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The effects of early exercise on brain damage and recovery after focal cerebral infarction in rats.

Matsuda F, Sakakima H, Yoshida Y - Acta Physiol (Oxf) (2011)

Bottom Line: We investigated whether treadmill running could reduce brain damage and enhance the expression of midkine (MK) and nerve growth factor (NGF), increase angiogenesis and decrease the expression of caspase-3.The infarct volume in the exercised group (12.4 ± 0.8%) subjected to treadmill running for 28 days was significantly decreased compared with that in the control group (19.8 ± 4.2%, P < 0.01).Our findings show that treadmill exercise improves motor behaviour and reduces neurological deficits and infarct volume, suggesting that it may aid recovery from central nervous system injury.

View Article: PubMed Central - PubMed

Affiliation: School of Health Sciences, Faculty of Medicine, Kagoshima University, Kagoshima, Japan. fumiyo@health.nop.kagoshima-u.ac.jp

ABSTRACT

Aim: Exercise can be used to enhance neuroplasticity and facilitate motor recovery after a stroke in rats. We investigated whether treadmill running could reduce brain damage and enhance the expression of midkine (MK) and nerve growth factor (NGF), increase angiogenesis and decrease the expression of caspase-3.

Methods: Seventy-seven Wistar rats were split into three experimental groups (ischaemia-control: 36, ischaemia-exercise: 36, sham-exercise: 5). Stroke was induced by 90-min left middle cerebral artery occlusion using an intraluminal filament. Beginning on the following day, the rats were made to run on a treadmill for 20 min once a day for a maximum of 28 consecutive days. Functional recovery after ischaemia was assessed using the beamwalking test and a neurological evaluation scale in all rats. Infarct volume, and the expression of MK, NGF, anti-platelet-endothelial cell adhesion molecule (PECAM-1), and caspase-3 were evaluated at 1, 3, 5, 7, 14 and 28 days after the induction of ischaemia.

Results: Over time motor coordination and neurological deficits improved more in the exercised group than in the non-exercised group. The infarct volume in the exercised group (12.4 ± 0.8%) subjected to treadmill running for 28 days was significantly decreased compared with that in the control group (19.8 ± 4.2%, P < 0.01). The cellular expression levels of MK, NGF and PECAM-1 were significantly increased while that of caspase-3 was decreased in the peri-infarct area of the exercised rats.

Conclusions: Our findings show that treadmill exercise improves motor behaviour and reduces neurological deficits and infarct volume, suggesting that it may aid recovery from central nervous system injury.

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Related in: MedlinePlus

Representative photographs of caspase-3-positive cells. Brain sections were immunohistochemically stained for caspase-3 as an apoptosis marker in the ipsilateral frontoparietal cortex including the motor cortex 14 days after ischaemic injury in the ischaemia-exercise (IE) (a) and ischaemia-non-exercised control (IC) (b) groups. Changes in the caspase-3 -immunoreactive areas on the infarction side after ischaemia (c) are shown. Quantitative analysis was conducted on caspase-3 immunoreactive cells from the motor cortex in the IE and IC groups for 14 days that indicated the occurrence of apoptosis. anova analysis demonstrated a significant increase in the number of caspase-3 labelled cells after exercise; *P < 0.05 (compared with IC group value). No caspase-3 immunoreactive cells were detected in the normal brains (SE group) or at 28 days after ischaemia. Values shown are mean ± SD (n = 6). Scale bar = 200 μm.
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fig07: Representative photographs of caspase-3-positive cells. Brain sections were immunohistochemically stained for caspase-3 as an apoptosis marker in the ipsilateral frontoparietal cortex including the motor cortex 14 days after ischaemic injury in the ischaemia-exercise (IE) (a) and ischaemia-non-exercised control (IC) (b) groups. Changes in the caspase-3 -immunoreactive areas on the infarction side after ischaemia (c) are shown. Quantitative analysis was conducted on caspase-3 immunoreactive cells from the motor cortex in the IE and IC groups for 14 days that indicated the occurrence of apoptosis. anova analysis demonstrated a significant increase in the number of caspase-3 labelled cells after exercise; *P < 0.05 (compared with IC group value). No caspase-3 immunoreactive cells were detected in the normal brains (SE group) or at 28 days after ischaemia. Values shown are mean ± SD (n = 6). Scale bar = 200 μm.

Mentions: Photomicrographs of caspase-3-positive cells are shown in Figure 7a,b. Caspase-3-immunopositive cells were detected in the infarct and peri-infarct regions after the induction of ischaemia in rats of the IE and IC groups, but not on the contralateral side nor in the brains of rats of the SE group. The area of caspase-3-positive cells was nearly zero mm2 in the SE group brain, but was markedly increased to 7.89 ± 3.68 mm2 in the IC group (Fig. 7d) and reduced to 3.29 ± 2.04 mm2 in the IE group by 14 days after surgery (Fig. 7c). Two-factor factorial anova revealed a significant effect of group (F1,60 = 16.38, P=0.0003) but no effect of day (F5,60 = 1.71, P=0.17) or of the interaction between group and day (F10,60 = 0.204, P=0.93). A subsequent one-way anova (day) revealed a significant difference among the groups with regard to the number of caspase-3-positive cells at 5 days (P<0.01) and 14 days (P=0.04), but not at other time points (data not shown). These findings showed that infarction enhanced caspase-3 expression in the ipsilateral frontoparietal cortex including the motor cortex and that treadmill exercise after MCA occlusion significantly suppressed ischaemia-induced increases in caspase-3 expression (Fig. 7c).


The effects of early exercise on brain damage and recovery after focal cerebral infarction in rats.

Matsuda F, Sakakima H, Yoshida Y - Acta Physiol (Oxf) (2011)

Representative photographs of caspase-3-positive cells. Brain sections were immunohistochemically stained for caspase-3 as an apoptosis marker in the ipsilateral frontoparietal cortex including the motor cortex 14 days after ischaemic injury in the ischaemia-exercise (IE) (a) and ischaemia-non-exercised control (IC) (b) groups. Changes in the caspase-3 -immunoreactive areas on the infarction side after ischaemia (c) are shown. Quantitative analysis was conducted on caspase-3 immunoreactive cells from the motor cortex in the IE and IC groups for 14 days that indicated the occurrence of apoptosis. anova analysis demonstrated a significant increase in the number of caspase-3 labelled cells after exercise; *P < 0.05 (compared with IC group value). No caspase-3 immunoreactive cells were detected in the normal brains (SE group) or at 28 days after ischaemia. Values shown are mean ± SD (n = 6). Scale bar = 200 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3045711&req=5

fig07: Representative photographs of caspase-3-positive cells. Brain sections were immunohistochemically stained for caspase-3 as an apoptosis marker in the ipsilateral frontoparietal cortex including the motor cortex 14 days after ischaemic injury in the ischaemia-exercise (IE) (a) and ischaemia-non-exercised control (IC) (b) groups. Changes in the caspase-3 -immunoreactive areas on the infarction side after ischaemia (c) are shown. Quantitative analysis was conducted on caspase-3 immunoreactive cells from the motor cortex in the IE and IC groups for 14 days that indicated the occurrence of apoptosis. anova analysis demonstrated a significant increase in the number of caspase-3 labelled cells after exercise; *P < 0.05 (compared with IC group value). No caspase-3 immunoreactive cells were detected in the normal brains (SE group) or at 28 days after ischaemia. Values shown are mean ± SD (n = 6). Scale bar = 200 μm.
Mentions: Photomicrographs of caspase-3-positive cells are shown in Figure 7a,b. Caspase-3-immunopositive cells were detected in the infarct and peri-infarct regions after the induction of ischaemia in rats of the IE and IC groups, but not on the contralateral side nor in the brains of rats of the SE group. The area of caspase-3-positive cells was nearly zero mm2 in the SE group brain, but was markedly increased to 7.89 ± 3.68 mm2 in the IC group (Fig. 7d) and reduced to 3.29 ± 2.04 mm2 in the IE group by 14 days after surgery (Fig. 7c). Two-factor factorial anova revealed a significant effect of group (F1,60 = 16.38, P=0.0003) but no effect of day (F5,60 = 1.71, P=0.17) or of the interaction between group and day (F10,60 = 0.204, P=0.93). A subsequent one-way anova (day) revealed a significant difference among the groups with regard to the number of caspase-3-positive cells at 5 days (P<0.01) and 14 days (P=0.04), but not at other time points (data not shown). These findings showed that infarction enhanced caspase-3 expression in the ipsilateral frontoparietal cortex including the motor cortex and that treadmill exercise after MCA occlusion significantly suppressed ischaemia-induced increases in caspase-3 expression (Fig. 7c).

Bottom Line: We investigated whether treadmill running could reduce brain damage and enhance the expression of midkine (MK) and nerve growth factor (NGF), increase angiogenesis and decrease the expression of caspase-3.The infarct volume in the exercised group (12.4 ± 0.8%) subjected to treadmill running for 28 days was significantly decreased compared with that in the control group (19.8 ± 4.2%, P < 0.01).Our findings show that treadmill exercise improves motor behaviour and reduces neurological deficits and infarct volume, suggesting that it may aid recovery from central nervous system injury.

View Article: PubMed Central - PubMed

Affiliation: School of Health Sciences, Faculty of Medicine, Kagoshima University, Kagoshima, Japan. fumiyo@health.nop.kagoshima-u.ac.jp

ABSTRACT

Aim: Exercise can be used to enhance neuroplasticity and facilitate motor recovery after a stroke in rats. We investigated whether treadmill running could reduce brain damage and enhance the expression of midkine (MK) and nerve growth factor (NGF), increase angiogenesis and decrease the expression of caspase-3.

Methods: Seventy-seven Wistar rats were split into three experimental groups (ischaemia-control: 36, ischaemia-exercise: 36, sham-exercise: 5). Stroke was induced by 90-min left middle cerebral artery occlusion using an intraluminal filament. Beginning on the following day, the rats were made to run on a treadmill for 20 min once a day for a maximum of 28 consecutive days. Functional recovery after ischaemia was assessed using the beamwalking test and a neurological evaluation scale in all rats. Infarct volume, and the expression of MK, NGF, anti-platelet-endothelial cell adhesion molecule (PECAM-1), and caspase-3 were evaluated at 1, 3, 5, 7, 14 and 28 days after the induction of ischaemia.

Results: Over time motor coordination and neurological deficits improved more in the exercised group than in the non-exercised group. The infarct volume in the exercised group (12.4 ± 0.8%) subjected to treadmill running for 28 days was significantly decreased compared with that in the control group (19.8 ± 4.2%, P < 0.01). The cellular expression levels of MK, NGF and PECAM-1 were significantly increased while that of caspase-3 was decreased in the peri-infarct area of the exercised rats.

Conclusions: Our findings show that treadmill exercise improves motor behaviour and reduces neurological deficits and infarct volume, suggesting that it may aid recovery from central nervous system injury.

Show MeSH
Related in: MedlinePlus