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Summary Hypoxic ischemic encephalopathy is a major complication of perinatal asphyxia, with high morbidity, mortality and neurologic sequelae as cerebral palsy, mostly in poor or developing countries. The difficulty in the diagnosis and management of newborns in these countries is astonishing, thus resulting in unreliable data on this pathology and bad outcomes regarding mortality and incidence of neurologic sequelae. The objective of this article is to present a new clinical diagnostic score to be started in the delivery room and to guide the therapeutic approach, in order to improve these results.
Resumo A encefalopatia hipóxico-isquêmica é a principal complicação da asfixia perinatal, com alta morbidade, mortalidade e incidência de sequelas neurológicas, como a paralisia cerebral, principalmente em países pobres e/ou em desenvolvimento. Nessas regiões, as dificuldades no diagnóstico e no manejo desses recém-nascidos é surpreendente, o que resulta em dados pouco confiáveis e em péssimos desfechos tanto no que se refere à mortalidade como à incidência de sequelas neurológicas. O objetivo deste artigo é apresentar um novo escore para o diagnóstico clínico ser iniciado na sala de parto e uma abordagem terapêutica com o intuito de melhorar esses resultados.
Subject(s)
Humans , Asphyxia Neonatorum/diagnosis , Asphyxia Neonatorum/therapy , Hypoxia-Ischemia, Brain/diagnosis , Hypoxia-Ischemia, Brain/therapy , Apgar Score , Societies, Medical , Severity of Illness IndexABSTRACT
This paper summarized the chemical structures and amounts of caffeoylquinic acids in Erigeron breviscapus, as well as its prevention and cure effects on ischemic stroke in clinical and possible pharmacological mechanism. The results showed 22 caffeoylquinic acids reported from E. breviscapus, accounting for 29% of all compounds from this herb; The average content of total polyphenols was 36.93%, and more than 95% of components in Erigeron Breviscapus Injection are caffeoylquinic acids, higher than that of scutellarin. Several high quality clinical studies confirmed that Erigeron Breviscapus Injection enhanced treatment performance and improve the neurological score in the treatment after ischemic stroke and had good safety. In pharmacological research, caffeoylquinic acid compounds display anti-oxidant, anti-free radical, anticoagulation, and anti-fibrosis effects, which can protect neuro, vascular endothelial cells, glial cells, and astrocytes. They are also able to inhibit inflammatory, suppress cytokines IL-1, TNF-α, and enhance SOD & GSH-Px, which play a role in different treatment stages of ischemic stroke. So, caffeoylquinic acid is a kind of important chemical in E. breviscapus.
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Objective To explore the appropriate dosage of drugs inducing experimental allergic en cephalomyelitis (EAE) in mice,and evaluate the modified model mice.Methods Different doses of myelin oligodendrocyte glycoprotein (MOG35-55:200 μg,100 μg,50 μg,25 μg),together with different doses of inactivation of mycobacterium tuberculosis (H37RA:800 μg,250 μg,100 μg) and pertussis toxin (500 ng,200 ng),were used to induce the EAE model.After immunized,the clinical disease severity of EAE mice was measured by the standard EAE grading clinical score daily.The open field test was used to detect the locomotion of mice.The Western blot and immunofluorescence were used to detect the level of myelin basic proteins (MBP) in different brain regions of mice.Results Compared with the EAE mice induced with high-dose drugs,the mice with low-dose drugs (25 μg MOG35-55,100 μg H37RA,200 ng pertussis toxin) had low neu rological scores.And they displayed normal locomotion compared with the control mice (day 16:group EAE (8.885±0.772) cm/s vs control group (8.933±0.567) cm/s,P＞0.05;day 31:group EAE (11.130±0.630) cm/s vs control group (10.670±0.959) cm/s,P＞0.05;day 55:group EAE (7.686±0.428) cm/s vs control group (8.313±0.918) cm/s,P＞0.05).Moreover,there was a significant decrease of MBP in the parahippocampal cortex (PHC) and fimbria-fornix of EAE mice induced with low-dose of drugs (PHC:group EAE (0.369±0.096) vs control group (1.000±0.163),P＜0.05;fimbria-fomix:group EAE (0.494±0.071) vs control group (1.000±0.143),P＜0.05).Conclusion The EAE mice induced with low-dose drugs(25 μg MOG35-55,100 μg H37RA,200 ng pertussis toxin) have low neurological scores,normal locomotion,and myelin impairment in the central neuronal system.And it can be used in the cognitive behavioral research of demyelination disease,such as multiple sclerosis.
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Aim To investigate the influence of the overexpression of CRMP2 on neural cell apoptosis after ischemia reperfusion injury in rats and its possible mechanism. Methods A total of 192 male adult SD rats were divided into four groups: sham group, cere-bral ischemia/reperfusion group( MCAO group) , cere-bral ischemia with blank plasmid control group( MCAO+GFP group ) , cerebral ischemia with CRMP2 eu-karyotic plasmid group ( MCAO + CRMP2/GFP group) . One day after injecting eukaryotic plasmid, the rats were operated for 120-min ischemia through MCA occlusion and reperfused. At 48 h and 1 wk, the expression of CRMP2 , p53 , Caspase-3 , Caspase-8 and BCL2 in brain tissue was tested by RT-PCR and West-ern blot. Apoptotic cells were observed by TUNEL test. TTC staining was use to detect cerebral infarction volume. The neural function of the rats were also eval-uated. Results Compared with the sham group, the expression levels of CRMP2 and BCL2 in MCAO group and MCAO +GFP group were significantly decreased ( P <0. 01 ) , while p53 , Caspase-3 , Caspase-8 and TUNEL positive cells were elevated(P<0. 01). Inter-vention of CRMP2 eukaryotic plasmid resulted in the increased expression of CRMP2 and BCL2 ( P<0. 01 ) and the decreased p53 , Caspase-3 and Caspase-8 ex-pression. In TUNEL test, overexpression of CRMP2 obviously decreased the number of TUNEL positive cells(P<0. 01). The expression of BDNF was upregu-lated after cerebral ischemic injury ( P<0. 01 ) , while overexpression of CRMP2 increased BDNF more signif-icantly ( P <0. 01 ) . TTC staining showed cerebral in-farction Volume of MCAO + CRMP2/GFP group was obviously decreased ( P <0. 01 ) , and neurologic defi-cits were significantly improved ( P <0. 01 ) . Conclu-sion The overexpression of CRMP2 reduces nerve cell apoptosis possibly by regulating the mitochondrial ap-optosis pathway after cerebral ischemia/reperfusion in-jury to protect nervous system.
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@#Objective To observe the effects of instant hyperbaric oxygen (HBO) therapy on brain edema and aquaporin-4 (AQP4) expression after cerebral ischemia in rats. Methods 18 healthy adult male Sprague-Dawley rats were randomly divided into sham group (n=6),control group (n=6) and HBO group (n=6). Middle cerebral artery occlusion model was established with modified Longa method in the control group and HBO group. HBO was administered after cerebral ischemia immediately in HBO group for 60 min. They were observed with the neurological function score, brain tissue water content and AQP4 experssion 6 h after operation. Results Compared with the control group, the neurological score in HBO group improved significantly (P<0.05), while the brain tissue water content and brain AQP4 expression decreased (P<0.05). Conclusion HBO may improve the neurological function and brain edema after cerebral ischemia, which may relate with inhibiting the expression of AQP4.
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Objective To observe the effects of instant hyperbaric oxygen (HBO) therapy on brain edema and aquaporin-4 (AQP4) ex-pression after cerebral ischemia in rats. Methods 18 healthy adult male Sprague-Dawley rats were randomly divided into sham group (n=6), control group (n=6) and HBO group (n=6). Middle cerebral artery occlusion model was established with modified Longa method in the con-trol group and HBO group. HBO was administered after cerebral ischemia immediately in HBO group for 60 min. They were observed with the neurological function score, brain tissue water content and AQP4 experssion 6 h after operation. Results Compared with the control group, the neurological score in HBO group improved significantly (P<0.05), while the brain tissue water content and brain AQP4 expres-sion decreased (P<0.05). Conclusion HBO may improve the neurological function and brain edema after cerebral ischemia, which may re-late with inhibiting the expression of AQP4.