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When this paper was first published the following ethical statement was omitted in error: The experiment was conducted in accordance with the welfare and ethical principles of experimental animals and the laws and regulations of experimental animals. Treat animals kindly, respect animal life, no maltreatment and brutality against animals, and take the least painful method to deal with animals. The authors would like to apologise for any inconvenience caused. DOI of original article: https://doi.org/10.1016/j.chmed.2019.03.005
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Objective To evaluate the efficacy and safety of stenting on symptomatic severe M1 segment stenosis (>80% lumen reduction) of the middle cerebral artery. Methods Thirty-two patients with symptomatic severe M1 segment stenosis of the middle cerebral artery, admitted to our hospital from July 2007 to August 2010, were included in this study. These patients were diagnosed by cerebral angiography and treated using balloon-expandable stents. Their clinical data were collected; the success rate of the treatment, perioperative management and complicatious, stroke during the follow-up period and reangiostenosis were further discussed. Results The success rate was 93.8% (30/32) for total lesions. During the perioperation, 2 patients had cerebral infarction and one of them was asymptomatic ischemic stroke; no other complications appeared. No recurrence of ischemic stroke or death appeared in these 32 patients during the mean 12.6 months of follow-up. Conclusion Stenting based on drug treatment appears to be an effective and feasible therapy for symptomatic severe M1 segment stenosis of the middle erebral artery, but also appears to have the perioperation complication.
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Objective To study the effects of stilbene glucoside(TSG)on calcium homeostasis and expression of RyR3 in pyramidal neurons of the rat hippocampus induced by β-amyloid(Aβ).Methods Eighty Wistar rats were equally randomized into 4 groups(n=20): control group,sham-operated group,model group and TSG inducement group.AD models in the later 3 groups were induced by stereotactic injection of Aβ1-42 to the rat hippocampus;and rats of the control group did not give any treatment.The mRNA expression of RyR3 was detected by real time PCR(RT-PCR) and monitored under laser scanning confocal microscope. Results The concentration of intracellular calcium between each 2 groups was significantly different(P<0.05);that in the model group was obviously higher than that in the control and sham-operated groups,and that in the TSG inducement group was obviously lower than that in the model group(P<0.05).Semi-quantitative RT-PCR indicated that the value of RyR3/β-actin in the model group was obviously decreased as compared with that in the control and sham-operated groups(P<0.05);the value of RyR3/β-actin in the TSG inducement group was slightly increased, but no significant difference was noted as compared with that in the control and sham-operated groups (P>0.05). Conclusion Aβ neurotoxicity causes disorder of intracellular calcium homeostasis,which is not through the pathway of Ca2+-induced Ca2+ release induced by RyR3,but through the changes of permeability of cytomembrane.TSG plays a protection role from Aβ neurotoxicity by calcium homeostasis.
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Objective To investigate the effects of human urinary kallidinogenase (HUK) on the abilities of spatial learning and memory and the expression of nestin in the peri-infarction cortex of rats after focal cerebral ischemia-reperfusion. Methods Sixty rats were equally randomized into 5 groups:sham-operated group, model group, low dose HUK treatment group (3.5 ×10-3 PNAU/kg), median dose HUK treatment group (8.75×10-3 PNAU/kg) and high dose HUK treatment group (17.5×10-3 PNAU/kg).The focal cerebral ischemia-reperfusion models in the model group and HUK treatment groups were established by introducing an intraluminal filament into the right middle cerebral artery of the rats. HUK was administered intraperitoneally right after the operation and afterward once daily for 2 weeks. The spatial learning and memory functions were studied by Morris water maze test, and the nestin expression in the peri-infarction cortex was measured by immunohistochemistry on the 15th d. Results The model group exhibited seriously spatial learning and memory deficits in both place navigation trail and spatial probe trial. In the place navigation trial, the mean values of escape latency in the median dose and high dose HUK treatment groups were shorter than those in the model group (P＜0.05). In the spatial probe trial, significant differences in the percentages of time spending in the former platform quadrant and frequency of crossing the former platform site were noted between the model group and both median dose and high dose HUK treatment groups (P＜0.05). Immunohistochemical analysis showed that the nestin expression in the peri-infarction cortex of median dose and high dose HUK treatment groups increased significantly as compared with that in the model group (P＜0.05). Conclusion Treatment with HUK improves the spatial learning and memory abilities in rats after focal cerebral ischemia-reperfusion, which may result from the increasing expression ofnestin and the proliferation of neural stem cells.
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Objective To explore the expressions of matrix metalloproteinase-9 (MMP-9) and tissue inhibitors of matrix metalloproteinase-1 (TIMP-1) after focal cerebral ischemia-repeffusion injury in rats. Methods Totally 40 Wistar rats were randomly divided into 2 groups: sham-operated group and iscbemia-reperfusion group. A middle cerebral artery occlusion model was constructed in the 25 rats with Longa's method. The expressions of MMP-9 and TIMP-1 were investigated with immunohistochemistry and HE staining at 6, 24, 48, 72 h and 7 d of reperfusion following 2 h ischemia. Results MMP-9 began to be expressed at 6 h reperfusion, and was obviously increased at 24 h and reached the peak level at 48 h, and then, the expression of MMP-9 began to decrease at 72 h to a low level at 7 d. TIMP-1 positive cells began to arise at 6 h reperfusion, peaked at 24 h, decreased at 48 h and remained a low level at 7 d. The expressions of MMP-9 and TIMP-1 were mainly located in vascular endothelial cells, neurons and gitter cells. The expressions of MMP-9 and TIMP-1 were negative in sham-operated group. Conclusion The expressions of MMP-9 and TIMP-1 are induced to increase by focal cerebral ischemia-reperfusion, and vascular endothelial injury may be the main cause to the high expressions of MMP-9 and TLMP-1.