scholarly journals Adenosine A1 and A2A receptors are involved on guanosine protective effects against oxidative burst and mitochondrial dysfunction induced by 6-OHDA in striatal slices

2021 ◽  
Author(s):  
C. M. Massari ◽  
L. C. Constantino ◽  
C. I. Tasca
Keyword(s):  
Mitochondrial Dysfunction ◽  
Oxidative Burst ◽  
Protective Effects ◽  
Striatal Slices ◽  
A2a Receptors ◽  
Adenosine A1

Involvement of Adenosine A1 and A2A Receptors in the Adenosinergic Modulation of the Discriminative-Stimulus Effects of Cocaine and Methamphetamine in Rats

2003 ◽  
Vol 307 (3) ◽  
pp. 977-986 ◽  
Author(s):  
Zuzana Justinova ◽  
Sergi Ferré ◽  
Pavan N. Segal ◽  
Katerina Antoniou ◽  
Marcello Solinas ◽  
...  
Keyword(s):  
Discriminative Stimulus ◽  
A2a Receptors ◽  
Discriminative Stimulus Effects ◽  
Adenosine A1 ◽  
Stimulus Effects

Roles of adenosine A1 and A2A receptors in the expression and development of methamphetamine-induced sensitization

2000 ◽  
Vol 388 (3) ◽  
pp. 249-254 ◽  
Author(s):  
Takao Shimazoe ◽  
Akiko Yoshimatsu ◽  
Atsuko Kawashimo ◽  
Shigenori Watanabe
Keyword(s):  
A2a Receptors ◽  
Adenosine A1

Adenosine A1 and A2a receptors modulate the nitrergic system in cell culture from dorsomedial medulla oblongata

2020 ◽  
Vol 229 ◽  
pp. 102737
Author(s):  
M.A. Costa ◽  
J.P.P. Matsumoto ◽  
D.C. Carrettiero ◽  
D.R. Fior-Chadi
Keyword(s):  
Cell Culture ◽  
Medulla Oblongata ◽  
A2a Receptors ◽  
Adenosine A1

scholarly journals Proanthocyanidins-Mediated Nrf2 Activation Ameliorates Glucocorticoid-Induced Oxidative Stress and Mitochondrial Dysfunction in Osteoblasts

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Liang Chen ◽  
Sun-Li Hu ◽  
Jun Xie ◽  
De-Yi Yan ◽  
She-Ji Weng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Low Dose ◽  
Distal Femur ◽  
Therapeutic Potential ◽  
Protective Effects ◽  
Nrf2 Pathway ◽  
Pathway Activation ◽  
Nrf2 Activation ◽  
Osteoblast Apoptosis

The widespread use of therapeutic glucocorticoids has increased the frequency of glucocorticoid-induced osteoporosis (GIOP). One of the potential pathological processes of GIOP is an increased level of oxidative stress and mitochondrial dysfunction, which eventually leads to osteoblast apoptosis. Proanthocyanidins (PAC) are plant-derived antioxidants that have therapeutic potential against GIOP. In our study, a low dose of PAC was nontoxic to healthy osteoblasts and restored osteogenic function in dexamethasone- (Dex-) treated osteoblasts by suppressing oxidative stress, mitochondrial dysfunction, and apoptosis. Mechanistically, PAC neutralized Dex-induced damage in the osteoblasts by activating the Nrf2 pathway, since silencing Nrf2 partly eliminated the protective effects of PAC. Furthermore, PAC injection restored bone mass and promoted the expression of Nrf2 in the distal femur of Dex-treated osteoporotic rats. In summary, PAC protect osteoblasts against Dex-induced oxidative stress and mitochondrial dysfunction via the Nrf2 pathway activation and may be a promising drug for treating GIOP.

scholarly journals Gating and the Need for Sleep: Dissociable Effects of Adenosine A1 and A2A Receptors

2019 ◽  
Vol 13 ◽  
Author(s):  
Michael Lazarus ◽  
Yo Oishi ◽  
Theresa E. Bjorness ◽  
Robert W. Greene
Keyword(s):  
A2a Receptors ◽  
Adenosine A1

scholarly journals Mitochondria-Targeted Antioxidants for Treatment of Hearing Loss: A Systematic Review

Antioxidants ◽  
2019 ◽  
Vol 8 (4) ◽  
pp. 109 ◽  
Author(s):  
Chisato Fujimoto ◽  
Tatsuya Yamasoba
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Mitochondrial Dysfunction ◽  
Cell Lines ◽  
Mitochondrial Gene ◽  
Protective Effects ◽  
Drug Induced ◽  
Age Related ◽  
Cochlear Damage ◽  
Age Related Hearing Loss

Mitochondrial dysfunction is associated with the etiologies of sensorineural hearing loss, such as age-related hearing loss, noise- and ototoxic drug-induced hearing loss, as well as hearing loss due to mitochondrial gene mutation. Mitochondria are the main sources of reactive oxygen species (ROS) and ROS-induced oxidative stress is involved in cochlear damage. Moreover, the release of ROS causes further damage to mitochondrial components. Antioxidants are thought to counteract the deleterious effects of ROS and thus, may be effective for the treatment of oxidative stress-related diseases. The administration of mitochondria-targeted antioxidants is one of the drug delivery systems targeted to mitochondria. Mitochondria-targeted antioxidants are expected to help in the prevention and/or treatment of diseases associated with mitochondrial dysfunction. Of the various mitochondria-targeted antioxidants, the protective effects of MitoQ and SkQR1 against ototoxicity have been previously evaluated in animal models and/or mouse auditory cell lines. MitoQ protects against both gentamicin- and cisplatin-induced ototoxicity. SkQR1 also provides auditory protective effects against gentamicin-induced ototoxicity. On the other hand, decreasing effect of MitoQ on gentamicin-induced cell apoptosis in auditory cell lines has been controversial. No clinical studies have been reported for otoprotection using mitochondrial-targeted antioxidants. High-quality clinical trials are required to reveal the therapeutic effect of mitochondria-targeted antioxidants in terms of otoprotection in patients.

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