Passage of spermidine across the blood–brain barrier in short recirculation periods following global cerebral ischemia: effects of mild hyperthermia

Diler, A. Sarper; Ziylan, Y. Ziya; Üzüm, Gülay; Lefauconnier, Jeanne-Marie; Seylaz, Jacques; Pinard, Elisabeth

doi:10.1016/s0168-0102(02)00059-7

Cited by 22 publications

(11 citation statements)

References 42 publications

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“…In spite of the potent neuroprotective capacity of spermidine in invertebrates, it remains elusive whether spermidine is able to cross the mammalian blood-brain barrier or even to regulate its integrity (116,117). At least after forebrain ischemia, spermidine is transported into several areas of the rat brain (117). Alternatively, spermidine may act on nervous tissue via systemic routes that involve regulation of inflammatory cytokines and immune cells capable of invading cerebral tissue.…”

Section: Neuromodulatory and Neuroprotective Mechanisms Of Spermidinementioning

confidence: 99%

Spermidine in health and disease

Madeo

Eisenberg

Pietrocola

et al. 2018

Science

705

633

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Interventions that delay aging and protect from age-associated disease are slowly approaching clinical implementation. Such interventions include caloric restriction mimetics, which are defined as agents that mimic the beneficial effects of dietary restriction while limiting its detrimental effects. One such agent, the natural polyamine spermidine, has prominent cardioprotective and neuroprotective effects and stimulates anticancer immunosurveillance in rodent models. Moreover, dietary polyamine uptake correlates with reduced cardiovascular and cancer-related mortality in human epidemiological studies. Spermidine preserves mitochondrial function, exhibits anti-inflammatory properties, and prevents stem cell senescence. Mechanistically, it shares the molecular pathways engaged by other caloric restriction mimetics: It induces protein deacetylation and depends on functional autophagy. Because spermidine is already present in daily human nutrition, clinical trials aiming at increasing the uptake of this polyamine appear feasible.

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Section: Neuromodulatory and Neuroprotective Mechanisms Of Spermidinementioning

confidence: 99%

Spermidine in health and disease

Madeo

Eisenberg

Pietrocola

et al. 2018

Science

705

633

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“…On the second day, under chloral hydrate anesthesia both CCA were occluded for 30 min. Rats with 4VO were only included if EEG was flattening during ischemia (Diler et al 2002). Seventy-two hours reperfusion was initiated by opening the carotid clamps after 30 min of ischemia.…”

Section: Surgery Proceduresmentioning

confidence: 99%

Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia

et al. 2014

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Global cerebral ischemia arises in patients who have a variety of clinical conditions including cardiac arrest, shock and asphyxia. In spite of advances in understanding of the brain ischemia and stroke etiology, therapeutic approaches to improve ischemic injury still remain limited. It has been established that metformin can attenuate cell death in cerebral ischemia. One of the main functions of metformin is proposed to be conducted via AMP-activated protein kinase (AMPK)-dependent pathway in the experimental cerebral ischemia model. It is also established that metformin can suppress inflammation and activate Nuclear factor erythroid 2-related factor (Nrf2) pathways in neurons. In the current study, the role of metformin in regulating inflammatory and antioxidant pathways in the global cerebral ischemia was investigated. Our results indicated that pretreatment of rats by metformin attenuated cellular levels of nuclear factor-κB, Tumor Necrosis Factor alpha and Cyclooxygenase-2 which are considered as three important proteins involved in the inflammation pathway. Pretreatment by metformin increased the level of Nrf2 and heme oxygenase-1 in the hippocampus of ischemic rats compared with untreated ischemic group. Moreover, pretreatment by metformin enhanced the level of glutathione and catalase activities compared with them in ischemic group. Such protective changes detected by metformin pretreatment were reversed by injecting compound c, an AMPK inhibitor. These findings suggested that metformin might protect cells through modulating inflammatory and antioxidant pathways via induction of AMPK. However, more experimental and clinical trial studies regarding neuroprotective potential of metformin and the involved mechanisms, especially in the context of cerebral ischemic injuries, are necessary.

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“…Due to their limited capacity to cross the blood-brain barrier [19], concentrations of polyamines in the brain are generally in the nanomolar range [20]. In fact, only agmatine and arginine are able to cross the blood-brain barrier [21].…”

Section: -Role Of Polyamines In Cnsmentioning

confidence: 99%

Suicide and the Polyamine System

Gross¹,

Turecki

2013

CNSNDDT

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Suicide is a significant worldwide public health problem. Understanding the neurobiology is important as it can help us to better elucidate underlying etiological factors and provide opportunities for intervention. In recent years, many lines of research have suggested that the polyamine system may be dysregulated in suicidal behaviors. Initial research in animals provided evidence of a dysfunctional polyamine stress response system, while later work using post-mortem human brain tissue has suggested that molecular mechanisms may be at play in the suicide brain. In this review, we will describe the research that suggests the presence of alterations in the polyamine system in mental disorders and behavioral phenotypes, with particular attention to work on suicide. In addition, we will also describe potential avenues for future work. KeywordsEpigenetics; Major Depressive Disorder; Neurobiology; Polyamines; Polyamine Stress Response; Spermidine/Spermine-N 1 -Acetyltransferase; Suicide -IntroductionSuicide, most often associated with major depressive disorder (MDD) [1], is an important cause of premature death around the world [2]. According to the World Health Organization (www.who.int, 2012), approximately one million people die by suicide annually, and the rate of suicide attempts is 20 times greater than that of suicide completion (www.who.int, 2012). As such, suicidal behaviors (SB) are an important source of public health concern. The etiology of suicide is complex [3], and commonly understood as resulting from the interaction of predisposing (distal) and precipitant (proximal) factors [4]. Biological alterations resulting from a combination of genetic and environmental risk factors underlie predisposition to suicide, but the exact molecular mechanisms at play remain largely unclear. As such, it is important that we gain a better understanding of the molecular processes associated with suicide in order to identify new avenues for prevention and intervention.Over the past several decades, molecular studies of suicide and MDD have focused on the monoamine system. Beginning in the late 1960s, research into the neurobiology of suicide

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Passage of spermidine across the blood–brain barrier in short recirculation periods following global cerebral ischemia: effects of mild hyperthermia

Cited by 22 publications

References 42 publications

Spermidine in health and disease

Spermidine in health and disease

Pre-treatment with metformin activates Nrf2 antioxidant pathways and inhibits inflammatory responses through induction of AMPK after transient global cerebral ischemia

Suicide and the Polyamine System

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