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Physical exercise promotes recovery of neurological function after ischemic stroke in rats.

ABSTRACT: Although physical exercise is an effective strategy for treatment of ischemic stroke, the underlying protective mechanisms are still not well understood. It has been recently demonstrated that neural progenitor cells play a vital role in the recovery of neurological function (NF) through differentiation into mature neurons. In the current study, we observed that physical exercise significantly reduced the infarct size and improved damaged neural functional recovery after an ischemic stroke. Furthermore, we found that the treatment not only exhibited a significant increase in the number of neural progenitor cells and neurons but also decreased the apoptotic cells in the peri-infarct region, compared to a control in the absence of exercise. Importantly, the insulin-like growth factor-1 (IGF-1)/Akt signaling pathway was dramatically activated in the peri-infarct region of rats after physical exercise training. Therefore, our findings suggest that physical exercise directly influences the NF recovery process by increasing neural progenitor cell count via activation of the IGF-1/Akt signaling pathway.

SUBMITTER: Zheng HQ

PROVIDER: S-EPMC4100192 | biostudies-literature | 2014 Jun

REPOSITORIES: biostudies-literature

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Physical exercise promotes recovery of neurological function after ischemic stroke in rats.

Zheng Hai-Qing HQ Zhang Li-Ying LY Luo Jing J Li Li-Li LL Li Menglin M Zhang Qingjie Q Hu Xi-Quan XQ

International journal of molecular sciences 20140618 6

Although physical exercise is an effective strategy for treatment of ischemic stroke, the underlying protective mechanisms are still not well understood. It has been recently demonstrated that neural progenitor cells play a vital role in the recovery of neurological function (NF) through differentiation into mature neurons. In the current study, we observed that physical exercise significantly reduced the infarct size and improved damaged neural functional recovery after an ischemic stroke. Furt ...[more]

PMID: 24945308

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Project description:AimVasculotide (VT), an angiopoietin-1 mimetic peptide, exerts neuroprotective effects in type one diabetic (T1DM) rats subjected to ischemic stroke. In this study, we investigated whether delayed VT treatment improves long-term neurological outcome after stroke in T1DM rats.MethodsMale Wistar rats were induced with T1DM, subjected to middle cerebral artery occlusion (MCAo) model of stroke, and treated with PBS (control), 2 µg/kg VT, 3 µg/kg VT, or 5.5 µg/kg VT. VT treatment was initiated at 24 h after stroke and administered daily (i.p) for 14 days. We evaluated neurological function, lesion volume, vascular and white matter remodeling, and inflammation in the ischemic brain. In vitro, we evaluated the effects of VT on endothelial cell capillary tube formation and inflammatory responses of primary cortical neurons (PCN) and macrophages.ResultsTreatment of T1DM-stroke with 3 µg/kg VT but not 2 µg/kg or 5.5 µg/kg significantly improves neurological function and decreases infarct volume and cell death compared to control T1DM-stroke rats. Thus, 3 µg/kg VT dose was employed in all subsequent in vivo analysis. VT treatment significantly increases axon and myelin density, decreases demyelination, decreases white matter injury, increases number of oligodendrocytes, and increases vascular density in the ischemic border zone of T1DM stroke rats. VT treatment significantly decreases MMP9 expression and decreases the number of M1 macrophages in the ischemic brain of T1DM-stroke rats. In vitro, VT treatment significantly decreases endothelial cell death and decreases MCP-1, endothelin-1, and VEGF expression under high glucose (HG) and ischemic conditions and significantly increases capillary tube formation under HG conditions when compared to non-treated control group. VT treatment significantly decreases inflammatory factor expression such as MMP9 and MCP-1 in macrophages subjected to LPS activation and significantly decreases IL-1? and MMP9 expression in PCN subjected to ischemia under HG conditions.ConclusionDelayed VT treatment (24 h after stroke) significantly improves neurological function, promotes vascular and white matter remodeling, and decreases inflammation in the ischemic brain after stroke in T1DM rats.

Project description:Purpose: Skin-derived Precursor Schwann cells (SKP-SCs) have been reported to provide neuroprotection for the injured and dysmyelinated nervous system. However, little is known about SKP-SCs on acute ischemic stroke (AIS). We aimed to explore the efficacy and the potential mechanism of action of SKP-SCs on AIS in a rat ischemic stroke model. Methods: Adult male Sprague-Dawley rats were subjected to a middle cerebral artery occlusion (MCAO) for 1.5 h on Day 0 and subsequently received an intracarotid injection of 2 × 106 green fluorescent protein (GFP) -labeled SKP-SCs or phosphate buffered saline (PBS) during reperfusion. Neurological function was assessed by behavioral tests on Days 1, 4, 7, 14, and 28. In a satellite cohort, rat brains were harvested and infarct volume was measured with 2,3,5-triphenyltetrazolium chloride (TTC) staining on Days 1 and 7, and migration and survival of SKP-SCs in the brain were traced by monitoring green fluorescence at 6 and12 h on Day 0, and on Days 1, 4, 7, 14, and 28. Histopathology and immunofluorescence staining were used to analyze the morphology, survival and apoptosis of neurons. Additionally, in an in vitro SKP-SC co-culture model using fetal rat primary cortical neurons underwent oxygen glucose deprivation/reoxygenation (OGD/R), Western blot was used to detect the expression of apoptosis indicators including activated caspase-3, Bax, and Bcl-2. TUNEL staining was used to count apoptotic cells. Results: Intracarotid transplantation of SKP-SCs effectively migrated to the periinfarct area and survived for at least 4 weeks. Transplanted SKP-SCs inhibited neuronal apoptosis, reduced infarct volume, and improved neurological recovery in the MCAO rats. Moreover, in vitro data showed that SKP-SCs treatment inhibited OGD/R-induced neuronal apoptosis and promoted survival of the cultured primary cortical neurons. Conclusions: Intracarotid transplantation of SKP-SCs promoted functional recovery in the rat AIS model and possesses the potential to be further developed as a novel therapy to treat ischemic stroke in humans.

Project description:Background: Stroke is the leading cause of death and disability. Exercise produces neuroprotection by improving neuroplasticity. Exercise can induce exosome production. According to several studies, exosomes are involved in repairing brain function, but the relationship and mechanism of exercise, exosomes, and neuroprotection have not been elucidated. This study intends to explore the relationship and potential mechanism by observing the changes in the exosome level, infarct volume, neurological function and behavioral scores, synapses, and corticospinal tract (CST). Methods: Rats were randomly divided into four groups: a sham operation (SHAM) group, middle cerebral artery occlusion (MCAO) with sedentary intervention (SED-MCAO) group, MCAO with exercise intervention (EX-MCAO) group, and MCAO with exercise intervention and exosome injection (EX-MCAO-EXO) group. The exercise intervention was started 1 day after MCAO and lasted for 4 weeks. All rats were assessed using the modified neurological severity score (mNSS). The levels of exosomes in serum and brain, gait analysis, and magnetic resonance scan were performed 1 and 4 weeks after the intervention. After 4 weeks of intervention, the number of synapses, synaptophysin (Syn), and postsynaptic density protein 95(PSD-95) expression was detected. Results: After 4 weeks of intervention, (1) the EX-MCAO and EX-MCAO-EXO groups showed higher serum exosome (p EX-MCAO = 0.000, p EX-MCAO-EXO = 0.000) and brain exosome (p EX-MCAO = 0.001, p EX-MCAO-EXO = 0.000) levels than the SED-MCAO group, of which the EX-MCAO group had the highest serum exosome (p = 0.000) and the EX-MCAO-EXO group had the highest brain exosome (p = 0.03) levels. (2) The number of synapses in the EX-MCAO (p = 0.032) and EX-MCAO-EXO groups (p = 0.000) was significantly higher than that in the SED-MCAO group. The EX-MCAO-EXO group exhibited a greater number of synapses than the EX-MCAO (p = 0.000) group. (3) The synaptic plasticity-associated proteins were expressed significantly higher in the EX-MCAO (p Syn = 0.010, p PSD-95 = 0.044) and EX-MCAO-EXO (p Syn = 0.000, p PSD-95 = 0.000) groups than in the SED-MCAO group, and the EX-MCAO-EXO group (p Syn = 0.000, p PSD-95 = 0.046) had the highest expression. (4) Compared with the SED-MCAO group, the EX-MCAO group had significantly improved infarct volume ratio (p = 0.000), rFA value (p = 0.000), and rADC (p = 0.000). Compared with the EX-MCAO group, the EX-MCAO-EXO group had a significantly improved infarct volume ratio (p = 0.000), rFA value (p = 0.000), and rADC value (p = 0.001). (5) Compared with the SED-MCAO group, the EX-MCAO group (p = 0.001) and EX-MCAO-EXO group (p = 0.000) had significantly lower mNSS scores and improved gait. (6) The brain exosome levels were negatively correlated with the mNSS score, infarct volume ratio, and rADC value and positively correlated with the rFA value, Syn, and PSD-95 expression. The serum and brain exosome levels showed a positive correlation. Conclusions: Exercise intervention increases the serum exosome level in MCAO rats, which are recruited into the brain, leading to improved synaptic growth and CST integrity, a reduced infarct volume, and improved neurological function and gait.

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Physical exercise promotes recovery of neurological function after ischemic stroke in rats.

Publications

Physical exercise promotes recovery of neurological function after ischemic stroke in rats.

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