Effects of detraining on preconditioning exercise-induced neuroprotective potential after ischemic stroke in rats

Otsuka, Shotaro; Sakakima, Harutoshi; Tani, Akira; Nakanishi, Kazuki; Takada, Seiya; Norimatsu, Kosuke; Maejima, Hiroshi; Maruyama, Ikuro

doi:10.1007/s00429-021-02317-5

Cited by 11 publications

(8 citation statements)

References 30 publications

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“…Twenty-eight male Sprague Dawley rats (CLEA Japan, Inc., Shizuoka, Japan) (7 weeks old, weight 240–270 g) were used in this study. The number of animals used was determined with reference to previous studies 9 , 37 . The rats were housed in the same manner as in our previous experiments with rats 23 , 38 .…”

Section: Methodsmentioning

confidence: 99%

Effects of different remote ischemia perconditioning methods on cerebral infarct volume and neurological impairment in rats

Otsuka

Itashiki

Tani

et al. 2023

Sci Rep

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Remote ischemic perconditioning (RIPerC) is a novel neuroprotective method against cerebral infarction that has shown efficacy in animal studies but has not been consistently neuroprotective in clinical trials. We focused on the temporal regulation of ischemia–reperfusion by RIPerC to establish an optimal method for RIPerC. Rats were assigned to four groups: 10 min ischemia, 5 min reperfusion; 10 min ischemia, 10 min reperfusion; 5 min ischemia, 10 min reperfusion; and no RIPerC. RIPerC interventions were performed during ischemic stroke, which was induced by a 60-min left middle cerebral artery occlusion. Infarct volume, sensorimotor function, neurological deficits, and cellular expressions of brain-derived neurotrophic factor (BDNF), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), and caspase 3 were evaluated 48 h after the induction of ischemia. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) was also performed. RIPerC of 10 min ischemia/10 min reperfusion, and 5 min ischemia/10 min reperfusion decreased infarct volume, improved sensorimotor function, decreased Bax, caspase 3, and TUNEL-positive cells, and increased BDNF and Bcl-2 expressions. Our findings suggest RIPerC with a reperfusion time of approximately 10 min exerts its neuroprotective effects via an anti-apoptotic mechanism. This study provides important preliminary data to establish more effective RIPerC interventions.

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Section: Methodsmentioning

confidence: 99%

Effects of different remote ischemia perconditioning methods on cerebral infarct volume and neurological impairment in rats

Otsuka

Itashiki

Tani

et al. 2023

Sci Rep

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“…However, exercise preconditioning-induced neuroprotective effect could be quickly lost after exercise cessation. This outcome is a reminder that regulating HIF-1α expression in a time-dependent manner may potentially focus on the further treatment of ischemic stroke ( Otsuka et al, 2021a ).…”

Section: Mechanism Of Exercise Preconditioning Induced Cerebral Ische...mentioning

confidence: 98%

Insight Into the Mechanism of Exercise Preconditioning in Ischemic Stroke

Zhu¹,

Sun²,

Hu³

et al. 2022

Front. Pharmacol.

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Exercise preconditioning has attracted extensive attention to induce endogenous neuroprotection and has become the hotspot in neurotherapy. The training exercise is given multiple times before cerebral ischemia, effectively inducing ischemic tolerance and alleviating secondary brain damage post-stroke. Compared with other preconditioning methods, the main advantages of exercise include easy clinical operation and being readily accepted by patients. However, the specific mechanism behind exercise preconditioning to ameliorate brain injury is complex. It involves multi-pathway and multi-target regulation, including regulation of inflammatory response, oxidative stress, apoptosis inhibition, and neurogenesis promotion. The current review summarizes the recent studies on the mechanism of neuroprotection induced by exercise, providing the theoretical basis of applying exercise therapy to prevent and treat ischemic stroke. In addition, we highlight the various limitations and future challenges of translational medicine from fundamental study to clinical application.

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“…Submitting rats to 20 min of a daily moderate treadmill for 2 weeks can significantly reduce adenosine triphosphate (ATP) and adenosine diphosphate (ADP) hydrolysis in the hippocampal synaptosomes and blood serum [ 23 ], suggesting lower activity of CD39. Possible modulation of A1R [ 4 ], A2AR, P2X2R, P2X6R [ 16 ], P2X4R [ 14 ], and P2X7R [ 15 ] by physical exercise was explored in complex regional pain syndrome type I (CRPS-I) mice, chronic constriction injury rats, stroke rats, and hypertensive rats. However, there is still a lack of information about the possible effects of physical training on some P2YRs.…”

Section: Exercise Improves Neurological Disorders By Regulating Bdnf ...mentioning

confidence: 99%

“…Following intracerebral hemorrhage, ATP administration had the ability to relieve cerebral hemorrhage–induced injury and improve cerebral neurological function by upregulating the mBDNF/proBDNF ratio and p38-MAPK. However, whether P2X7R has a clear regulatory effect on BDNF has not been clearly demonstrated in the area of stroke improvement [ 15 ].…”

Section: Exercise Improves Stroke Probably By Activating P2x7r and Bdnfmentioning

confidence: 99%

“…Moreover, preconditioning exercise decreased P2X4 receptor (P2X4R) and BDNF, decreased inflammatory cytokines, and ceased prior to sciatic injury [ 14 ]. It has been reported that P2X7 receptor (P2X7R) and BDNF are probably involved in neuron structural and functional modifications that culminate in the enhancement of sensorimotor function after exercise [ 15 ]. Here, we provide support for the hypothesis that P2X4R and P2X7R activate the BDNF signaling pathway in the neuroprotection of exercise (Figure 1 ), which mainly contributes to anti-inflammatory and neuroplasticity.…”

Section: Introductionmentioning

confidence: 99%

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Neuroprotection of exercise: P2X4R and P2X7R regulate BDNF actions

Sun

Peng

Liu

et al. 2022

Purinergic Signalling

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The neurotrophin brain-derived neurotrophic factor (BDNF), which acts as a transducer, is responsible for improving cerebral stroke, neuropathic pain, and depression. Exercise can alter extracellular nucleotide levels and purinergic receptors in central nervous system (CNS) structures. This inevitably activates or inhibits the expression of BDNF via purinergic receptors, particularly the P2X receptor (P2XR), to alleviate pathological progression. In addition, the significant involvement of sensitive P2X4R in mediating increased BDNF and p38-MAPK for intracerebral hemorrhage and pain hypersensitivity has been reported. Moreover, archetypal P2X7R blockade induces mouse antidepressant-like behavior and analgesia by BDNF release. This review summarizes BDNF-mediated neural effects via purinergic receptors, speculates that P2X4R and P2X7R could be priming molecules in exercise-mediated changes in BDNF, and provides strategies for the protective mechanism of exercise in neurogenic disease.

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Effects of detraining on preconditioning exercise-induced neuroprotective potential after ischemic stroke in rats

Cited by 11 publications

References 30 publications

Effects of different remote ischemia perconditioning methods on cerebral infarct volume and neurological impairment in rats

Effects of different remote ischemia perconditioning methods on cerebral infarct volume and neurological impairment in rats

Insight Into the Mechanism of Exercise Preconditioning in Ischemic Stroke

Neuroprotection of exercise: P2X4R and P2X7R regulate BDNF actions

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