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Forced exercise enhances functional recovery after focal cerebral ischemia in spontaneously hypertensive rats.

Park S, Shin J, Hong Y, Kim S, Lee S, Park K, Lkhagvasuren T, Lee SR, Chang KT, Hong Y - Brain Sci (2012)

Bottom Line: Expression of caveolins was decreased in MCAo brain tissue, whereas the levels of iNOS and glial fibrillary acidic protein (GFAP) increased.Additionally, LC3-II and beclin-1 levels were elevated in the MCAo groups.These results suggest that forced exercise may be beneficial for promoting functional recovery following cerebral ischemia through caveolin-dependent mechanisms or interactions between caveolins and these signaling molecules in ischemic brain regions.

View Article: PubMed Central - PubMed

Affiliation: Cardiovascular & Metabolic Disease Center, College of Biomedical Science & Engineering, Inje University, Gimhae 621-749, Korea. charm-soo@hanmail.net.

ABSTRACT
Caveolin is the principal protein of caveolae and has been implicated in the pathogenesis of cerebral ischemia. To investigate whether changed expression of caveolins has a pivotal role in focal cerebral ischemia, we induced middle cerebral artery occlusion (MCAo)-reperfusion and examined expression of caveolins, inflammatory activation markers, and mediators of autophagic cell death. We also treated MCAo rats with forced exercise to determine its effects on neurological outcome. Particularly, spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were used to compare the effects of hypertension on focal cerebral ischemia. All MCAo groups showed neurological deficiencies, motor dysfunction, and disruption of balancing ability; however, these pathological changes were more severe in SHR than WKY rats. Expression of caveolins was decreased in MCAo brain tissue, whereas the levels of iNOS and glial fibrillary acidic protein (GFAP) increased. Additionally, LC3-II and beclin-1 levels were elevated in the MCAo groups. Forced exercise attenuated both molecular and behavioral changes in MCAo animals, but SHR rats showed delayed functional recovery and residual molecular changes when compared to WKY rats. These results suggest that forced exercise may be beneficial for promoting functional recovery following cerebral ischemia through caveolin-dependent mechanisms or interactions between caveolins and these signaling molecules in ischemic brain regions.

No MeSH data available.


Related in: MedlinePlus

2,3,5-triphenyltetrazolium chloride (TTC)-defined volume of ischemic lesions in WKY and SHR rats after middle cerebral artery occlusion (MCAo) surgery. (A) Representative TTC staining of brain slices in rats after MCAo. After 24 h, WKY and SHR rats were sacrificed, and their brains were removed and cut into coronal slices. (B) Lesion volumes were determined for all brain slices. For each slice, the lesion volume is expressed as the percentage of the total ipsilateral hemispheric slice volume. Brains were cut into coronal slices of 2-mm thickness between the bregma levels of +4 mm (anterior) and −6 mm (posterior), yielding six coronal slices. Brain slices were labeled a to f in sequence. Data shown are means ± SEM, * p < 0.05 in WKY-MCAo and SHR-MCAo.
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brainsci-02-00483-f002: 2,3,5-triphenyltetrazolium chloride (TTC)-defined volume of ischemic lesions in WKY and SHR rats after middle cerebral artery occlusion (MCAo) surgery. (A) Representative TTC staining of brain slices in rats after MCAo. After 24 h, WKY and SHR rats were sacrificed, and their brains were removed and cut into coronal slices. (B) Lesion volumes were determined for all brain slices. For each slice, the lesion volume is expressed as the percentage of the total ipsilateral hemispheric slice volume. Brains were cut into coronal slices of 2-mm thickness between the bregma levels of +4 mm (anterior) and −6 mm (posterior), yielding six coronal slices. Brain slices were labeled a to f in sequence. Data shown are means ± SEM, * p < 0.05 in WKY-MCAo and SHR-MCAo.

Mentions: To determine the effects of hypertension on cerebral infarction due to MCAo, MCAo rats in WKY and SHR were sacrificed and compared cerebral infarction volume at 24 h after MCAo surgery. The brains were removed and cut into six 2-mm-thick coronal slices between the bregma levels of +4 mm (anterior) and −6 mm (posterior). Lesion volumes were determined for all brain slices and are expressed as a percent of the total ipsilateral hemispheric slice volume (see Figure 2A). The cerebral infarction volume of the first brain slice was 16.5% ± 1.50% and 26.5% ± 1.50% in WKY and SHR rats, respectively (p < 0.05). The cerebral infarction volume of the second brain slice was 35% ± 1.0% and 67% ± 2.0% in WKY and SHR rats (p < 0.05), respectively. Lesions were also evident in the third (45.5% ± 3.50% and 62% ± 2.0%) and fourth brain slices (41% ± 1.0% and 64% ± 3.0%) in both WKY and SHR rats (p < 0.05), respectively (see Figure 2B). These results demonstrated that SHR rats had more severe cerebral infarction volumes as compared with control WKY rats after MCAo surgery. Thus, hypertension appears to be a risk factor affecting extent of lesion size after focal cerebral ischemia.


Forced exercise enhances functional recovery after focal cerebral ischemia in spontaneously hypertensive rats.

Park S, Shin J, Hong Y, Kim S, Lee S, Park K, Lkhagvasuren T, Lee SR, Chang KT, Hong Y - Brain Sci (2012)

2,3,5-triphenyltetrazolium chloride (TTC)-defined volume of ischemic lesions in WKY and SHR rats after middle cerebral artery occlusion (MCAo) surgery. (A) Representative TTC staining of brain slices in rats after MCAo. After 24 h, WKY and SHR rats were sacrificed, and their brains were removed and cut into coronal slices. (B) Lesion volumes were determined for all brain slices. For each slice, the lesion volume is expressed as the percentage of the total ipsilateral hemispheric slice volume. Brains were cut into coronal slices of 2-mm thickness between the bregma levels of +4 mm (anterior) and −6 mm (posterior), yielding six coronal slices. Brain slices were labeled a to f in sequence. Data shown are means ± SEM, * p < 0.05 in WKY-MCAo and SHR-MCAo.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4061815&req=5

brainsci-02-00483-f002: 2,3,5-triphenyltetrazolium chloride (TTC)-defined volume of ischemic lesions in WKY and SHR rats after middle cerebral artery occlusion (MCAo) surgery. (A) Representative TTC staining of brain slices in rats after MCAo. After 24 h, WKY and SHR rats were sacrificed, and their brains were removed and cut into coronal slices. (B) Lesion volumes were determined for all brain slices. For each slice, the lesion volume is expressed as the percentage of the total ipsilateral hemispheric slice volume. Brains were cut into coronal slices of 2-mm thickness between the bregma levels of +4 mm (anterior) and −6 mm (posterior), yielding six coronal slices. Brain slices were labeled a to f in sequence. Data shown are means ± SEM, * p < 0.05 in WKY-MCAo and SHR-MCAo.
Mentions: To determine the effects of hypertension on cerebral infarction due to MCAo, MCAo rats in WKY and SHR were sacrificed and compared cerebral infarction volume at 24 h after MCAo surgery. The brains were removed and cut into six 2-mm-thick coronal slices between the bregma levels of +4 mm (anterior) and −6 mm (posterior). Lesion volumes were determined for all brain slices and are expressed as a percent of the total ipsilateral hemispheric slice volume (see Figure 2A). The cerebral infarction volume of the first brain slice was 16.5% ± 1.50% and 26.5% ± 1.50% in WKY and SHR rats, respectively (p < 0.05). The cerebral infarction volume of the second brain slice was 35% ± 1.0% and 67% ± 2.0% in WKY and SHR rats (p < 0.05), respectively. Lesions were also evident in the third (45.5% ± 3.50% and 62% ± 2.0%) and fourth brain slices (41% ± 1.0% and 64% ± 3.0%) in both WKY and SHR rats (p < 0.05), respectively (see Figure 2B). These results demonstrated that SHR rats had more severe cerebral infarction volumes as compared with control WKY rats after MCAo surgery. Thus, hypertension appears to be a risk factor affecting extent of lesion size after focal cerebral ischemia.

Bottom Line: Expression of caveolins was decreased in MCAo brain tissue, whereas the levels of iNOS and glial fibrillary acidic protein (GFAP) increased.Additionally, LC3-II and beclin-1 levels were elevated in the MCAo groups.These results suggest that forced exercise may be beneficial for promoting functional recovery following cerebral ischemia through caveolin-dependent mechanisms or interactions between caveolins and these signaling molecules in ischemic brain regions.

View Article: PubMed Central - PubMed

Affiliation: Cardiovascular &amp; Metabolic Disease Center, College of Biomedical Science &amp; Engineering, Inje University, Gimhae 621-749, Korea. charm-soo@hanmail.net.

ABSTRACT
Caveolin is the principal protein of caveolae and has been implicated in the pathogenesis of cerebral ischemia. To investigate whether changed expression of caveolins has a pivotal role in focal cerebral ischemia, we induced middle cerebral artery occlusion (MCAo)-reperfusion and examined expression of caveolins, inflammatory activation markers, and mediators of autophagic cell death. We also treated MCAo rats with forced exercise to determine its effects on neurological outcome. Particularly, spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were used to compare the effects of hypertension on focal cerebral ischemia. All MCAo groups showed neurological deficiencies, motor dysfunction, and disruption of balancing ability; however, these pathological changes were more severe in SHR than WKY rats. Expression of caveolins was decreased in MCAo brain tissue, whereas the levels of iNOS and glial fibrillary acidic protein (GFAP) increased. Additionally, LC3-II and beclin-1 levels were elevated in the MCAo groups. Forced exercise attenuated both molecular and behavioral changes in MCAo animals, but SHR rats showed delayed functional recovery and residual molecular changes when compared to WKY rats. These results suggest that forced exercise may be beneficial for promoting functional recovery following cerebral ischemia through caveolin-dependent mechanisms or interactions between caveolins and these signaling molecules in ischemic brain regions.

No MeSH data available.


Related in: MedlinePlus