微小牛蜱Enolase基因在昆虫细胞中的表达及鉴定

为对微小牛蜱烯醇酶(Enolase)基因进行真核表达及免疫反应原性分析,本研究采用RT-PCR方法扩增微小牛蜱Enolase基因的开放阅读框(ORF)序列,将其克隆至pFastBac1载体中构建重组质粒pFastBac1-Enolase,随后转化至大肠杆菌DH10Bac细胞中制备了重组杆粒Bacmid-Enolase,转染至SF9细胞以获得重组Enolase蛋白。通过双酶切、PCR及测序鉴定显示Enolase基因正确插入。利用SDS-PAGE分析表达产物,结果显示目的蛋白大小约为48 ku。利用western blot对重组蛋白进行分析,结果表明目的蛋白能被微小牛蜱抗原免疫兔阳性血清识别,具有良好的免疫反应原性。凝血酶时间(TT)的测定结果显示,Enolase重组蛋白能显著延长TT,具有抗凝血活性。本研究首次采用Bac-to-Bac杆状病毒表达系统对微小牛蜱Enolase基因进行真核表达,并鉴定了重组蛋白的免疫反应原性,为开展Enolase免疫原性分析及功能研究奠定了基础。

α-enolase蛋白在口腔鳞状细胞癌组织中的表达及其临床意义

目的探讨α-enolase蛋白在口腔鳞状细胞癌组织中的表达及其与口腔鳞癌发生发展的关系。方法采用ELISA法对40例口腔鳞癌组织、10例口腔正常粘膜组织中α-enolase蛋白的表达情况进行检测。结果 1.口腔鳞状细胞癌组织中α-enolase蛋白表达明显高于正常粘膜组织(P<0.01)。2.α-enolase蛋白在低、中、高分化口腔鳞状细胞癌组织中的表达均有差异(P<0.05),差异具有统计学意义,高分化鳞癌的α-enolase浓度>中分化鳞癌>低分化鳞癌;3.有淋巴结转移、TNM分期为III+IV期者α-enolase的表达分别明显高于无淋巴结转移、TNM分期为I+II期者(P<0.05)。4.α-enolase在口腔鳞状细胞癌中的表达与淋巴结转移、TNM分期、肿瘤分化程度密切相关(P<0.05),而与患者的年龄、性别无关(P>0.05)。结论口腔鳞状细胞癌组织中α-enolase蛋白表达上调,α-enolase可能在口腔鳞状细胞癌的发生、发展中起重要作用。

表面蛋白烯醇化酶Enolase在S.suis 2感染中的角色

目的通过克隆表达,在获得具有酶活性的猪链球菌2型(S.suis2)05ZYH33重组烯醇化酶Enolase蛋白的基础上,旨在继续探索其在细菌粘附和引发免疫下调作用中的角色。方法流式细胞术(FCM)、Hep2细胞粘附竞争试验、免疫空斑试验。结果流式细胞术FCM的细胞定位显示Enolase可以部分存在S.suis205ZYH33细菌的表面;Hep2细胞粘附竞争试验表明猪链球菌表面Enolase参与细菌对宿主细胞的黏附作用;免疫空斑实验的结果揭示Enolase在抑制宿主特异性免疫应答中发挥作用。结论 Enolase作为一个表面蛋白,确实在S.suis2感染中扮演一定的角色。

Enolase在鸭疫里默氏杆菌侵袭鸭脑微血管内皮细胞中的作用

旨在明确鸭疫里默氏杆菌烯醇化酶(Enolase)在其侵袭鸭脑微血管内皮细胞(DBMEC)以及血脑屏障(BBB)中的作用。本研究以鸭疫里默氏杆菌RA-LZ01株为亲本株,利用同源重组和结合转移的方法构建enolase基因缺失株ΔEnolase和回复株cΔEnolase,并测定RA-LZ01、ΔEnolase和cΔEnolase对DBMEC黏附和侵袭能力的差异;用上述菌株感染雏鸭,测定雏鸭血液和脑组织中的载菌量。结果表明,与亲本株RA-LZ01相比,缺失株ΔEnolase对DBMEC的黏附率和入侵率均极显著降低;回复株cΔEnolase恢复了对DBMEC的黏附和入侵能力。感染RA-LZ01、ΔEnolase和cΔEnolase菌株的雏鸭的血液载菌量无显著差异;与感染RA-LZ01和cΔEnolase菌株的雏鸭相比,感染ΔEnolase菌株的雏鸭脑组织中的载菌量极显著降低。以上结果说明,Enolase与鸭疫里默氏杆菌黏附和入侵DBMEC以及入侵雏鸭脑组织显著相关,可能为介导鸭疫里默氏杆菌突破鸭血脑屏障的毒力因子。

牛环形泰勒虫enolase基因的原核表达及生物信息学分析

【目的】获得牛环形泰勒虫(Theileria annulata)新疆株enolase基因,并分析其生物学特性及反应原性。【方法】对牛环形泰勒虫enolase基因进行扩增和克隆,构建原核表达载体pGEX-4T-1-enolase,诱导表达enolase重组蛋白并进行蛋白纯化,通过Western blotting验证enolase重组蛋白反应原性。利用生物信息学方法对enolase基因编码蛋白的理化性质、亲疏水性、跨膜区、信号肽、磷酸化、亚细胞定位及蛋白互作网络进行预测分析。【结果】PCR扩增出大小为1248 bp的牛环形泰勒虫enolase基因片段,enolase重组蛋白大小约70 ku;Western blotting结果表明,该重组蛋白与牛环形泰勒虫阳性血清发生反应。enolase基因编码416个氨基酸,理论等电点为5.91,有38个磷酸化位点;二级结构主要由α-螺旋(43.03%)和无规则卷曲(33.17%)组成;具有17个B细胞抗原表位,亚细胞定位主要位于细胞质中;enolase蛋白与磷酸甘油酸变位酶(PGAM)、二磷酸核苷激酶(NDK)、磷酸甘油酸激酶(PGK)、热休克蛋白70(HSP70)存在相互作用。【结论】本试验成功克隆出新疆牛环形泰勒虫enolase基因,蛋白互作网络预测其与糖酵解和能量代谢相关的蛋白相互作用。研究结果为牛环形泰勒虫能量代谢途径基因的相关研究奠定基础。

Regulation of enolase activation to promote neural protection and regeneration in spinal cord injury

Spinal cord injury(SCI)is a debilitating condition characterized by damage to the spinal cord resulting in loss of function,mobility,and sensation with no U.S.Food and Drug Administration-approved cure.Enolase,a multifunctional glycolytic enzyme upregulated after SCI,promotes pro-and anti-inflammatory events and regulates functional recovery in SCI.Enolase is normally expressed in the cytosol,but the expression is upregulated at the cell surface following cellular injury,promoting glial cell activation and signal transduction pathway activation.SCI-induced microglia activation triggers pro-inflammatory mediators at the injury site,activating other immune cells and metabolic events,i.e.,Rho-associated kinase,contributing to the neuroinflammation found in SCI.Enolase surface expression also activates cathepsin X,resulting in cleavage of the C-terminal end of neuron-specific enolase(NSE)and non-neuronal enolase(NNE).Fully functional enolase is necessary as NSE/NNE C-terminal proteins activate many neurotrophic processes,i.e.,the plasminogen activation system,phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B,and mitogen-activated protein kinase/extracellular signal-regulated kinase.Studies here suggest an enolase inhibitor,ENOblock,attenuates the activation of Rho-associated kinase,which may decrease glial cell activation and promote functional recovery following SCI.Also,ENOblock inhibits cathepsin X,which may help prevent the cleavage of the neurotrophic C-terminal protein allowing full plasminogen activation and phosphatidylinositol-4,5-bisphosphate 3-kinase/mitogen-activated protein kinase activity.The combined NSE/cathepsin X inhibition may serve as a potential therapeutic strategy for preventing neuroinflammation/degeneration and promoting neural cell regeneration and recovery following SCI.The role of cell membrane-expressed enolase and associated metabolic events should be investigated to determine if the same strategies can be applied to other neurodegenerative diseases.Hence,this review discusses the importance of enolase activation and inhibition as a potential therapeutic target following SCI to promote neuronal survival and regeneration.

Implications of enolase in the RANKL-mediated osteoclast activity following spinal cord injury

Spinal Cord Injury(SCI)is a debilitating condition characterized by damage to the spinal cord,resulting in loss of function,mobility,and sensation.Although increasingly prevalent in the US,no FDA-approved therapy exists due to the unfortunate complexity of the condition,and the difficulties of SCI may be furthered by the development of SCI-related complications,such as osteoporosis.SCI demonstrates two crucial stages for consideration:the primary stage and the secondary stage.While the primary stage is suggested to be immediate and irreversible,the secondary stage is proposed as a promising window of opportunity for therapeutic intervention.Enolase,a metabolic enzyme upregulated after SCI,performs non-glycolytic functions,promoting inflammatory events via extracellular degradative actions and increased production of inflammatory cytokines and chemokines.Neuron-specific enolase(NSE)serves as a biomarker of functional damage to neurons following SCI,and the inhibition of NSE has been demonstrated to reduce signs of secondary injury of SCI and to ameliorate dysfunction.This Viewpoint article involves enolase activation in the regulation of RANK-RANKL pathway and summarizes succinctly the mechanisms influencing osteoclast-mediated resorption of bone in SCI.Our laboratory proposes that inhibition of enolase activation may reduce SCI-induced inflammatory response and decrease osteoclast activity,limiting the chances of skeletal tissue loss in SCI.

Serum neuron-specific enolase:A promising biomarker of silicosis

BACKGROUND Silicosis is a type of chronic pulmonary fibrosis caused by long-term inhalation of silica dust particles.There has been no ideal biomarker for the diagnosis and differential diagnosis of silicosis until now.Studies have found that elevated neuron-specific enolase(NSE)concentration in the serum of silicosis patients is helpful for diagnosis and severity assessment of the disease.However,the number of cases in these studies was not enough to arouse attention.AIM To investigate the clinical significance of serum NSE in the diagnosis and staging of silicosis.METHODS From January 2017 to June 2019,326 cases of silicosis confirmed in Quanzhou First Hospital Affiliated to Fujian Medical University were included in the silicosis group.A total of 328 healthy individuals or medical patients without silicosis were included in the control group.Serum NSE concentrations of all subjects were determined by electrochemical luminescence.RESULTS There were no significant differences in sex,age,smoking index and complications between the silicosis and control groups.The mean serum NSE concentration was 26.57±20.95 ng/mL in the silicosis group and 12.42±2.68 ng/mL in the control group.The difference between the two groups was significant(U=15187,P=0.000).Among the 326 patients with silicosis,103 had stage I silicosis,and the mean serum NSE concentration was 15.55±6.23 ng/mL.The mean serum NSE concentration was 21.85±12.05 ng/mL in 70 patients with stage II silicosis.The mean serum NSE concentration was 36.14±25.72 ng/mL in 153 patients with stage III silicosis.Kruskal-Wallis H test suggested that the difference in serum NSE concentration in silicosis patients in the three groups was significant(H=130.196,P=0.000).Receiver operating characteristic curve analysis indicated that the area under the curve was 0.858(95%confidence interval:0.828-0.888;P=0.000).When the NSE concentration was 15.82 ng/mL,the Jorden index was the largest,the sensitivity was 72%,and the specificity was 90%.CONCLUSION Serum NSE concentration may be a promising biomarker for the diagnosis and assessment of severity of silicosis.

Changes in plasma calcitonin gene-related peptide and serum neuron specific enolase in rats with acute cerebral ischemia after low-frequency electrical stimulation with different waveforms and intensities

Following acute cerebral ischemia in rats, plasma calcitonin gene-related peptide decreased and the level of serum neuron specific enolase and the volume of the infarction increased. Square-wave and triangular-wave electrical stimulation with low or high intensities could increase the plasma calcitonin gene-related peptide, decrease the serum neuron specific enolase and reduce the infarction volume in the brain in rats with cerebral ischemia. There was no significant difference between different wave forms and intensities. The experimental findings indicate that low-frequency electrical stimulation with varying waveforms and intensities can treat acute cerebral ischemia in rats.

Neuron-specific enolase expression in a rat model of radiation-induced brain injury following vascular endothelial growth factor-modified neural stem cell transplantation

BACKGROUND： Previous studies have shown that transplantation of vascular endothelial growth factor （VEGF）-modified neural stem cells （NSC） provides better outcomes, compared with neural stem cells, in the treatment of brain damage. OBJECTIVE： To compare the effects of VEGF-modified NSC transplantation and NSC transplantation on radiation-induced brain injury, and to determine neuron-specific enolase （NSE） expression in the brain. DESIGN, TIME, AND SETTING： The randomized, controlled study was performed at the Linbaixin Experimental Center, Second Affiliated Hospital, Sun Yat-sen University, China from November 2007 to October 2008. MATERIALS： VEGF-modified C17.2 NSCs were supplied by Harvard Medical School, USA. Streptavidin-biotin-peroxidase-complex kit （Boster, China） and 5, 6-carboxyfluorescein diacetate succinimidyl ester （Fluka, USA） were used in this study. METHODS： A total of 84 Sprague Dawley rats were randomly assigned to a blank control group （n = 20）, model group （n = 20）, NSC group （n = 20）, and a VEGF-modified NSC group （n = 24）. Rat models of radiation-induced brain injury were established in the model, NSC, and VEGF-modified NSC groups. At 1 week following model induction, 10 pL （5 ×10^4 cells/μL） VEGF-modified NSCs or NSCs were respectively infused into the striatum and cerebral cortex of rats from the VEGF-modified NSC and NSC groups. A total of 10μL saline was injected into rats from the blank control and model groups. MAIN OUTCOME MEASURES： NSE expression in the brain was detected by immunohistochemistry following VEGF-modified NSC transplantation. RESULTS： NSE expression was significantly decreased in the brains of radiation-induced brain injury rats （P 〈 0.05）. The number of NSE-positive neurons significantly increased in the NSC and VEGF-modified NSC groups, compared with the model group （P 〈 0.05）. NSE expression significantly increased in the VEGF-modified NSC group, compared with the NSC group, at 6 weeks following transplantation （P 〈 0.05）. CONCLUSION： VEGF-modified NSC transplantation increased NSE expression in rats with radiation-induced brain injury, and the outcomes were superior to NSC transplantation.

Flunarizine and lamotrigine prophylaxis effects on neuron-specific enolase, S-100, and brain-specific creatine kinase in a fetal rat model of hypoxic-ischemic brain damage

BACKGROUND： Calcium antagonists may act as neuroprotectants, diminishing the influx of calcium ions through voltage-sensitive calcium channels. When administered prophylactically, they display neuroprotective effects against hypoxic-ischemic brain damage in newborn rats. OBJECTIVE： To investigate the neuroprotective effects of flunarizine （FNZ）, lamotrigine （LTG） and the combination of both drugs, on hypoxic-ischemic brain damage in fetal rats. DESIGN AND SETTING： This randomized, complete block design was performed at the Department of Pediatrics, Shenzhen Fourth People＇s Hospital, Guangdong Medical College. MATERIALS： Forty pregnant Wistar rats, at gestational day 20, were selected for the experiment and were randomly divided into FNZ, LTG, FNZ ＋ LTG, and model groups, with 10 rats in each group. METHODS： Rats in the FNZ, LTG, and FNZ ＋ LTG groups received intragastric injections of FNZ （0.5 mg/kg/d）, LTG （10 mg/kg/d）, and FNZ （0.5 mg/kg/d） ＋ LTG （10 mg/kg/d）, respectively. Drugs were administered once a day for 3 days prior to induction of hypoxia-ischemia. Rats in the model group were not administered any drugs. Three hours after the final administration, eight pregnant rats from each group underwent model establishment hypoxia-ischemia brain damage to the fetal rats. Cesareans were performed at 6, 12, 24, and 48 hours later; and 5 fetal rats were removed from each mother and kept warm. Two fetuses without model establishment were removed by planned cesarean at the same time and served as controls. A total of 0.3 mL serum was collected from fetal rats at 6, 12, 24, and 48 hours, respectively, following birth. MAIN OUTCOME MEASURES： Serum protein concentrations of neuron-specific enolase and S-100 were measured by ELISA. Serum concentrations of brain-specific creatine kinase were measured using an electrogenerated chemiluminescence method. RESULTS： Serum concentrations of neuron-specific enolase, S-100, and brain-specific creatine kinase were significantly higher in the hypoxic-ischemic fetal rats, compared with the non-hypoxic-ischemic group. Serum concentrations of neuron-specific enolase, S-100, and brain-specific creatine kinase were significantly less in the FNZ, LTG, and FNZ ＋ LTG groups following ischemia, compared with the model group （P 〈 0.01）. However, these values were significantly greater in the FNZ and LTG groups, compared with the FNZ ＋ LTG group, following ischemia （P 〈 0.01）. CONCLUSION： Preventive antenatal use of oral FNZ and LTG has positive neuroprotective effects on intrauterine hypoxic-ischemic brain damage. The combined effect of these two drugs is superior.

Plasma level of neuron specific enolase in patients with acute cerebral infarction:A case-control study

BACKGROUND： The plasma level of neuron specific enolase （NSE） can be used to diagnose and evaluate neuronal injury and predict early prognosis. OBJECTIVE： To observe the dynamic changes in plasma levels of NSE in patients with acute cerebral infarction, and to investigate its correlations with disease severity and prognosis. DESIGN, TIME AND SETTING： This non-randomized, concurrent case-control experiment was performed at the Department of Neurology, First Hospital Affiliated to Heilongjiang University of Traditional Chinese Medicine between May and July 2007. PARTICIPANTS： Eighteen patients with acute cerebral infarction, who received treatment at the Department of Neurology, First Hospital Affiliated to Heilongjiang University of Traditional Chinese Medicine between May and July 2007, were recruited into the patient group. An additional 10 healthy individuals, who received health examinations simultaneously, were included as controls. METHODS： Following admission （within 3 days） and at days 6, 12, and 30 subsequent to acute cerebral infarction attack, 3 mL venous blood was taken from each patient before the morning meal to determine the plasma level of NSE by enzyme-labeled immunosorbent assay. One-time blood extraction was performed in each healthy subject during the health examination for the same purpose as in patients. At 6 and 30 days following acute cerebral infarction attack, CT examination was performed for calculation of cerebral infarction volume according to the Tada formula. Following admission and at 30 days of disease invasion, all patients were scored by the National Institutes of Health Stroke Scale （NIHSS, 13 items）. MAIN OUTCOME MEASURES： Comparison of NSE plasma level between acute cerebral infarction patients and healthy individuals; correlations of NSE plasma level in acute cerebral infarction patients with cerebral infarction volume, NIHSS score, and prognosis. RESULTS： Following admission and at days 6 and 12 of disease invasion, the plasma level of NSE was significantly higher in the patient group than in the control group （P 〈 0.05）. Following admission and at day 30 of disease invasion, the NIHSS scores of the patient group were 17.706 and 11.222, respectively. Following admission and at day 6 of disease invasion, the plasma level of NSE was positively correlated with cerebral infarction volume （r = 0.503, 0.435, P 〈 0.05）, but it was negatively correlated with NIHSS score （r = -0.571, 0.368, P 〈 0.05）. The plasma level of NSE was mostly correlated with cerebral infarction volume, followed by NIHSS score, and lastly prognosis, with regression coefficients of 0.386, 0.343, and 0.340, respectively. CONCLUSION： The plasma level of NSE is higher in patients with acute cerebral infarction than in the healthy population. It can reflect infarct severity and predict early prognosis of acute cerebral infarction.

The diagnostic value of neuron specific enolase in patients with gliomas

Objective: In order ic look into the alterations and effects of neuron specific enolase (NSE) in cerebralspinal fluid (CSF ) and serum of foe paticnts with glioma and meningiomas. Methods: We studied CSF and serumlevels of NSE in 40 patients with gliomas and 10 with meningiomas;3 days before and after operation byradioimmunoassay. Results: Compared with the value of NSE: in CSF and serum from 10 control patients. samplesfrom patients with malignant gliomas contained abnormally high level of NSE before operation (P < 0. 05 ) butnormal level after operation (P >0. 05 ). However. samples from patients with low grade gliomas andmeningiomas were within normal range before and after operation (P >0. 05). Gliomas with totall refectionshowed normal NSE values but with sub lotal removal presented high levels of NSE after surgery (P < 0. 05).Conclusion: The increased value of NSE in patients with malignant gliomas may be associated with elevated rate of glucolysis. As one of the new tumor markers NSE Is postulated to play an important role in the diagnosi followup and monitoring of gliomas.

微小扇头蜱Enolase基因序列特征及其编码蛋白结构与抗原表位预测

目的 分析微小扇头蜱Enolase基因序列特征,并预测其所编码Enolase蛋白二、三级结构及抗原表位。方法 2022年6月25日在湖南省怀化市芷江县某黄牛养殖场采集62只雌性饱血微小扇头蜱,提取其DNA,PCR扩增其Enolase基因,PCR扩增产物克隆、测序并表达。采用软件Clustal X分析Enolase基因序列特征,并将基因序列翻译成氨基酸序列。采用PRABI软件推导出Enolase蛋白二、三级结构,并对其理化性质进行分析;采用ABCpred Prediction、Scratch、IEDB和NetCTL软件预测Enolase蛋白B、T细胞抗原表位。结果 微小扇头蜱Enolase基因序列全长1 323 bp,碱基A、T、G、C含量分别为24.5%、22.5%、27.0%、26.0%,A+T含量为47.0%、G+C含量为53.0%。该基因共编码434个氨基酸;Enolase蛋白分子量大小为47.12 k Da,其二级结构含186个(42.86%)α-螺旋、32个(7.37%)β-转角、144个(33.18%)无规卷曲、72个(16.59%)扩展链。Enolase蛋白存在于细胞质中的概率最大(76.7%),其次是线粒体(39.1%)和细胞核(21.7%),该蛋白无信号肽和跨膜结构域。Enolase蛋白预计有14个B细胞优势抗原表位和8个T细胞优势抗原表位。结论 微小扇头蜱Enolase基因序列呈GC偏好;其所编码的Enolase蛋白为酸性亲水性蛋白,以α-螺旋和无规卷曲为主要结构,且具有B、T细胞优势抗原表位,是微小扇头蜱疫苗研发的一种理想靶标。

奶牛源无乳链球菌enolase重组蛋白制备及其免疫保护性研究

奶牛乳房炎是奶牛养殖场常见疾病,为了有效预防奶牛乳房炎,降低药物残留,提高奶牛养殖的生产效益,为牛源无乳链球菌亚单位疫苗的制备提供一定的依据,本研究选取无乳链球菌免疫原性较好的enolase蛋白为靶标,克隆enolase基因、构建重组表达质粒。经过诱导、表达和纯化获得重组enolase蛋白。用纯化的蛋白加以佐剂对小鼠进行二次免疫,测定免疫后小鼠的血清抗体水平,评价enolase蛋白亚单位疫苗的免疫效果和安全性。最终,成功从无乳链球菌分离株MN686586中扩增出enolase基因,构建出重组表达质粒pET-32a-enolase,经IPTG体外诱导表达,获得分子质量大小为67 ku的重组蛋白。用enolase亚单位疫苗免疫小鼠,间接ELISA检测小鼠血清抗体水平显示,二免后第14天小鼠血清抗体水平效价达到1∶25 600,并且相对免疫保护率(RPS)为100%。结果表明,enolase亚单位疫苗能够刺激小鼠产生一定的免疫应答和产生特异性抗体,已初步制备出针对牛源无乳链球菌的亚单位疫苗。

基于绵羊肺炎支原体Enolase蛋白建立间接ELISA抗体检测方法

旨在建立一种检测绵羊肺炎支原体(Mo)血清抗体的间接ELISA方法,笔者构建了Mo Enolase基因原核表达载体,诱导表达后,纯化的重组蛋白用Western-blot分析其反应原性。以重组蛋白为包被抗原,建立了Mo间接ELISA抗体检测方法。结果显示,重组蛋白得到可溶性表达,Western-blot证实具有良好的反应原性。间接ELISA反应条件优化结果显示,包被抗原浓度为2 mg/L,37℃2 h,封闭条件为含10 g/L BSA的PBS,4℃过夜,待检血清稀释度为1∶50,37℃1 h,酶标二抗最佳稀释度为1∶4000,37℃1 h,底物最佳显色条件为37℃避光10 min。分别利用38份阴性血清、38份阳性血清确定临界值为S/P=0.365。用该方法与间接血凝法对180份血清进行检测,两者符合率为81.11%。结果表明,本研究建立的间接ELISA方法敏感、特异,具有良好的临床应用前景。

Use of neuron-specific enolase to predict mild brain injury in motorcycle crash patients with maxillofacial fractures: A pilot study

Purpose: Mild traumatic brain injury (TBI) is common but accurate diagnosis and its clinical consequences have been a problem. Maxillofacial trauma does have an association with TBI. Neuron-specific enolase (NSE) has been developed to evaluate neuronl damage. The objective of this study was to investigate the accuracy of NSE serum levels to detect mild brain injury of patients with sustained maxillofacial fractures during motor vehicle accidents. Methods: Blood samples were drawn from 40 healthy people (control group) and 48 trauma patients who has sustained isolated maxillofacial fractures and mild brain injury in motor vehicle accidents. Brain injuries were graded by Glasgow Coma Scale. In the trauma group, correlations between the NSE serum value and different facial fracture sites were also assessed. Results: The NSE serum level (mean ± SD, ng/ml) in the 48 patients with maxillofacial fractures and mild TBI was 13.12 ± 9.68, significantly higher than that measured in the healthy control group (7.72 ± 1.82, p < 0.001). The mean NSE serum level (ng/ml) in the lower part of the facial skeleton (15.44 with SD 15.34) was higher than that in the upper facial part (12.42 with SD 7.68);and the mean NSE level (ng/ml) in the middle-and lower part (11.97 with SD 5.63) was higher than in the middle part (7.88 with SD 2.64). Conclusion: An increase in NSE serum levels can be observed in patients sustained maxillofacial fractures and mild brain injury.

Neuron specific enolase is a potential target for regulating neuronal cell survival and death: implications in neurodegeneration and regeneration

Enolase is a multifunctional enzyme primarily involved in catalyzing the conversion of 2-phosphoglycerate to phosphoenolpyruvate during glycolysis and the reverse reaction during gluconeogenesis[1-4].Though typically expressed in the cytosol,enolase has been shown to migrate to the cell surface upon inflammatory signal[3].

Significance of serum neuron-specific enolase in patients with acute traumatic brain iniurv

Objective: To study the association between serum neuron-specific enolase (NSE) and the extent of brain damage and the outcome after acute traumatic brain injury (TBI). Methods: The release patterns of serum NSE in 78 patients after acute TBI were analyzed by using the enzyme linked immunosobent assay. The levels of NSE were compared with Glasgow coma scale, the category of brain injury and the outcome after 6 months of injury. Results: There were different NSE values in patients with minor (12.96 μg/L±2.39 μg/L), moderate (23.44 μg/L±5.33 μg/L) and severe brain injury (42.68 μg/L±4.57 μg/L). After severe TBI, the concentration of NSE in patients with epidural hematomas was 13.38 μg/L±4.01 μg/L, 24.03 μg/L±2.85 μg/L in brain contusion without surgical intervention group, 55.20 μg/L±6.35 μg/L in brain contusion with surgical intervention group, and 83.85 μg/L±15.82 μg/L in diffuse brain swelling group. There were close correlations between NSE values and Glasgow coma scale (r=-0.608, P<0.01) and the extent of brain injury (r=0.75, P<0.01). Patients with poor outcome had significantly higher initial and peak NSE values than those with good outcome (66.40 μg/L±9.46 μg/L, 94.24 μg/L±13.75 μg/L vs 32.16 μg/L±4.21 μg/L, 34.08 μg/L±4.40 μg/L, P<0.01, respectively). Initial NSE values were negatively related to the outcome (r=-0.501, P<0.01). Most patients with poor outcomes had persisting or secondary elevated NSE values. Conclusions: Serum NSE is one of the valuable neurobiochemical markers for assessment of the severity of brain injury and outcome prediction.

NEURON-SPECIFIC ENOLASE IN PATIENTS WITH ACUTE ISCHEMIC STROKE AND RELATED DEMENTIA

Neuron-specific enolase (NSE) levels of cerebrospinal fluid (CSF) were measured in 39 patients with ischemic stroke and 15 controls. There was a significant increase of CSF NSE in acute ischemic stroke patients as compared with the controls. The altered CSF NSE levels correlated well with the infarct size in CT scan. The CSF NSE levels were higher in 6-multiinfarct dementia (MID) patients who were diagnosed after 6-month follow-up than those in 22 non-MID patients of this series. Our research supports the view that CSF NSE can be a useful biochemical marker for brain ischemia. The importance of CSF NSE in the study of dementia related to ischemic stroke is worth further studies.