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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

Schematic diagram of experimental design. WKY and SHR rats were randomly divided into four groups: Sham, Sham + Ex, MCAo, and MCAo + Ex groups. The brain tissue of the core infarction region was analyzed for expression of caveolins, inflammatory activation markers (NOS isoforms (iNOS and nNOS) and GFAP), and mediators of autophagic cell death (LC3 and beclin-1). Motor dysfunction due to MCAo was also evaluated.
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brainsci-02-00483-f006: Schematic diagram of experimental design. WKY and SHR rats were randomly divided into four groups: Sham, Sham + Ex, MCAo, and MCAo + Ex groups. The brain tissue of the core infarction region was analyzed for expression of caveolins, inflammatory activation markers (NOS isoforms (iNOS and nNOS) and GFAP), and mediators of autophagic cell death (LC3 and beclin-1). Motor dysfunction due to MCAo was also evaluated.

Mentions: As shown at Figure 1A, both WKY and SHR rats were randomly divided into four groups: Sham, sham with exercise (Sham + Ex), MCAo, and exercise after MCAo (MCAo + Ex). In the Sham group (n = 6), as a normal state without injury, exercise was not administered. The Sham + Ex group (n = 6) performed motor-driven treadmill exercise. In the MCAo group (n = 6), MCAo was induced, and exercise was not administered. In the MCAo + Ex group (n = 6), MCAo was induced, and the animals exercised on a motor-driven treadmill. Rats were sacrificed 28 days after injury, and brain tissue was obtained for histological and biochemical analysis (see Figure 6).


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)

Schematic diagram of experimental design. WKY and SHR rats were randomly divided into four groups: Sham, Sham + Ex, MCAo, and MCAo + Ex groups. The brain tissue of the core infarction region was analyzed for expression of caveolins, inflammatory activation markers (NOS isoforms (iNOS and nNOS) and GFAP), and mediators of autophagic cell death (LC3 and beclin-1). Motor dysfunction due to MCAo was also evaluated.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

brainsci-02-00483-f006: Schematic diagram of experimental design. WKY and SHR rats were randomly divided into four groups: Sham, Sham + Ex, MCAo, and MCAo + Ex groups. The brain tissue of the core infarction region was analyzed for expression of caveolins, inflammatory activation markers (NOS isoforms (iNOS and nNOS) and GFAP), and mediators of autophagic cell death (LC3 and beclin-1). Motor dysfunction due to MCAo was also evaluated.
Mentions: As shown at Figure 1A, both WKY and SHR rats were randomly divided into four groups: Sham, sham with exercise (Sham + Ex), MCAo, and exercise after MCAo (MCAo + Ex). In the Sham group (n = 6), as a normal state without injury, exercise was not administered. The Sham + Ex group (n = 6) performed motor-driven treadmill exercise. In the MCAo group (n = 6), MCAo was induced, and exercise was not administered. In the MCAo + Ex group (n = 6), MCAo was induced, and the animals exercised on a motor-driven treadmill. Rats were sacrificed 28 days after injury, and brain tissue was obtained for histological and biochemical analysis (see Figure 6).

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