Combination treatment with progesterone and rehabilitation training further promotes behavioral recovery after acute ischemic stroke in mice

Jiang-bi, Wang; Xiang, Feng; Du, Yi; Wang, Lei; Zhang, Shengxiang

doi:10.3233/rnn-130312

Cited by 6 publications

(5 citation statements)

References 77 publications

(80 reference statements)

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“…Rehabilitation could increase reorganization of cortical maps whereas the progesterone might reduce the infarct volume through its neuroprotective effect by targeting excitotoxicity. Although this combination had no additional effect in reducing infarct volume, functional recovery effectiveness was promoted as shown by the increased rotarod performance and forelimb grip strength at all time points within 7 days after ischemic stroke [ 32 ].…”

Section: Beneficial Effect Of Physical Training Rehabilitation In mentioning

confidence: 99%

Physical Exercise as a Diagnostic, Rehabilitation, and Preventive Tool: Influence on Neuroplasticity and Motor Recovery after Stroke

Pin-Barre

Laurin

2015

Neural Plasticity

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Stroke remains a leading cause of adult motor disabilities in the world and accounts for the greatest number of hospitalizations for neurological disease. Stroke treatments/therapies need to promote neuroplasticity to improve motor function. Physical exercise is considered as a major candidate for ultimately promoting neural plasticity and could be used for different purposes in human and animal experiments. First, acute exercise could be used as a diagnostic tool to understand new neural mechanisms underlying stroke physiopathology. Indeed, better knowledge of stroke mechanisms that affect movements is crucial for enhancing treatment/rehabilitation effectiveness. Secondly, it is well established that physical exercise training is advised as an effective rehabilitation tool. Indeed, it reduces inflammatory processes and apoptotic marker expression, promotes brain angiogenesis and expression of some growth factors, and improves the activation of affected muscles during exercise. Nevertheless, exercise training might also aggravate sensorimotor deficits and brain injury depending on the chosen exercise parameters. For the last few years, physical training has been combined with pharmacological treatments to accentuate and/or accelerate beneficial neural and motor effects. Finally, physical exercise might also be considered as a major nonpharmacological preventive strategy that provides neuroprotective effects reducing adverse effects of brain ischemia. Therefore, prestroke regular physical activity may also decrease the motor outcome severity of stroke.

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Section: Beneficial Effect Of Physical Training Rehabilitation In mentioning

confidence: 99%

Physical Exercise as a Diagnostic, Rehabilitation, and Preventive Tool: Influence on Neuroplasticity and Motor Recovery after Stroke

Pin-Barre

Laurin

2015

Neural Plasticity

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“…The second consideration is whether early locomotor exercise combined with other rehabilitative treatments or drugs is more reasonable than locomotor exercise only. 146,147 A related rehabilitative treatment may be functional electrical stimulation, acupuncture, music stimulus, light stimulus, skilled training, and so on. Drugs can include multiple agents that alleviate inflammatory response and neuronal apoptosis and promote angiogenesis and neurogenesis.…”

Section: Summary and Prospectsmentioning

confidence: 99%

“…, 86 , 115 There are many locomotor exercise manipulations that could be used conveniently, but so far this is no unified standard to assist in choosing the optimum type. The second consideration is whether early locomotor exercise combined with other rehabilitative treatments or drugs is more reasonable than locomotor exercise only 146 147 A related rehabilitative treatment may be functional electrical stimulation, acupuncture, music stimulus, light stimulus, skilled training, and so on.…”

Section: Summary and Prospectsmentioning

confidence: 99%

Neuroprotection of Early Locomotor Exercise Poststroke: Evidence From Animal Studies

Zhang

Jia

Yang

et al. 2015

Can. J. Neurol. Sci.

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Early locomotor exercise after stroke has attracted a great deal of attention in clinical and animal research in recent years. A series of animal studies showed that early locomotor exercise poststroke could protect against ischemic brain injury and improve functional outcomes through the promotion of angiogenesis, inhibition of acute inflammatory response and neuron apoptosis, and protection of the blood-brain barrier. However, to date, the clinical application of early locomotor exercise poststroke was limited because some clinicians have little confidence in its effectiveness. Here we review the current progress of early locomotor exercise poststroke in animal models. We hope that a comprehensive awareness of the early locomotor exercise poststroke may help to implement early locomotor exercise more appropriately in treatment for ischemic stroke.RÉSUMÉ: Neuroprotection conférée par l'exercice locomoteur précoce après un accident vasculaire cérébral : données tirées des études chez l'animal. L'exercice locomoteur précoce après un accident vasculaire cérébral (AVC) a retenu l'attention en recherche clinique et en recherche chez l'animal au cours des dernières années. Plusieurs études chez l'animal ont montré que l'exercice locomoteur précoce après un AVC protégerait contre une lésion ischémique du cerveau et pourrait améliorer l'issue fonctionnelle en favorisant l'angiogenèse, l'inhibition de la réponse inflammatoire aiguë et l'apoptose neuronale ainsi que la protection de la barrière hémato-encéphalique. Cependant, à ce jour, le recours en clinique à l'exercice locomoteur précoce après un AVC a été limité parce que certains cliniciens ont peu confiance en son efficacité. Nous revoyons les progrès actuels dans le domaine de l'exercice locomoteur précoce après un AVC chez des modèles animaux. Nous espérons qu'une sensibilisation à l'exercice locomoteur précoce après un AVC pourra favoriser une utilisation de l'exercice locomoteur précoce de façon plus appropriée dans le traitement de l'AVC ischémique.

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“…Progesterone treatment can improve the neurological function of rats with brain injury, and its mechanism may be related to the regulatory of progesterone on immuneinflammatory after brain injury [6]. In animal experiments of acute toxic injury, traumatic injury, spinal cord injury, and the central nervous system stroke, the application of progesterone therapy can delay the necrosis and apoptosis of nerve cells in model animals, reduce the inflammatory reaction and brain edema caused by ischemic brain injury, promote the synthesis of brain myelin sheath, and promote the reconstruction of the blood-brain barrier [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

Progesterone Reduces ATP-Induced Pyroptosis of SH-SY5Y Cells

Cui

Wang

Zhang

et al. 2022

BioMed Research International

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Aim. To investigate the mechanism of progesterone inhibiting the scorch death of SH-SY5Y cells induced by exogenous adenosine triphosphate (ATP). Methods. SH-SY5Y cells with good logarithmic growth were used in the experiment. The cells were randomly divided into 5 groups: normal control group, DMSO group, BBG group, ATP group, and ATP+progesterone group. The cell survival rate of each group was measured by CCK-8 method. The expressions of P2X7 receptor, caspase-1, caspase-11, and IL-1β were detected by western blotting. Results. (1) After SH-SY5Y cells were treated with ATP at different concentrations (1, 3, 6, and 9 mmol/L) for 2 hours, the cell survival rate decreased in a concentration-dependent manner compared with the normal blank group. The results showed that the optimal lethal concentration of ATP was 6 mmol/L. SH-SY5Y cells were preincubated with progesterone at different concentrations (3, 10, 30, and 100 nmol/L) for 30 minutes and then incubated with 6 mmol/L ATP. The cell survival rate of this group was significantly improved ( P < 0.01 ). The optimal concentration of progesterone to improve cell survival and inhibit cell death was 30 nmol/L. (2) Compared to the control group, there was no significant difference ( P > 0.05 ) in P2X7 receptor, caspase-1, caspase-11, and IL-1β with the DMSO group (0.001% DMSO, 24 h) and BBG group (bbg1 mmol/L, 24 h). (3) In the ATP group, the expression of P2X7 receptor and caspase-1 (the key protein of classical cell death pathway) increased significantly ( P < 0.01 ), which was related to inflammatory factor IL-1β with consistent performance ( P < 0.01 ). There was no significant change in caspase-11 (the key protein of nonclassical focal death pathway) ( P > 0.05 ). (4) The expression of P2X7 receptor, caspase-1, and inflammatory factor IL-1β in the progesterone+ATP group was significantly downregulated ( P < 0.01 ). There was no significant change in caspase-11 ( P > 0.05 ). Conclusion. Certain dose of progesterone can inhibit the focal death of SH-SY5Y cells induced by extracellular high concentration ATP. It can reduce the expression of P2X7 receptor, inhibit the conduction pathway of cell death, reduce the release of inflammatory factor IL-1β, and improve cell survival.

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Combination treatment with progesterone and rehabilitation training further promotes behavioral recovery after acute ischemic stroke in mice

Cited by 6 publications

References 77 publications

Physical Exercise as a Diagnostic, Rehabilitation, and Preventive Tool: Influence on Neuroplasticity and Motor Recovery after Stroke

Physical Exercise as a Diagnostic, Rehabilitation, and Preventive Tool: Influence on Neuroplasticity and Motor Recovery after Stroke

Neuroprotection of Early Locomotor Exercise Poststroke: Evidence From Animal Studies

Progesterone Reduces ATP-Induced Pyroptosis of SH-SY5Y Cells

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