Exercise-Induced Overexpression of Angiogenic Factors and Reduction of Ischemia / Reperfusion Injury in Stroke

Ding, Yun; Luan, Xiaodong; Li, Jie; Rafols, José A.; Guthinkonda, M.; Díaz, Fernando G.; Ding, Yuchuan

doi:10.2174/1567202043361875

Cited by 132 publications

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“…These trophic factors generate more abundant neuronal and synaptic networks, and they have also been shown to be protective of the neural and cerebrovascular systems. BDNF and NGF mRNA levels have been shown to be upregulated following several weeks of continuous exercise (Ding et al, 2004b), which has been specifically seen in astrocytes and neuronal cells. In addition, providing exercise in an enriched environment, including running wheels, toy balls, ladders, and wooden planks, increased synaptogenesis and neurologic functioning even more than previously seen with basic exercise preconditioning, which was also associated with an increase in BDNF and NGF mRNA levels (Neeper et al, 1996;Ickes et al, 2000).…”

Section: Neurotrophin Expressionmentioning

confidence: 99%

“…Through its beneficial effects on hypertension, lipid profiles, obesity, and diabetes, exercise training has been associated with decreased stroke incidence and better outcomes after stroke (Evenson et al, 1999;Gillum et al, 1996;Hu et al, 2004). Despite risk factor management, exercise has also been shown to provide endogenous neuroprotection, preserving neuronal viability in the setting of ischemia/ reperfusion injury, resulting in decreased infarct volume and improved neurologic recovery (Chaudhry et al, 2010;Curry et al, 2009;Davis et al, 2007;Ding et al, 2004aDing et al, , 2004bDing et al, , 2005Ding et al, , 2006aDing et al, , 2006bGuo et al, 2008a;Liebelt et al, 2010;Zwagerman et al, 2010aZwagerman et al, , 2010b. These beneficial endogenous effects of exercise preconditioning have been seen even after multivariate analysis has controlled for risk factor alterations (Hu et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…

Preconditioning modalities

While various modalities, such as treadmill running, voluntary running, simple and complex exercise, have been shown to provide variable amounts of neuroprotection.

…”

mentioning

confidence: 99%

“…Another study revealed that the neuroprotective effects of exercise preconditioning appear to be long-lasting, showing that 3 weeks after cessation of exercise, rats still maintained lower levels of neurologic deficit and decreased stroke volume when compared to non-exercise rats (Ding et al, 2004b). Future human studies ought to determine the exact duration needed for maximal endogenous neuroprotection.…”

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Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

Dornbos¹,

Ding²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia -Reperfusion Injury 301 neuroprotection after exercise has stopped.Another study revealed that the neuroprotective effects of exercise preconditioning appear to be long-lasting, showing that 3 weeks after cessation of exercise, rats still maintained lower levels of neurologic deficit and decreased stroke volume when compared to non-exercise rats (Ding et al., 2004b). Future human studies ought to determine the exact duration needed for maximal endogenous neuroprotection. Preconditioning modalitiesWhile various modalities, such as treadmill running, voluntary running, simple and complex exercise, have been shown to provide variable amounts of neuroprotection. When comparing forced exercise on a treadmill to voluntary running on a running wheel, rats forced to exercise on a treadmill tend to have better neurologic outcomes after stroke (Hayes et al., 2008). Previous studies have shown that forced exercise on a treadmill is slower but more constant than voluntary exercise occurs in shorter spurts with faster speed, although the total distance is equal in the two groups (Noble et al., 1999). This neuroprotection in forced exercise subjects led to decreased stroke volume, lessened neurologic deficit, upregulation of heat shock proteins, increased neurogenesis and cerebral metabolism (Hayes et al., 2008;Kinni et al., 2011;Leasure and Jones, 2008). These findings show that moderate exercise over a longer time period conveys more efficient and greater neuroprotection than more vigorous exercise over shorter time periods. In addition to the studies assessing forced and voluntary exercise, differences have also been established when comparing simple and complex exercise. This study analyzed simple exercise as the repetitive movements of treadmill running, whereas complex exercise constituted enriched activities which required both balance and coordination (Ding et al., 2003). Following ischemia/reperfusion injury, rats preconditioned with complex exercise demonstrated increased synaptogenesis and improved neurologic outcomes when compared to simple treadmill exercise (Ding et al., 2003;Jones et al., 1999). Simple exercise training also alleviates much of the injury following ischemia/reperfusion, but its benefit is less pronounced than what is observed with complex exercise training. Although no human studies have definitively shown the most effective means of exercise for enhanced neuroprotection, these animal studies provide a solid framework for the development of appropriate exercise regimens. Moderate exercise intensity, including components of balance, coordination and stress, taking place over a sustained duration seem to be the most neuroprotective when compared to other exercise modalities and intensities.

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Section: Neurotrophin Expressionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…

Preconditioning modalities

While various modalities, such as treadmill running, voluntary running, simple and complex exercise, have been shown to provide variable amounts of neuroprotection.

…”

mentioning

confidence: 99%

mentioning

confidence: 99%

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Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

Dornbos¹,

Ding²

2012

Brain Injury - Pathogenesis, Monitoring, Recovery and Management

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“…Original Article growth factors in the brain, and protects against ischemic cell damage [10]. Further, physical activity enhances the neuronal plasticity and the excitability of neuronal pathways.…”

Section: Introductionmentioning

confidence: 99%

The effect of physical training on glutamate transporter expression in an experimental ischemic stroke rat model

Kim¹,

Kim²

2013

PTRS

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Objective: The present study was aimed at determining the effect of physical training on glutamate transporter activity in a middle cerebral artery occlusion (MCAO)-induced ischemia injury rat model. Design: Randomized controlled trial. Methods: In this study, we randomly divided them into three groups. Group I included non-occlusion sham controls (n=10), Group II included non-physical training after MCAO (n=10), and Group III included rats that were subjected to physical training after MCAO (n=10). Rats in the physical training group underwent treadmill training, which began at 24 h after MCAO and continued for 14 consecutive days. The training intensity was gradually increased from 5 m/min on the first day to 12 m/min on day 3, and it was maintained until day 14. Focal cerebral ischemia was examined in adult male Sprague-Dawley rats by using the MCAO model. We determined the functional outcomes for each rat on days 1, 7, and 14. Glutamate transporter-1 (GLT-1) activity in the cortex of rats from all three groups was examined at the end of the experiment. Results: Out result show that MCAO rats exhibited severe neurological deficits on the 1 day, and there was no statistically significant in each groups. We observed that the functional outcomes were improved at days 7 and 14 after middle cerebral artery occlusion, and GLT-1 activity was increased in the physical training group (p<0.05). Conclusions: These results indicated that physical training after focal cerebral ischemia exerts neuroprotective effects against ischemic brain injury by improving motor performance and increasing the levels of GLT-1 activity.

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Biochemical‐ and Biophysical‐Induced Barriergenesis in the Blood–Brain Barrier: A Review of Barriergenic Factors for Use in In Vitro Models

Schofield

Rodrigo‐Navarro

Dalby

et al. 2021

Advanced NanoBiomed Research

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Central nervous system (CNS) pathologies are a prevalent problem in aging populations, creating a need to understand the underlying events in these diseases and develop efficient CNS‐targeting drugs. The importance of the blood–brain barrier (BBB) is evident, acting both as a physical barrier to drug entry into the CNS and potentially as the cause or aggravator of CNS diseases. The development of a biomimetic BBB in vitro model is required for the understanding of BBB‐related pathologies and in the screening of drugs targeting the CNS. There is currently great interest in understanding the influence of biochemical and biophysical factors, as these have the potential to greatly improve the barrier function of brain microvascular endothelial cells (BMECs). Recent advances in understanding how these may regulate barriergenesis in BMECs help promote the development of improved BBB in vitro models and therefore novel interventional therapies for pathologies related to its disruption. Herein, an overview of specific biochemical and biomechanical cues in the formation of the BBB, with a focus on in vitro models and how these might recapitulate the BBB function, is provided.

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Exercise-Induced Overexpression of Angiogenic Factors and Reduction of Ischemia / Reperfusion Injury in Stroke

Cited by 132 publications

References 0 publications

Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

Mechanisms of Neuroprotection Underlying Physical Exercise in Ischemia - Reperfusion Injury

The effect of physical training on glutamate transporter expression in an experimental ischemic stroke rat model

Biochemical‐ and Biophysical‐Induced Barriergenesis in the Blood–Brain Barrier: A Review of Barriergenic Factors for Use in In Vitro Models

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