ABSTRACT
Objective To study the expression of smad2/3 protein and the effects of flunarizine on the its expression in braln tissue following transient cerebral ischemie reperfusion in gerbils. Methods A cerebral ischemia-reperfusion model in gerbils was established by clamping both common carotids. Thirty-five gerbils were randomly divided into three groups, sham operation group, cerebral ischemia-reperfusion group and flunarizine treatment group. The expression of smad2/3 protein in brain tissue was detected by immunohistochemistry technique. Results Experimental results revealed that smad2/3 protein was expressed in neuroeyte in 35 gerbil brain. Compared with sham operation group, the expression of smad2/3 protein in neurecytes of cerebral isehemia-reperfusion group was evidently increased at the lst day, 3rd day and 7th day (P <0. 01). Compared with cerebral ischemia-reperfusion group, the expression of smad2/3 protein in neurecytes of gerbils in flunarizine treatment group was evidently decreased at these time point (P < 0.05). Condusions Smad2/3 protein was expressed in nettrcvytes of gerbils. Expression of smad2/3 protein in neuroeytes of gerbils was evidently increased following cerebral ischemic reperfusion, and its expression in flunarizine treatment group was evidently decreased.
ABSTRACT
Objective To investigate the changes of neuroglobin (Ngb) expression in the CA1 hippocampus after cerebral ischemia and the effect of limb ischemic preconditioning (LIP) on it in young and aged rats. Methods SD rats aged 3 months and 21-23 months with permanently occluding bilateral vertebral arteries were randomly divided into cerebral ischemic group and LIP + cerebral ischemic group, respectively. The expression of Ngb mRNA and protein in the hippocampus were investigated by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot methods. The profile of delayed neuronal death (DND) of pyramidal neurons in the hippocampus CA1 was evaluated by using thionin staining under light microscope by determining the neuronal density (ND) and histological grade (HG). Results Ngb mRNA and protein expressions were 0.16±0.02 and 0.32±0.07, 0.52±0.04 and 0.91±0.06, 0.09±0.01 and 0.22±0.08, 0.21±0.01 and 0.66± 0. 06 in young cerebral ischemia group, LIP + young cerebral ischemia group, aged cerebral ischemia group and LIP + aged cerebral ischemia group, respectively. The expressions of Ngb mRNA and protein after cerebral ischemia for 8 minutes in aged rats were decreased compared with those in the young rats which suffered an identical cerebral ischemia with the aged rats (P<0.05). LIP up-regulated Ngb mRNA and protein expressions in both young and aged rats which suffered cerebral ischemia (P<0.05). However, the up-regulation of Ngb expression in aged rats was significantly less than that in young rats (P<0.05). Neuropathological evaluation showed that ND was 38.8±10.9, 171.5±16.9, 21.2±12.2 and 102.7±15.4 in young cerebral ischemic group, LIP + young cerebral ischemic group, aged cerebral ischemic group and LIP + aged cerebral ischemic group, respectively. It showed that obvious DND of pyramidal neurons was found in young and aged rats after cerebral ischemia. Although LIP effectively protected the pyramidal neurons in the CA1 hippocampus against DND normally induced by ischemic insult, the neuroprotection of LIP for aged rats was less effective than that for young rats. Conclusions The expression of Ngb and the up-regulation effect of LIP on the expression in aged rats are significantly decreased compared to those in young rats when the rats suffer cerebral ischemia. These differences may be one of underlying reasons why the aged rats exhibit severe DND after cerebral ischemia and why the neuroprotective effect of LIP is less in the aged rats than that in the young rats.
