Effect of Cyclopentyladenosine on Lipid Peroxidation during Focal Cerebral Ischemia

Суфианова, Г. З.; Sufianov, Albert; Шапкин, А. Г.

doi:10.1007/s10517-014-2531-z

Cited by 7 publications

(5 citation statements)

References 4 publications

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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%

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Manual Therapy Reduces Pain Behavior and Oxidative Stress in a Murine Model of Complex Regional Pain Syndrome Type I

et al. 2019

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Complex regional pain syndrome type I (CRPS-I) is a chronic painful condition. We investigated whether manual therapy (MT), in a chronic post-ischemia pain (CPIP) model, is capable of reducing pain behavior and oxidative stress. Male Swiss mice were subjected to ischemia-reperfusion (IR) to mimic CRPS-I. Animals received ankle joint mobilization 48h after the IR procedure, and response to mechanical stimuli was evaluated. For biochemical analyses, mitochondrial function as well as oxidative stress thiobarbituric acid reactive substances (TBARS), protein carbonyls, antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) levels were determined. IR induced mechanical hyperalgesia which was subsequently reduced by acute MT treatment. The concentrations of oxidative stress parameters were increased following IR with MT treatment preventing these increases in malondialdehyde (MDA) and carbonyls protein. IR diminished the levels of SOD and CAT activity and MT treatment prevented this decrease in CAT but not in SOD activity. IR also diminished mitochondrial complex activity, and MT treatment was ineffective in preventing this decrease. In conclusion, repeated sessions of MT resulted in antihyperalgesic effects mediated, at least partially, through the prevention of an increase of MDA and protein carbonyls levels and an improvement in the antioxidant defense system.

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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%

Manual Therapy Reduces Pain Behavior and Oxidative Stress in a Murine Model of Complex Regional Pain Syndrome Type I

et al. 2019

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“…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%

Adenosine A1 receptor: A neuroprotective target in light induced retinal degeneration

et al. 2018

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Light induced retinal degeneration (LIRD) is a useful model that resembles human retinal degenerative diseases. The modulation of adenosine A1 receptor is neuroprotective in different models of retinal injury. The aim of this work was to evaluate the potential neuroprotective effect of the modulation of A1 receptor in LIRD. The eyes of rats intravitreally injected with N6-cyclopentyladenosine (CPA), an A1 agonist, which were later subjected to continuous illumination (CI) for 24 h, showed retinas with a lower number of apoptotic nuclei and a decrease of Glial Fibrillary Acidic Protein (GFAP) immunoreactive area than controls. Lower levels of activated Caspase 3 and GFAP were demonstrated by Western Blot (WB) in treated animals. Also a decrease of iNOS, TNFα and GFAP mRNA was demonstrated by RT-PCR. A decrease of Iba 1+/MHC-II+ reactive microglial cells was shown by immunohistochemistry. Electroretinograms (ERG) showed higher amplitudes of a-wave, b-wave and oscillatory potentials after CI compared to controls. Conversely, the eyes of rats intravitreally injected with dipropylcyclopentylxanthine (DPCPX), an A1 antagonist, and subjected to CI for 24 h, showed retinas with a higher number of apoptotic nuclei and an increase of GFAP immunoreactive area compared to controls. Also, higher levels of activated Caspase 3 and GFAP were demonstrated by Western Blot. The mRNA levels of iNOS, nNOS and inflammatory cytokines (IL-1β and TNFα) were not modified by DPCPX treatment. An increase of Iba 1+/MHC-II+ reactive microglial cells was shown by immunohistochemistry. ERG showed that the amplitudes of a-wave, b-wave, and oscillatory potentials after CI were similar to control values. A single pharmacological intervention prior illumination stress was able to swing retinal fate in opposite directions: CPA was neuroprotective, while DPCPX worsened retinal damage. In summary, A1 receptor agonism is a plausible neuroprotective strategy in LIRD.

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“…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%

Adenosine and Oxygen/Glucose Deprivation in the Brain

Pedata

Dettori

Gaviano

et al. 2018

The Adenosine Receptors

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Extracellular adenosine concentrations in the brain increase dramatically during ischemia in concentrations that able to stimulate all (A 1 , A 2A , A 2B , and A 3) receptors. Adenosine exerts a clear neuroprotective effect through A 1 receptors during ischemia mainly by reducing precocious excitotoxic phenomena. Unfortunately, the use of selective A 1 agonists is hampered by undesirable peripheral effects. Evidence indicates that A 2A receptor antagonists administered early after ischemia provide protection centrally by reducing excitotoxicity. After ischemia, the primary damage due to the early massive increase of extracellular glutamate is followed by activation of resident immune cells, i.e., microglia, and production or activation of inflammation mediators and blood cell infiltration. Evidences are that agonists at A 2A, A 2B , and A 3 receptors mainly acting on blood and vascular endothelial cells provide protection by controlling neuroinflammation, endothelial leaking, and massive blood cell infiltration in the hours and days after brain ischemia. Since ischemia is a multifactorial pathology characterized by different events evolving in the time and protracted neuroinflammation is recognized as the predominant mechanism of secondary brain injury progression, adenosinergic drugs aimed at dampening damage in the hours/days after ischemia appear promising.

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Effect of Cyclopentyladenosine on Lipid Peroxidation during Focal Cerebral Ischemia

Cited by 7 publications

References 4 publications

Manual Therapy Reduces Pain Behavior and Oxidative Stress in a Murine Model of Complex Regional Pain Syndrome Type I

Manual Therapy Reduces Pain Behavior and Oxidative Stress in a Murine Model of Complex Regional Pain Syndrome Type I

Adenosine A1 receptor: A neuroprotective target in light induced retinal degeneration

Adenosine and Oxygen/Glucose Deprivation in the Brain

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