Résumé
Objective To investigate the dynamic levels of autophagy after intimal injury of carotid artery. Meth-ods In this study ,40 male SD rats were randomly assigned to operated(n=20)and control groups(n=20). Balloon inju-ry was induced in the left carotid artery in operated groups .Rats in control groups just received carotid artery exposure without injury. Western blot was used to detect the levels of Beclin-1, LC3 and p62 at the third and seventh days. Immu-nofluorescence was used to examine the expression of Beclin-1 and LC3 at the third and seventh days. Results The ex-pression levels of Beclin-1 and LC3 were increased while the levels of P62 were decreased at the third and seventh days after carotid balloon injury. Beclin-1 and LC3 were present in neointima and medintima. The numbers of both Beclin-1 positive cells and LC3 positive cells were increased at the third and seventh days after carotid injury. The numbers of Be-clin-1 positive cells were 18.60 ± 1.34 in neointima and 6.40 ± 0.55 in medintima at third day, (27.6 ± 2.19 in neointima and 6.40±0.55 in medinitima at the seventh day,(all P=0.000,n=5). The numbers of LC3 positive cells were 10.60±1.52 in neointima and 3.00 ± 0.71 in medintima at third day, (P=0.000,n=5;at the seventh day 21.20 ± 2.49;3.00 ± 0.71,P=0.000,n=5). Conclusions This study domenstrates that autophagy was activated after carotid injury and the chang is dy-namic, which may contribute to neointima formation.
Résumé
Objective To examine the expression of inhibitory chondroitin sulfate proteoglycans (CSPGs) and in-vestigate their potential effects on neural plasticity in the peri-infarct cortex and ipsilateral thalamus after focal cerebral infarction in hypertensive rats. Methods Twenty-four adult renovascular hypertensive Sprague-Dawley rats per group were subjected to permanent right middle cerebral artery occlusion(MCAO) or sham operation. Twelve rats which were se-lected randomly from per group at each time point were decapitated and their brains were removed and cut into coronal sections at 7 and 14 days post MCAO. The expression of CSPGs, NG2 and Neurocan was examined using immunostaining and western blot. Results All rats displayed neurological deficits to varying degrees and the expression of CSPGs, NG2 and full length Neurocan was increased in the peri-infarct cortex and ipsilateral thalamus at 7 and 14 days (P0.05). Conclusions CSPGs may play a negative role in neural plasticity through induction of inhibitory environment in the peri-infarct cortex and ipsilat-eral thalamus following focal cerebral infarction in hypertensive rats.