Effect of ligustrazine on nNOS expression and neuranagenesis in adult rats after cerebral ischemia-reperfusion injury / 南方医科大学学报
Journal of Southern Medical University
;
(12): 771-774, 2007.
Artigo
em Chinês
| WPRIM
| ID: wpr-337388
ABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of ligustrazine on cell proliferation in the subventricular zone (SVZ) and dentate gyrus (DG) and nNOS expression in rat brain after cerebral ischemia-reperfusion injury.</p><p><b>METHODS</b>Male SD rats were randomly divided into normal control group, sham operation group, model group and ligustrazine treatment group. The latter two groups were further divided into 5 subgroups for observation at 1, 3, 7, 14 and 21 days after reperfusion following a 2-hour middle cerebral artery occlusion (MCAO). The cells in S phase were labeled with BrdU, and immunohistochemistry was employed to detect BrdU- and nNOS-positive cells. The numbers of BrdU-positive cells in the SVZ and DG were measured. The expression of nNOS was detected by Western blotting.</p><p><b>RESULTS</b>nNOS expression increased significantly in the model group as compared to the sham operation group (P<0.05), and ligustrazine treatment significantly lowered the expression level in comparison with the model group (P<0.05). Compared with the model group, a significant increase in BrdU-positive cells occurred in the SVZ of rats 1 and 3 days after igustrazine treatment (P<0.05), along with an increase of DG BrdU-positive cells.</p><p><b>CONCLUSION</b>Ligustrazine significantly restrains ischemia-reperfusion injury-induced nNOS activity enhancement and promotes cell proliferation in the SVZ and DG of adult rats after ischemia-reperfusion injury.</p>
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Índice:
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Assunto principal:
Patologia
/
Farmacologia
/
Pirazinas
/
Encéfalo
/
Imuno-Histoquímica
/
Traumatismo por Reperfusão
/
Distribuição Aleatória
/
Isquemia Encefálica
/
Ventrículos Cerebrais
/
Anti-Inflamatórios não Esteroides
Limite:
Animais
Idioma:
Chinês
Revista:
Journal of Southern Medical University
Ano de publicação:
2007
Tipo de documento:
Artigo
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