2014
DOI: 10.1007/s10517-014-2531-z
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Effect of Cyclopentyladenosine on Lipid Peroxidation during Focal Cerebral Ischemia

Abstract: The antioxidant effect of an adenosine A1 receptor agonist cyclopentyladenosine was studied on the model of focal cerebral ischemia. Ischemic injury of the brain was accompanied by changes in LPO processes (in the blood and brain tissue) and failure of some factors for antioxidant protection (peroxidase and catalase) that inactivate reactive metabolites. Changes in the ratio between LPO and antioxidant protection were less pronounced after treatment with cyclopentyladenosine.

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Cited by 7 publications
(5 citation statements)
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“…Changes in lipid peroxidation (LPO) processes in the brain and blood tissue were demonstrated following ischemic brain injury. Changes in the ratio between LPO and antioxidant protection were less pronounced after cyclopentyladenosine treatment [30]. Current thought is that signaling activated by adenosine and/or other receptors (such as opioid or bradykinin) converge on key targets like mitochondrial K ATP channels or the mitochondrial permeability transition pore (MPTP) [49,50,51,52].…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Changes in lipid peroxidation (LPO) processes in the brain and blood tissue were demonstrated following ischemic brain injury. Changes in the ratio between LPO and antioxidant protection were less pronounced after cyclopentyladenosine treatment [30]. Current thought is that signaling activated by adenosine and/or other receptors (such as opioid or bradykinin) converge on key targets like mitochondrial K ATP channels or the mitochondrial permeability transition pore (MPTP) [49,50,51,52].…”
Section: Discussionmentioning
confidence: 99%
“…Moreover, the activation of the CB 2 receptor may generate inhibitory signaling that directly suppresses the production of ROS stimulated by the activation of the receptor CB 1 [29]. In addition, the adenosinergic system is known to modulate oxidative stress especially via activation of the A 1 receptor [30].…”
Section: Introductionmentioning
confidence: 99%
“…In rod photoreceptors, the observed neuroprotective effect of CPA could be mediated by the inhibition of calcium influx as it is known that adenosine inhibits calcium influx through L-type calcium channels [ 53 ]. Also the observed protective effect of CPA on photoreceptors could be mediated by its antioxidant effect as CPA inhibits lipid peroxidation and potentiates the antioxidant defense mechanisms (peroxidase and catalase enzymes) [ 54 ]. In addition, the activation of A1 receptors inhibits adenylate cyclase (AC) and decrease intracellular cAMP concentration.…”
Section: Discussionmentioning
confidence: 99%
“…In addition, the activation of A1 receptors inhibits adenylate cyclase (AC) and decrease intracellular cAMP concentration. These changes decrease cell metabolism and neuronal energy requirements enhancing cell survival [ 54 , 55 ].…”
Section: Discussionmentioning
confidence: 99%
“…CCPA administered i.c.v. before focal ischemia reduces lipid peroxidation in the cerebral cortex (Sufianova et al 2014). Chronic coadministration of CCPA and vitamin C i.p.…”
Section: Adenosine a 1 Receptors Are Protectivementioning
confidence: 99%