Adenosine A1 Receptor Induced Delayed Cardioprotection: Investigation into Time-Course and Cellular Mechanisms

1999 ◽  
Vol 97 (s41) ◽  
pp. 12P-12P
Author(s):  
A Dana ◽  
DM Yellon
Keyword(s):  
Time Course ◽  
Adenosine A1 Receptor ◽  
Cellular Mechanisms ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Delayed Cardioprotection

Time course of action of three adenosine A1 receptor agonists with differing lipophilicity in rats: comparison of pharmacokinetic, haemodynamic and EEG effects

1997 ◽  
Vol 356 (6) ◽  
pp. 827-837 ◽  
Author(s):  
E. A. van Schaick ◽  
C. Kulkarni ◽  
J. K. von Frijtag Drabbe Künzel ◽  
R. A. A. Mathôt ◽  
G. Cristalli ◽  
...  
Keyword(s):  
Time Course ◽  
Adenosine A1 Receptor ◽  
Receptor Agonists ◽  
Course Of Action ◽  
Adenosine A1 ◽  
A1 Receptor

Adenosine A1 Receptor Antagonist Up-regulates Casp3 and Stimulates Apoptosis Rate in Breast Cancer Cell Line T47D

2020 ◽  
Vol 9 (1) ◽  
pp. 14-20
Author(s):  
Mohammad Zamani Rarani ◽  
Fahimeh Zamani Rarani ◽  
Ali Valiani ◽  
Zeinolabedin Shrifian Dastjerdi ◽  
Elias Kargar Abargouei ◽  
...  
Keyword(s):  
Cell Line ◽  
Cancer Cell Line ◽  
P53 Gene ◽  
T47d Cell ◽  
Adenosine A1 Receptor ◽  
T47d Cells ◽  
Apoptosis Rate ◽  
Adenosine A1 ◽  
T47d Cell Line ◽  
A1 Receptor

Background: Adenosine receptor family, especially A1 type is-overexpressed in breast-derived tumor cells and the P53 gene is mutant in some of these cells while the casps gene is of wild type as well. The aim of this study was to evaluate the effect of the A1 receptor function on cell programmed death or proliferation, as well as the relationship between this receptor stimulation/inhibition and caspase 3 (casp3) expression in T47D cell line that has a mutant and non-functional P53 gene. Materials and Methods: The expression of casps3 was measured by real-time polymerase chain reaction and then flow cytometery and MTT assay were used to assess the apoptotic and proliferation cell rate after the treatment of T47D cells with specific agonist N6-cyclopentyladenosine (CPA) and antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) of this receptor 24, 48, and 72 hours after treatment. Result: Our results indicated that DPCPX significantly induces apoptosis in T47D cells and the rate of survival cell after the reduction of this treatment, especially 72 hours after treatment. Finally, the expression of casp3 was up-regulated by DPCPX treatment, especially in 72 hours while CPA treatment had opposite results (P>0.05). Conclusion: In general, DPCPX could up-regulate casp3 gene expression and subsequently increase the apoptosis rate in T47D cells with casp3 expression without the P53 gene interference. Therefore, adenosine A1 receptor antagonists may be introduced as anti-cancer agents.

scholarly journals Activation of Adenosine A1 Receptor in Ischemic Stroke: Neuroprotection by Tetrahydroxy Stilbene Glycoside as an Agonist

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1112
Author(s):  
Lingyu Ruan ◽  
Guanghui Li ◽  
Wenlong Zhao ◽  
Huihui Meng ◽  
Qi Zheng ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Glutamate Release ◽  
Chinese Herb ◽  
Adenosine A1 Receptor ◽  
Polygonum Multiflorum ◽  
Stroke Treatment ◽  
Cardiovascular Side Effects ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
Underlying Mechanisms

Ischemic stroke is the main cause of death/disability, posing a great menace to human health. Though efforts to search for therapeutic drugs are ongoing, few of them have succeeded. Adenosine A1 receptor (A1R) activation could ameliorate ischemic injury, representing a very tempting target for stroke treatment. Tetrahydroxy stilbene glycoside (TSG), a potent antioxidant from the well-known Chinese herb Polygonum multiflorum Thunb., has been reported to have notable neuroprotective activities but the underlying mechanisms are elusive. This study investigated the mechanism of TSG focusing on A1R. TSG markedly decreased mortality, neurological deficit score, cerebral infarct size and brain water content of MCAO rats, and ameliorated the disorders in purine metabolism, energy metabolism and antioxidative defense system. TSG helped the survival of SH-SY5Y cells in OGD/R by alleviating oxidative stress and glutamate release, and by maintaining calcium homeostasis. TSG effects were abolished by A1R antagonist DPCPX. Docking and binding assays confirmed the binding of TSG with A1R. In addition, TSG upregulated the A1R level lowered by MCAO and OGD/R. The downstream signals of A1R activation, ERK1/2, HIF-1α and NF-κB contributed to the neuroprotection of TSG. Moreover, void of “well-known” cardiovascular side effects of classical A1R agonists, TSG showcased its great potential for stroke treatment.

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