Hypothermic preconditioning reduces Purkinje cell death possibly by preventing the over-expression of inducible nitric oxide synthase in rat cerebellar slices after an in vitro simulated ischemia

Yuan, Hui-Bih; Huang, Yongye; Zheng, Shaoyong; Zuo, Zhiyi

doi:10.1016/j.neuroscience.2006.06.053

Cited by 16 publications

(8 citation statements)

References 55 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Several clinical trials have addressed the effects of huperzine A on VaD [9]. Our previous studies show that, besides inhibiting AChE, huperzine A has a range of neuroprotective activities against neurotoxicity induced by glutamate, hydrogen peroxide, b-amyloid peptide fragments [25][26][27][28][29][30][31][32][33][34][35] and staurosporine [9]. We also demonstrate the neuroprotective effects of huperzine A on several ischemic models in vitro and in vivo [8,10].…”

Section: Introductionsupporting

confidence: 56%

See 1 more Smart Citation

Huperzine A protects C6 rat glioma cells against oxygen–glucose deprivation‐induced injury

Wang

Tang

2007

FEBS Letters

View full text Add to dashboard Cite

The protective effects of huperzine A against oxygenglucose deprivation (OGD)-induced injury in C6 cells were investigated. OGD for 6 h and reoxygenation for 6 h enhanced phosphorylation and degradation of IjBa and nuclear translocation of nuclear factor-kappa B (NF-jB), triggered overexpression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2) and nitric oxide (NO) in C6 cells. Along with inhibiting acetylcholinesterase activity, treatment with 1 lM huperzine A inhibited activation of NF-jB, attenuated iNOS, COX-2 and NO overexpression, and promoted survival in C6 cells subjected to OGD insult. The protective effects of huperzine A were partly mediated by ''cholinergic anti-inflammatory pathway'' through a7 nicotinic acetylcholine receptor.

show abstract

Section: Introductionsupporting

confidence: 56%

“…Compelling evidences have indicated the roles of iNOS and COX‐2 in OGD‐induced cell death [26,27]. Furthermore, iNOS or COX‐2 inhibitors were also reported to prevent cell death from OGD injury [28,29]. INOS and COX‐2 are therefore among the most promising pharmacological targets for the treatment of cerebral ischemia [11].…”

Section: Discussionmentioning

confidence: 99%

Huperzine A protects C6 rat glioma cells against oxygen–glucose deprivation‐induced injury

Wang

Tang

2007

FEBS Letters

View full text Add to dashboard Cite

show abstract

“…Similar mild hypothermic exposure was also reported to have a preconditioning effect at an acute phase of tolerance in in vitro models of ischemia. Hypothermic preconditioning (33°C for 20 minutes) applied 0 to 3 hours before OGD effectively prevented OGD-induced Purkinje cell death in rat cerebellar slices (Yuan et al , 2004, 2006). This rapid neuroprotection induced by hypothermic preconditioning appeared dependent on the activation of signaling molecules and increased gene expression (Yuan et al , 2004, 2006).…”

Section: 0 Preconditioning Stimulimentioning

confidence: 97%

Preconditioning provides neuroprotection in models of CNS disease: Paradigms and clinical significance

Stetler

Leak

Gan

et al. 2014

Progress in Neurobiology

171

140

View full text Add to dashboard Cite

Preconditioning is a phenomenon in which brief episodes of a sublethal insult induce robust protection against subsequent lethal injuries. Preconditioning has been observed in multiple organisms and can occur in the brain as well as other tissues. Extensive animal studies suggest that the brain can be preconditioned to resist acute injuries, such as ischemic stroke, neonatal hypoxia/ischemia, trauma, and agents that are used in models of neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. Effective preconditioning stimuli are numerous and diverse, ranging from transient ischemia, hypoxia, hyperbaric oxygen, hypothermia and hyperthermia, to exposure to neurotoxins and pharmacological agents. The phenomenon of “cross-tolerance,” in which a sublethal stress protects against a different type of injury, suggests that different preconditioning stimuli may confer protection against a wide range of injuries. Research conducted over the past few decades indicates that brain preconditioning is complex, involving multiple effectors such as metabolic inhibition, activation of extra- and intracellular defense mechanisms, a shift in the neuronal excitatory/inhibitory balance, and reduction in inflammatory sequelae. An improved understanding of brain preconditioning should help us identify innovative therapeutic strategies that prevent or at least reduce neuronal damage in susceptible patients. In this review, we focus on the experimental evidence of preconditioning in the brain and systematically survey the models used to develop paradigms for neuroprotection, and then discuss the clinical potential of brain preconditioning. In a subsequent components of this two-part series, we will discuss the cellular and molecular events that are likely to underlie these phenomena.

show abstract

“…Крайне низкое содержание HSP70 положительных клеток у интактных животных, вероятно, может быть свидетельством того, что в этой нейрональной популя ции реализуются иные механизмы защиты клеток. Дей ствительно, на модели кислородно глюкозной деприва ции in vitro показано, что предупреждение гибели клеток Пуркинье после ишемии было связано с ингиби рованием синтеза индуцибельной NO синтазы, в то время как экспрессии HSP70 в этих нейронах не обна ружено [31,32]. Установлено также, что экспрессия ин дуцируемых ишемией белков существенно зависит не только от специфики и тяжести воздействия, но и так же и от типа нейрональной популяции [10].…”

Section: рисunclassified

Individual Typological Features of Postresuscitative Cerebral Changes: Role of Heat Shock Proteins HSP70

Аврущенко¹,

Острова²,

Заржецкий³

et al. 2008

rmt

View full text Add to dashboard Cite

Цель исследования. Установить, как в постреанимационном периоде реализуются протективные свойства белков семейст ва HSP70 в зависимости от индивидуально типологических особенностей организма. Материал и методы. Проведено сравнительное морфометрическое и иммуногистохимическое исследование состояния нейрональных популяций клеток Пуркинье мозжечка, секторов СА1 и СА4 гиппокампа, V слоя сенсомоторной коры головного мозга у крыс, перенесших 12 минутную клиническую смерть и различающихся по результатам выработки условного рефлекса активного избегания (УРАИ). Иммунореактивность к белкам теплового шока определяли непрямым пероксидазно антипероксидазным мето дом с использованием поликлональных антител к HSP70. Плотность и состав нейрональных популяций определяли с по мощью морфометрического анализа. Результаты. Установлено, что контрольные животные с разной способностью к вы работке УРАИ характеризуются отличиями по составу нейрональных популяций сектора СА4 гиппокампа и клеток Пуркинье мозжечка. Выраженные постреанимационные повреждения нейронов обнаружены только у обучившихся крыс. Выявлено, что в контроле иммунореактивность к HSP70 в популяциях пирамидных клеток секторов СА1 и СА4 гиппокам па больше у обучившихся крыс по сравнению с необучившимися. В постреанимационном периоде происходит увеличение иммунореактивности к HSP70 нейрональных популяций секторов СА1 и СА4 гиппокампа, но только у необучившихся жи вотных. Заключение. В целом результаты настоящей работы свидетельствуют о том, что иммунореактивность нейрональ ных популяций к HSP70 взаимосвязана с индивидуально типологическими свойствами организма. Отличия в иммунореак тивности нейрональных популяций к HSP70 между животными с различной способностью к обучению имеются в норме и проявляются в постреанимационном периоде. Особенности реализации нейропротективных свойств HSP70 в зависимости от индивидуально типологических свойств организма являются одним из важных факторов формирования неодинаковой устойчивости мозга к постреанимационным повреждениям. Ключевые слова: остановка сердца, индивидуально типологи ческие особенности, HSP70, иммуногистохимия, нейрональные популяции.Objective: to establish how the protective properties of HSP70 family proteins are realized in the postresuscitative period depending on the organism's individual typological features. Materials and methods. Neuronal populations of the CA1 and CA4 region of the hippocampus, cerebral sensorimotor cortex V and Purkinje's cells of the cerebellum were comparatively morpho metrically and immunohistochemically studied in the rats who had sustained 12 minute clinical death and differed in the results of active avoidance conditioning (AAC). Immunological responsivness to heat shock proteins was determined by peroxidase antiperoxidase assay using polyclonal antibodies to HSP70. The density and composition of the neuronal populations were ascer tained by morphometric analysis. Results. The control animals having varying capacity for AAC were found to have differences in the composition of neuronal populatio...

show abstract

Hypothermic preconditioning reduces Purkinje cell death possibly by preventing the over-expression of inducible nitric oxide synthase in rat cerebellar slices after an in vitro simulated ischemia

Cited by 16 publications

References 55 publications

Huperzine A protects C6 rat glioma cells against oxygen–glucose deprivation‐induced injury

Huperzine A protects C6 rat glioma cells against oxygen–glucose deprivation‐induced injury

Preconditioning provides neuroprotection in models of CNS disease: Paradigms and clinical significance

Individual Typological Features of Postresuscitative Cerebral Changes: Role of Heat Shock Proteins HSP70

Contact Info

Product

Resources

About