The neuroprotective effects of preconditioning exercise on brain damage and neurotrophic factors after focal brain ischemia in rats

Otsuka, Shotaro; Sakakima, Harutoshi; Sumizono, Megumi; Takada, Seiya; Terashi, Takuto; Yoshida, Yasuhiko

doi:10.1016/j.bbr.2016.01.049

Cited by 77 publications

(70 citation statements)

References 45 publications

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“…Midkine is known to exert neuroprotective effects in some of these pathologies including Alzheimer's disease [18] and brain ischemia [39]. Thus, it is reasonable to hypothesize that the ability of MK to limit neuroinflammation could contribute to its neuroprotective actions in different pathological contexts.…”

Section: Discussionmentioning

confidence: 99%

Midkine Is a Novel Regulator of Amphetamine-Induced Striatal Gliosis and Cognitive Impairment: Evidence for a Stimulus-Dependent Regulation of Neuroinflammation by Midkine

Vicente-Rodríguez

Fernández-Calle

Gramage

et al. 2016

Mediators of Inflammation

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Midkine (MK) is a cytokine that modulates amphetamine-induced striatal astrogliosis, suggesting a possible role of MK in neuroinflammation induced by amphetamine. To test this hypothesis, we studied astrogliosis and microglial response induced by amphetamine (10 mg/kg i.p. four times, every 2 h) in different brain areas of MK−/− mice and wild type (WT) mice. We found that amphetamine-induced microgliosis and astrocytosis are enhanced in the striatum of MK−/− mice in a region-specific manner. Surprisingly, LPS-induced astrogliosis in the striatum was blocked in MK−/− mice. Since striatal neuroinflammation induced by amphetamine-type stimulants correlates with the cognitive deficits induced by these drugs, we also tested the long-term effects of periadolescent amphetamine treatment (3 mg/kg i.p. daily for 10 days) in a memory task in MK−/− and WT mice. Significant deficits in the Y-maze test were only observed in amphetamine-pretreated MK−/− mice. The data demonstrate for the first time that MK is a novel modulator of neuroinflammation depending on the inflammatory stimulus and the brain area considered. The data indicate that MK limits amphetamine-induced striatal neuroinflammation. In addition, our data demonstrate that periadolescent amphetamine treatment in mice results in transient disruption of learning and memory processes in absence of endogenous MK.

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Section: Discussionmentioning

confidence: 99%

Midkine Is a Novel Regulator of Amphetamine-Induced Striatal Gliosis and Cognitive Impairment: Evidence for a Stimulus-Dependent Regulation of Neuroinflammation by Midkine

Vicente-Rodríguez

Fernández-Calle

Gramage

et al. 2016

Mediators of Inflammation

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“…; Otsuka et al. ). Limited but consistent evidence of neuroprotection from exercise in animal models has been found in various retinal degenerative diseases, although the type and protocol of exercise were inconsistent and not comparable in these studies.…”

Section: Neuroprotection Of Physical Exercise In Glaucomamentioning

confidence: 97%

“…Physical exercise has been investigated to promote neuronal plasticity and enhance resistance to neurodegeneration in the brain, spinal cord and cardiovascular system in both humans and experimental animals (Michelini & Stern 2009;Alvarez-Mejia et al 2015;Sandrow-Feinberg & Houle 2015;Chali et al 2016;Huttenrauch et al 2016;Li et al 2016;Otsuka et al 2016). Limited but consistent evidence of neuroprotection from exercise in animal models has been found in various retinal degenerative diseases, although the type and protocol of exercise were inconsistent and not comparable in these studies.…”

Section: Neuroprotection Of Physical Exercise In Glaucomamentioning

confidence: 99%

Physical exercise and glaucoma: a review on the roles of physical exercise on intraocular pressure control, ocular blood flow regulation, neuroprotection and glaucoma‐related mental health

Zhu

Lai

Choy

et al. 2018

Acta Ophthalmologica

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The benefits of physical exercise on health and well-being have been studied in a wide range of systemic and ocular diseases, including glaucoma, a progressive optic neuropathy characterized by accelerated apoptosis of retinal ganglion cells (RGCs). Elevated intraocular pressure (IOP) and insufficient ocular perfusion have been postulated to be the two main theories in glaucoma development and progression. The effects of exercise in these two aspects have been demonstrated by numerous researches. A review in 2009 focusing on these two theories concluded that exercise results in transient IOP reduction but an inconsistent elevation in ocular perfusion. However, the majority of the studies had been conducted in healthy subjects. Over the past decade, technological advancement has brought forth new and more detailed evidence regarding the effects of exercise. Moreover, the neuroprotective effect of exercise by upregulation of neurotrophin and enhancement of mitochondrial function has been a focus of interest. Apart from visual impairment, the mental health issues in patients with glaucoma, which include anxiety and depression, should also be addressed. In this review, we mainly focus on publications from the recent years, so as to provide a comprehensive review on the impact of physical exercise on IOP, ocular perfusion, neuroprotection and mental health in patients with glaucoma.

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“…Choi et al () reported that treadmill exercise in a rat model of vascular dementia improved spatial memory and increased the number of neuronal progenitor cells in the hippocampus. In another study, preconditioning exercise ameliorated motor function, reduced neuronal apoptosis, and increased angiogenesis and astrocyte proliferation in rats (Otsuka et al, ).…”

Section: Introductionmentioning

confidence: 96%

Treadmill exercise attenuates 3,4‐methylenedioxymethamphetamine‐induced memory impairment through a decrease apoptosis in male rat hippocampus

Gharebaghi

Amiri

Salehi

et al. 2017

J of Neuroscience Research

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3,4-methylenedioxymethamphetamine (MDMA) leads to apoptosis in the hippocampus with consequent induction of learning and memory impairment. In this study, we have investigated the effects of treadmill exercise on memory in relation to apoptosis and oxidative stress in the hippocampi of MDMA-treated rats. Male Wistar rats received multiple intraperitoneal (IP) injections of MDMA (10 mg/kg) and exercised for one month on a treadmill (simultaneously or asynchronously with MDMA). We assessed memory function with the Morris water maze (MWM) test. Lipid peroxidation (LPO) and expression of caspase 3, Bax, and Bcl-2 were examined by the thiobarbituric acid assay (TBA) and western blot, respectively. Our results showed that asynchronous treadmill exercise could significantly improve MDMA-induced memory impairment in the MWM test. Caspase 3 expression decreased in the exercise group compared to the MDMA group. Although MDMA treatment caused an increase in the Bax/Bcl-2 ratio, the treadmill exercise reduced this ratio. Simultaneous exercise caused a reduction in lipid peroxidation in the hippocampus. This data suggests that treadmill exercise can be a useful strategy for treating memory impairment in persons with neurodegenerative disease and stimulant drug users. © 2017 Wiley Periodicals, Inc.

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The neuroprotective effects of preconditioning exercise on brain damage and neurotrophic factors after focal brain ischemia in rats

Cited by 77 publications

References 45 publications

Midkine Is a Novel Regulator of Amphetamine-Induced Striatal Gliosis and Cognitive Impairment: Evidence for a Stimulus-Dependent Regulation of Neuroinflammation by Midkine

Midkine Is a Novel Regulator of Amphetamine-Induced Striatal Gliosis and Cognitive Impairment: Evidence for a Stimulus-Dependent Regulation of Neuroinflammation by Midkine

Physical exercise and glaucoma: a review on the roles of physical exercise on intraocular pressure control, ocular blood flow regulation, neuroprotection and glaucoma‐related mental health

Treadmill exercise attenuates 3,4‐methylenedioxymethamphetamine‐induced memory impairment through a decrease apoptosis in male rat hippocampus

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