Hypoxic preconditioning modifies the activity of prond antioxidant systems in rat hippocampus

Ms, Kislin; Sa, Stroev; Ts, Glushchenko; Ei, Tiul'kova; Pelto-Huikko, M; Mo, Samoĭlov

doi:10.18097/pbmc20135906673

Cited by 7 publications

(3 citation statements)

References 19 publications

(26 reference statements)

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“…Our study confirmed it: ischemia in the preconditioned animals was not accompanied by any signs of oxidative stress, nor was there any pronounced activation of ROS-induced processes as observed in the control animals with Ischemia. The application of compounds with an antioxidant activity in the CPreC protocol may lead to the weakening of the cytoprotective effect induced by preconditioning due to the inhibition of ROS, which play a signaling role in the mechanism of organism adapting to hypoxia (Kislin et al 2013). In our study, this was not observed.…”

Section: Resultscontrasting

confidence: 53%

“…This may be due to the time interval taken to evaluate the ROS-induced processes. For example, in Kislin et al (2013), it was shown that immediately after hypoxic PreC in the brain tissue, there was an activation of free radical reactions, but 3 hrs and 24 hrs later, on the contrary, they were inhibited, resulting in a decrease in SOD expression.…”

Section: Resultsmentioning

confidence: 99%

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Activity of ROS-induced processes in the combined preconditioning with amtizol before and after cerebral ischemia in rats

Левченкова¹,

Новиков²,

Vorobyova³

et al. 2021

RRP

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Introduction: The dose-dependent effect of reactive oxygen species (ROS) in tissues in preconditioning (PreC) and oxidative stress, as well as NO-synthase participation in mitochondrial ROS production determined the study aim – to assess the impact of the neuroprotective method of combined preconditioning (CPreC) on free radical reactions (FRRs) in brain in normoxia and in cerebral ischemia, including in NO-synthase blockade. Materials and methods: The intensity of FRR by iron-induced chemiluminescence (CL), the content of lipid peroxidation products and antioxidant enzyme activity were investigated 1 hr (early period) and 48 hrs (delayed period) after CPreC (amtizol and hypobaric hypoxia) in Wistar rat brain. Some animal groups were operated (common carotid artery bilateral ligation) 1 hr and 48 hrs after CPreC, as well as with preliminary introduction of L-NAME and aminoguanidine. Results and discussion: In normoxia, CPreC led to increase the CL maximum level (Fmax) in the delayed PreC period. The amount of thiobarbituric acid reactive products (TBA-RP), activity of superoxide dismutase (SOD) and catalase in mitochondrial fraction of rat brain did not change in comparison with the intact control in both PreC periods. In cerebral ischemia, oxidative stress was observed. The CPreC use before ischemia caused a decrease in CL parameters and TBA-RP in brain, the maintenance of SOD and high catalase activity. NO-synthase inhibitors partially abolished the antioxidant effect of CPreC in ischemia. Conclusion: CPreC had no influence on FRRs in brain tissue in normoxia, but prevented their excessive activation after ischemia, especially in the delayed period. NO-synthase was involved in the CPreC neuroprotection.

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Section: Resultscontrasting

confidence: 53%

Section: Resultsmentioning

confidence: 99%

Activity of ROS-induced processes in the combined preconditioning with amtizol before and after cerebral ischemia in rats

Левченкова¹,

Новиков²,

Vorobyova³

et al. 2021

RRP

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“…It was noted that in the hippocampus and cerebellum, the proportion of necrotic neurons is significantly higher than in other cerebral structures. Histochemical studies of localization of free radical oxidation (FRO) products in the brain of animals, which had cardiac arrest, showed that neurons of selectively vulnerable hippocampal areas are primal targets for FRO in the brain during reperfusion [1].…”

Section: Introductionmentioning

confidence: 99%

Dynamics of changes in the concentration of heat shock protein (HSP70) in the cerebral cortex and hippocampus in experimental violation of cerebral circulation: the ability to regulate this process through positive modulation of thiol-disulfide system

Бєленічев¹,

Горбачева²,

Bukhtiyarova³

et al. 2016

bmgt

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Objective: Ischemic brain damage is the main factor of pathogenesis of various CNS disorders, which are observed in clinical practice. Nowadays, it is established that the parts of the brain are differ in their sensitivity to ischemia. It 108 I. F. Belenichev et al. was noted that in the hippocampus and cerebellum, the proportion of necrotic neurons is significantly higher than in other cerebral structures. The goal of this research was estimation of possible pharmacological regulation of endogenous neuroprotective factor (HSP70 -heat shock protein) by the positive modulators of thiol-disulfide system in the neuronal cortex and hippocampus in the different periods after experimental cerebral vascular accident.Methods: Experiments were carried out on outbred rats of both sexes weighing 180-200 g. Experimental animals were divided on six groups: pseudo operated animals, control group and four groups of animals, that were treated by Thiotriazoline, Angioline, Thiocetam or lipoic acid. Cerebral vascular accident was reproduced by bilateral common carotid arteries ligation. In the brain homogenate we defined the content of HSP70 and recovered glutathione at different periods of ischemia (day 1, day 4 and day 18).Results: Modeling of cerebral vascular accident led to the different changes in the transcription of genes, which coded heat shock protein. We found decreasing of HSP70 content and recovered glutathione concentration in brain of animals with cerebral vascular accident. Such dynamics was observed during all period of observation until the day 18. Administration of thiol-disulfide system modulators to the experimental animals caused positive effect on HSP70 concentration in neurons of hippocampus and cortex. These could be explained by ability of these medicines to increase the content of recovered glutathione in the neuronal tissue. The most pronounced effect showed Angioline and Thiotriazoline.Conclusions: Analysis of obtained results confirms the idea that ischemic neuronal damage is accompanied by changes in the functional state of the components of heat shock proteins and glutathione system. Injection of thioldisulfide system modulators caused directly increasing of recovered glutathione content and indirectly led to the activation of expression of HSP70.

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Combining hypobaric hypoxia or hyperbaric oxygen postconditioning with memantine reduces neuroprotection in 7-day-old rat hypoxia-ischemia

Gamdzyk

Ziembowicz

Bratek

et al. 2016

Pharmacological Reports

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Hypoxic preconditioning modifies the activity of prond antioxidant systems in rat hippocampus

Cited by 7 publications

References 19 publications

Activity of ROS-induced processes in the combined preconditioning with amtizol before and after cerebral ischemia in rats

Activity of ROS-induced processes in the combined preconditioning with amtizol before and after cerebral ischemia in rats

Dynamics of changes in the concentration of heat shock protein (HSP70) in the cerebral cortex and hippocampus in experimental violation of cerebral circulation: the ability to regulate this process through positive modulation of thiol-disulfide system

Combining hypobaric hypoxia or hyperbaric oxygen postconditioning with memantine reduces neuroprotection in 7-day-old rat hypoxia-ischemia

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