
Jeong-Hyeon Ko ◽  
Ju-Hee Kang ◽  
Chang-Shin Park ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Shiba Niu ◽  
Weibo Shi ◽  
Yingmin Li ◽  
Shanyong Yi ◽  
Yang Li ◽  
...  

An increasing number of people are in a state of stress due to social and psychological pressures, which may result in mental disorders. Previous studies indicated that mesencephalic dopaminergic neurons are associated with not only reward-related behaviors but also with stress-induced mental disorders. To explore the effect of stress on dopaminergic neuron and potential mechanism, we established stressed rat models of different time durations and observed pathological changes in dopaminergic neurons of the ventral tegmental area (VTA) through HE and thionine staining. Immunohistochemistry coupled with microscopy-based multicolor tissue cytometry (MMTC) was employed to investigate the number changes of dopaminergic neurons. Double immunofluorescence labelling was used to investigate expression changes of endoplasmic reticulum stress (ERS) protein GRP78 and CHOP in dopaminergic neurons. Our results showed that prolonged stress led to pathological alteration in dopaminergic neurons of VTA, such as missing of Nissl bodies and pyknosis in dopaminergic neurons. Immunohistochemistry with MMTC indicated that chronic stress exposure resulted in a significant decrease in dopaminergic neurons. Double immunofluorescence labelling showed that the endoplasmic reticulum stress protein took part in the injury of dopaminergic neurons. Taken together, these results indicated the involvement of ERS in mesencephalic dopaminergic neuron injury induced by stress exposure.


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