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ObjectiveIn cerebral ischemia, free radicals form in large quantities and activate the inflammasome nod-like recepter protein 3(NLRP3), thereby exacerbating brain damage. Edaravone has the effect of scavenging free radicals, but the relationgship between its neuroprotective effect and inflammasome NLRP3 has not been reported. To study the neuroprotective effects of edaravone on inflammasome NLRP3 and associated protein of the blood-brain barrier against cerebral ischemia injury.Methods60 male Sprague-Dawley rats were randomly divided into Sham group, cerebral embolism group and edaravone group, respectively. Rat thromboembolic MCAO models were established and edaravone (3mg/kg) was intravenous injected immediately after occlusion and 4 hours after occlusion. In the sham group, cervical blood vessels were separated only, and no embolus was injected. At 24 hours after thrombi injected, mNSS score was used to evaluate neurological function deficits. Brain infarct volume was estimated by TTC staining. The expression of inflammasome NLRP3, occludin and ZO-1 was detected by Western blot. Immunohistochemistry was used to measure IgG leakage.ResultsThe mNSS score and infarct volume of cerebral embolism group at 24 hours after stroke were significantly higher than Sham group (P<0.05). The expression of inflammasome NLRP3 in the brain increased (P<0.05), occludin and ZO-1 blood brain barrier associated protein decreased (P<0.05), and IgG leakage increased. But compared with cerebral embolism group, the mNSS score（4.50±2.12 vs 6.50±1.35, P<0.05）and infarct volume （19.29±11.92 vs 29.99±7.56, P<0.05）decreased when treated with edaravone. Edaravone treatment significantly attenuated inflammasome NLRP3 expression in cerebral ischemic area (0.97±0.47 vs 1.58±0.86, P<0.05), degradation of BBB components (occludin, ZO-1) (1.04±0.19 vs 0.53±0.09, 0.66±0.05 vs 0.30±0.04,P<0.05) and IgG leakage decreased.ConclusionInflammasome NLRP3 play an important role in acute cerebral ischemia injury. Edaravone may provide neuroprotection by inhibiting expression of inflammasome NLRP3 and degradation of associated protein of blood brain barrier.
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Objective To study the cerebral vascular anomalies in patients with posterior circulation infarction and their risk factors.Methods The clinical data of 337 consecutive patients with first-onset of posterior circulation infarction,extracted from Nanjing Stroke Registry Program from January 2007 to June 2010,were collected.Computerized tomography angiography(CTA),magnetic resonance imaging angiography(MRA)and digital subtraction angiography(DSA)were performed in all the patients to clarify the site of vascular anomalies and their mechanisms; and their relation with their risk factors were analyzed.Results One hundred and ninety-five patients with posterior circulation infarction(57.9％)had vascular anomalies with 394 lesions.There were 115 lesions in the ostial vertebral artery,81 lesions in the V4 of vertebral artery,49 lesions in the basilar artery and 47 lesions in the posterior cerebral artery.Hypertension(64.9％)was the most common risk factors in patients with posterior circulation infarction smoking,followed by diabetes mellitus,drinking,and hyperhomocysteinemia.In patients with vascular anomalies,patients with hypertension enjoyed significantly higher incidence of vascular anomalies than those without hypertension,while those with cardiac disease were not(P＜0.05).Conclusion The incidence of posterior circular anomalies in patients with posterior circulation infarction is high,especially in the patients with hypertension and diabetes mellitus.
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Objective To investigate the influencing factors of diagnostic time in adult moyamoya disease (MMD) and provide evidence for its early diagnosis. Methods The clinical data of 65 consecutive patients, admitted to our hopspital from August 2008 to December 2009, were retrospectively analyzed. Logistic regression nalysis was employed to confirm the relevant factors of diagnostic time. Results The 65 patients with early diagnosis and late diagnosis were 41 (63.1%) and 24 (36.9%), respectively. The percentage of patients firstly visiting a hospital with the third grade, patients with high education and high income, and patients having initial hemorrhage of the early diagnosis group was significantly higher than that in those of late diagnosis group (P<0.05). Through a logistic regression analysis, the grade of initial hospital, the level of education, initial symptom and economic level were significantly associated with the early diagnosis, and the patients having initial hemorrhage and firstly visiting a hospital with higher grade were diagnosed earlier (OR=3.401, 95%CI 1.301-8.892, P=0.013;OR=26.351, 95%CI 4.953-140.193, P=0.000). Conclusion Patients with MMD having initial hemorrhage and firstly visiting a hospital with the third grade can be early diagnosed.
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<p><b>OBJECTIVE</b>To investigate the effects of montelukast on atherosclerosis and monocyte chemoattractant protein-1 expression in a hypercholesterolemic rabbit model.</p><p><b>METHODS</b>Thirty four male New Zealand white rabbits were randomized into four groups including normal control group (n = 6), placebo group (n = 8), atorvastatin group (1.5 mgxkg(-1)xd(-1), beginning at 8(th) weeks for 4 weeks, n = 10) and montelukast group (1 mgxkg(-1)xd(-1), beginning at 8(th) weeks for 4 weeks, n = 10). Rabbits except those in normal control group were fed a high cholesterol diet for 12 weeks. Serum lipids were measured at 0, 8 and 12 weeks after intervention. The intima/media ratio, percentages of macrophages or smooth muscle cells in intima and the expression of MCP-1 mRNA were examined.</p><p><b>RESULTS</b>Atherosclerosis was evidenced in placebo group and atorvastatin or montelukast treatment significantly reduced neointima (0.32 +/- 0.12 and 0.34 +/- 0.10 vs. 1.12 +/- 0.36, P < 0.05) and macrophage content [(9.8 +/- 4.6)% and (11.2 +/- 3.7)% vs. (34.6 +/- 8.8)%, P < 0.05], increased SMC content [(18.6 +/- 6.9)% and (19.2 +/- 8.6)% vs. (5.2 +/- 2.3)%, P < 0.05] and inhibited expression of MCP-1 mRNA (0.42 +/- 0.08 and 0.40 +/- 0.06 vs. 2.36 +/- 0.48, P < 0.01). Montelukast had similar anti-atherogenetic effects as atorvastatin but had no influence on plasma lipids.</p><p><b>CONCLUSIONS</b>Montelukast could attenuate atherosclerosis in this hypercholesterolemic rabbit model which might be attributed to its anti-inflammatory effects.</p>
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Animais , Coelhos , Aterosclerose , Metabolismo , Quimiocina CCL2 , Metabolismo , Hipercolesterolemia , Macrófagos , Metabolismo , Túnica ÍntimaRESUMO
Objective To evaluate the neuronal injury induced by organophosphorus(OP) compound exposurein rats andinvestigate andthepossible mechanisms. Methods Eighteen SD rats were randomly divided into OP groups(n=12)and the control group(n=6).SD rats were given intramuscular sarin inection followed 1 min later by intraperitoneal injection of atropine sulphate and pralidoxime,and the rats with typical toxic reactions were used for subsequent experiment.The rats in the control group received normal saline injections in identical manners.Twenty-four hours later,the brain tissue of the rats were taken for HE staining and neuronal nuclei antigen(NeuN)immunohistochemistry to quantitatively assess the neuronal damages in the pyriform cortex,hippocampus CAl and striatum.Results HE staining showed massive degeneration of the neurons in the pyriform cortex,hippocampus CAland striatum of rats with satin injection.Compared to the rats with saline injections,the rats exposed to satin presented with significantly decreased number of NeuN-positive neurons(P<0.05).Conclusion OP Can induce acute neuronal death in rat brain and cause a series of symptoms in the central nervous system,probably by such noncholinergic mechanisms as glutamic acid-induced eytotoxieity and oxidative stress.
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Objective To study the effect of intranasal(IN)delivery of nerve growth factor(NGF) on pyriform cortex of satin-poisoned rats.Methods Sprague-Dawley rats were treated with satin and atropine sulphate, pralidoxime to establish satin-poisoned rat model.Then NGF or saline was administered via the olfactory pathway.24 hours later, damaged and residual healthy neurons were estimated and quantified on pyriform cortex using hematoxylin-eosin(HE)staining and neuronal nuclei antigen(NeuN) immunohistochemistry.Results A massive quantity of degenerating neurons were seen in the pyriform cortex of rats with intranasal saline.And compared to the normal rats, the number of neurons of rats with intranasal saline was significantly reduced by 39.44% [(404.75?25.17)/mm~2].But the number of neurons in rats with intranasal NGF [(651.94?36.02)/mm~2] didn't change significantly compared to the normal rats.Conclusion Intranasal delivery of NGF, reducing the degenerating neurons on pyriform cortex of satin-exposure rats, is a potential treatment for satin intoxication.