乌司他丁联合连续性肾脏替代疗法对急性重症胰腺炎患者炎症因子及免疫球蛋白的影响

目的:探讨乌司他丁联合连续性肾脏替代疗法(CRRT)对急性重症胰腺炎(SAP)患者炎症因子及免疫球蛋白的影响。方法:选取2013年2月至2017年8月期间我院收治的SAP患者148例为研究对象,根据随机数字表法分为对照组(n=74)与观察组(n=74),两组均给予常规治疗以及乌司他丁药物治疗,观察组则在此基础上联合CRRT治疗,两组均治疗28d后,观察并比较两组患者的临床疗效,治疗前后白细胞介素-6(IL-6)、C-反应蛋白(CRP)、降钙素原(PCT)及IgA、IgG、IgM水平的变化。结果:观察组的总有效率为90.54%(67/74),显著高于对照组的67.57%(50/74)(P0.05)。两组患者治疗28d后血清IL-6、CRP、PCT水平较治疗前均显著降低,且观察组低于对照组(P0.05)。两组患者治疗28d后IgA、IgG、IgM较治疗前均显著升高,且观察组IgG、IgM显著高于对照组(P0.05)。治疗后观察组ICU住院时间短于对照组(P0.05),两组患者病死率比较差异无统计学意义(P0.05)。结论:乌司他丁联合CRRT治疗SAP效果显著,可有效降低患者炎症因子水平,调节免疫系统,改善患者预后,值得临床推广应用。     

连续性血液净化治疗联合乌司他丁对急性胰腺炎患者TLR4、血浆炎症因子及白介素的影响

目的:探究连续性血液净化联合乌司他丁对急性胰腺炎患者TLR4、白介素及血浆炎症因子的影响。方法:选择2014年1月至2016年1月我院接诊的72例急性胰腺炎患者,并采用随机的方法分为实验组与对照组各36例。实验组与对照组均进行基础治疗和乌司他丁治疗,而实验组还要进行连续性血液净化治疗。记录治疗后APACHEⅡ评分、住院时间、腹痛消失时间、血清淀粉酶恢复时间,测量患者治疗前和治疗一周后的TLR4、血浆炎症因子及白介素水平。结果:(1)实验组患者治疗后住院时间、血清淀粉酶恢复时间、APACHEⅡ评分、腹痛消失时间均显著低于或少于对照组患者(P0.05)。(2)相较于治疗前,两组患者治疗一周后的TLR4、CRP、IL-6和TNF-α水平均显著降低(p0.05);实验组患者治疗一周后的TLR4、CRP、IL-6和TNF-α的水平均显著低于对照组(p0.05)。(3)实验组的治愈率(34.29%)和总有效率(74.29%)均显著高于对照组的治愈率(14.29%)和总有效率(48.57%)。结论:连续性血液净化治疗联合乌司他丁对急性胰腺炎患者的抗炎效果相较于单独使用乌司他丁疗效显著,能更好地降低炎症反应,使得TLR4、血浆炎症因子及白介素等炎症因子降低。     

乌司他丁治疗急性胰腺炎的临床疗效及对患者血清炎性因子水平的影响

目的:观察乌司他丁在急性胰腺炎临床治疗中的作用效果,分析其临床治疗价值。方法:选取我院治疗的急性胰腺炎患者178例,根据治疗方法不同分为观察组和对照组,每组89例。对照组患者采用奥曲肽治疗,观察组患者采用乌司他丁与奥曲肽联合治疗。观察并比较治疗前后患者APACHEⅡ评分和血清炎症因子变化及临床疗效。结果:入院时,两组血清CRP、IL-1、IL-6、TNF-α、APACHEⅡ评分无统计差异(P0.05),治疗后,组内CRP、IL-1、IL-6、TNF-α、APACHEⅡ评分明显下降(P0.05);观察组CRP、IL-1、IL-6、TNF-α、APACHEⅡ评分显著低于参照组(P0.05);观察组临床总有效率(86.52%)显著高于参照组(71.91%),观察组并发症(12.36%)明显低于参照组(24.72%),P0.05,组间有统计差异。结论:乌司他丁能够显著提升急性胰腺炎的临床疗效,促进患者康复,其作用机制可能与抑制炎症因子表达有关。     

乌司他丁治疗急性胰腺炎的临床疗效及机制研究

目的:探讨乌司他丁对急性胰腺炎患者的临床疗效及可能机制。方法:收集我院收治的重症急性胰腺炎患者66例,随机分为实验组和对照组。所有患者均给予禁食水、充分补液、纠正电解质紊乱等常规支持对症治疗。对照组予奥曲肽,实验组予乌司他丁,共治疗7天。测定两组患者治疗前、后各血清白介素-6(IL-6)、白介素-8(IL-8)及肿瘤坏死因子-α(TNF-α)水平;治疗前、治疗第1、3天及治疗后进行血常规检测,观察白细胞计数(WBC),并进行血淀粉酶(AMS)、尿淀粉酶(UAMY)测定;分别记录两组患者临床症状及体征恢复时间,判定临床疗效。结果:1治疗后,两组患者血清IL-6、IL-8及TNF-α水平均较治疗前显著下降,且实验组较对照组下降更明显(P0.05);2治疗后,两组患者白细胞计数及血、尿淀粉酶水平均较治疗前明显下降,且实验组较对照组下降更明显(P0.05);3治疗后,实验组各项临床症状及体征消失时间均明显短于对照组(P0.05)。结论:乌司他丁可有效改善急性胰腺胰腺炎患者的各项临床症状,这可能与其显著降低其血清IL-6、IL-8、TNF-α、淀粉酶水平、白细胞计数及尿淀粉酶水平有关。     

细菌溶解产物联合匹多莫德对反复呼吸道感染儿童炎性因子水平及免疫功能的影响

目的:探讨细菌溶解产物联合匹多莫德(PDT)治疗儿童反复呼吸道感染(RRTI)的临床效果及对血清炎性因子水平及免疫功能的影响。方法:选取我院2015年1月~2017年1月收治的122例RRTI患儿,采用随机数字表法均分为两组。对照组予以PDT治疗,观察组在对照组基础上加用细菌溶解产物治疗。比较两组治疗前后血清白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-10(IL-10)、免疫球蛋白(IgA、IgG、IgM)水平的变化及临床疗效。结果:与治疗前对比,两组治疗3个月后血清IL-6、TNF-α水平均显著下降(P0.01),血清IL-10、IgA、IgG、IgM水平均显著升高(P0.01),且观察组血清IL-6、TNF-α水平均显著低于对照组,血清IL-10、IgA、IgG、IgM水平明显高于对照组(P0.01)。治疗3个月后,观察组总有效率为93.4%,较对照组明显升高(80.3%)(P0.05)。结论:反复呼吸道感染儿童应用细菌溶解产物联合匹多莫德治疗更能有效调节机体促炎-抗炎介质平衡、增强免疫功能,临床疗效显著。     

乌司他丁联合前列地尔对急性胰腺炎的临床疗效及对血清TNF-α、IL-1β、HMGB1、HSP的影响

目的:探讨乌司他丁联合前列地尔治疗急性胰腺炎的临床疗效及对血清肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素(Interleukin-1 beta,IL-1β)、高迁移率组蛋白1(HMGB1)、热休克蛋白(HSP)的影响。方法:选择72例我院收治的急性胰腺炎患者并将其随机平均分为观察组和对照组。对照组按照常规方法治疗,观察组在常规治疗方法上采用乌司他丁联合前列地尔加入葡萄糖注射治疗。比较两组患者临床症状及体征恢复时间、治疗前后血清TNF-α、IL-1β、HMGB1、HSP水平的变化及血淀粉酶水平的恢复情况。结果:治疗后,观察组的总有效率为97.2%,对照组的总有效率为69.7%,观察组显著高于对照组(P0.05);观察组多个体征恢复时间均明显短于对照组(P0.05);两组血清TNF-α、IL-1β、HMGB1、HSP水平均较治疗前明显下降,且观察组以上指标均显著低于对照组(P0.05);观察组血淀粉酶水平恢复率明显高于对照组(P0.05)。结论:乌司他丁联合前列地尔治疗急性胰腺炎能有效提高其临床疗效,显著缩短临床症状及体征恢复时间、血淀粉酶恢复时间,降低患者血清TNF-α、IL-1β、HMGB1、HSP水平。     

姜黄素预处理对干热环境下中暑大鼠肾组织NF-κB p65及炎症因子表达的影响

目的:探讨不同剂量姜黄素对沙漠干热环境下大鼠肾组织炎症因子及NF-κB p65表达的影响。方法:将50只SD大鼠随机(随机数字法)分为五组(n=10):常温对照组、干热对照组、姜黄素低浓度组(50 mg/kg)、姜黄素终浓度组(100 mg/kg)、姜黄素高浓度组(200 mg/kg)。常温对照组及干热对照组均给予0.9%生理盐水灌胃,姜黄素组大鼠给予不同浓度姜黄素溶液灌胃,连续7天。在干热环境中放置150分钟后,麻醉处死大鼠,留取血液、肾组织进行分析。观察各组大鼠肾组织形态,检测肾组织中IL-1β、IL-6、TNF-α以及NF-κB p65表达及血清肌酐、尿素氮以及尿液中肾损伤分子1(KIM-1)、中性粒细胞明胶酶相关载脂蛋白(NGAL)的水平。结果:干热对照组大鼠血清肌酐、尿素以及尿液中KIM-1、NGAL水平均较常温对照组明显升高(P0.05),不同浓度姜黄素预处理组大鼠血清肌酐、尿素以及尿液中KIM-1、NGAL均较干热对照组有所下降,且差异具有统计学意义(P0.05)。干热对照组大鼠肾组织中IL-1β、IL-6、TNF-α以及NF-κB p65、磷酸化IκB-α的表达较常温对照组显著增加(P0.05)。姜黄素处理组大鼠随着姜黄素浓度的升高各指标较干热对照组呈不同程度的下降趋势(P0.05)。结论:姜黄素对于干热环境下大鼠肾损伤的保护作用,可能是与抑制NF-κB的表达降低细胞炎症反应水平有关。     

醋酸奥曲肽联合乌司他丁对重症急性胰腺炎患者血清ET、MCP-1、TNF-α、IL-6水平及预后的影响

目的:探讨醋酸奥曲肽联合乌司他丁对重症急性胰腺炎血清内皮素(ET)、单核细胞趋化因子蛋白1(MCP-1)、肿瘤坏死因子-α(TNF-α)、白介素-6(IL-6)水平及预后的影响。方法:纳入我院2017年1月至2018年9月收治的94例重症急性胰腺炎患者,并依据随机数字表法将其分为对照组47例与观察组47例。对照组患者给予乌司他丁治疗,观察组在对照组基础上结合醋酸奥曲肽治疗,两组疗程均为7～14 d。比较两组治疗的疗效,血淀粉酶和尿淀粉酶恢复正常时间,腹痛缓解时间、肠鸣音恢复时间和腹胀缓解时间,治疗前后血清ET、MCP-1、TNF-α、IL-6水平的变化及预后。结果:观察组治疗总有效率(93.62%)显著高于对照组(72.34%)(P0.05)。观察组血淀粉酶和尿淀粉酶恢复时间、腹痛缓解时间、肠鸣音恢复时间和腹胀缓解时间明显短于对照组(P0.05)。两组治疗后血清ET、MCP-1、TNF-α和IL-6水平均较治疗前降低(P0.05),且观察组以上指标均显著低于对照组(P0.05)。观察组出院时生存率高于对照组,但差异无统计学意义(P0.05)。结论:与单用乌司他丁相比,醋酸奥曲肽联合乌司他丁治疗重症急性胰腺炎患者疗效更好,其可显著降低患者血清ET、MCP-1、TNF-α和IL-6水平。     

乌司他丁联合利奈唑胺对重症肺炎患者血清PCT、CRP、TNF-α及白细胞计数的影响

目的:探讨乌司他丁联合利奈唑胺对重症肺炎患者血清降钙素原(PCT)、C-反应蛋白(CRP)、肿瘤坏死因子-α(TNF-α)及白细胞计数的影响。方法:选择2014年2月-2018年2月在我院住院诊治的重症肺炎患者128例,根据治疗方法的不同分为观察组68例与对照组60例,对照组给予利奈唑胺治疗,观察组在对照组治疗的基础上给予乌司他丁治疗,两组都治疗观察2周,检测和比较两组治疗后临床疗效,治疗前后1秒钟用力呼气量占用力肺活量比值(FEV1/FVC)、血清PCT、CRP、TNF-α水平及白细胞计数的变化情况。结果:观察组与对照组的治疗总有效率分别为94.1%和76.7%,观察组的总有效率显著高于对照组(P0.05)。观察组与对照组治疗后的FEV1/FVC值、白细胞计数均显著高于治疗前(P0.05),且观察组以上指标明显高于对照组(P0.05)。观察组与对照组治疗后的血清PCT、CRP、TNF-α水平都显著低于治疗前(P0.05),且观察组以上指标均显著低于对照组(P0.05)。结论:乌司他丁联合利奈唑胺治疗重症肺炎患者能显著提高临床疗效,改善患者肺功能,可能与其降低血清PCT、CRP、TNF-α水平,提高白细胞计数有关。     

乌司他丁联合参麦注射液治疗创伤后早期急性肺损伤疗效及对血清TNF-α、IL-6水平的影响

目的:探讨乌司他丁联合参麦注射液治疗创伤后早期急性肺损伤疗效及对血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)水平的影响。方法:收集我院于2012年6月~2016年6月间收治的创伤后早期急性肺损伤(ALI)患者200例。通过随机数表法分为常规组及实验组各100例,常规组患者给予常规西医方案治疗,实验组患者在常规组治疗方案的基础上加用乌司他丁及参麦注射液联合治疗。统计比较两组患者临床疗效,重症监护室(ICU)天数、住院总天数及急性呼吸窘迫综合征(ARDS)发生率;检测两组患者治疗前后血气分析指标变化;采用酶联免疫吸附实验(ELISA)于治疗前、治疗1 d后、治疗3 d后、治疗7 d后检测两组患者血清TNF-α、IL-6水平。结果:实验组疗效总有效率为88.00%,明显高于常规组的75.00%,差异有统计学意义(P0.05)。实验组ICU天数及住院总天数、ARDS发生率均低于常规组,差异均有统计学意义(P0.05)。实验组患者治疗后动脉氧分压(Pa O2)、氧合指数(Pa O2/FIO2)后水平均高于常规组,差异有统计学意义(P0.05)。实验组患者治疗3 d后、治疗7 d后血清TNF-α、IL-6水平均低于常规组,差异有统计学意义(P0.05)。结论:采用乌司他丁联合参麦注射液治疗ALI患者疗效显著,可有效降低组织氧化应激损伤,改善肺部微循环功能,降低ICU时间及住院时间,改善ALI患者肺氧合功能,降低血清TNF-α和IL-6水平。     

Temporal expression profile of CXC chemokines in serum of patients with spinal cord injury

Chemokines, a subclass of cytokine superfamily have both pro-inflammatory and migratory role and serve as chemoattractant of immune cells during the inflammatory responses ensuing spinal cord injury (SCI). The chemokines, especially CXCL-1, CXCL-9, CXCL-10 and CXCL-12 contribute significant part in the inflammatory secondary damage of SCI. Inhibiting chemokine’s activity and thereby the secondary damage cascades has been suggested as a chemokine-targeted therapeutic approach to SCI. To optimize the inhibition of secondary injury through targeted chemokine therapy, accurate knowledge about the temporal profile of these cytokines following SCI is required. Hence, the present study was planned to determine the serum levels of CXCL-1, CXCL-9, CXCL-10 and CXCL-12 at 3–6 h, 7 and 28 days and 3 m after SCI in male and female SCI patients (n = 78) and compare with age- and sex-matched patients with non-spinal cord injuries (NSCI, n = 70) and healthy volunteers (n = 100). ANOVA with Tukey post hoc analysis was used to determine the differences between the groups. The data from the present study show that the serum level of CXCL-1, CXCL-9 and CXCL-10 peaked on day 7 post-SCI and then declined to the control level. In contrast, significantly elevated level of CXCL-12 persisted for 28 days post SCI. In addition, post-SCI expression of CXCL-12 was found to be sex-dependent. Male SCI patients expressed significantly higher CXCL-12 when compared to control and SCI female. We did not observe any change in chemokines level of NSCI. Further, the age of the patients did not influence chemokines expression after SCI. These observations along with SCI-induced CSF-chemokine level should contribute to the identification of selective and temporal chemokine targeted therapy after SCI.     

Towards reducing impact-induced brain injury: lessons from a computational study of army and football helmet pads

We use computational simulations to compare the impact response of different football and U.S. Army helmet pad materials. We conduct experiments to characterise the material response of different helmet pads. We simulate experimental helmet impact tests performed by the U.S. Army to validate our methods. We then simulate a cylindrical impactor striking different pads. The acceleration history of the impactor is used to calculate the head injury criterion for each pad. We conduct sensitivity studies exploring the effects of pad composition, geometry and material stiffness. We find that (1) the football pad materials do not outperform the currently used military pad material in militarily relevant impact scenarios; (2) optimal material properties for a pad depend on impact energy and (3) thicker pads perform better at all velocities. Although we considered only the isolated response of pad materials, not entire helmet systems, our analysis suggests that by using larger helmet shells with correspondingly thicker pads, impact-induced traumatic brain injury may be reduced.     

Neuron-glia communication: metallothionein expression is specifically up-regulated by astrocytes in response to neuronal injury

Recent data suggests that metallothioneins (MTs) are major neuroprotective proteins within the CNS. In this regard, we have recently demonstrated that MT-IIA (the major human MT-I/-II isoform) promotes neural recovery following focal cortical brain injury. To further investigate the role of MTs in cortical brain injury, MT-I/-II expression was examined in several different experimental models of cortical neuron injury. While MT-I/-II immunoreactivity was not detectable in the uninjured rat neocortex, by 4 days, following a focal cortical brain injury, MT-I/-II was found in astrocytes aligned along the injury site. At latter time points, astrocytes, at a distance up to several hundred microns from the original injury tract, were MT-I/-II immunoreactive. Induced MT-I/-II was found both within the cell body and processes. Using a cortical neuron/astrocyte co-culture model, we observed a similar MT-I/-II response following in vitro injury. Intriguingly, scratch wound injury in pure astrocyte cultures resulted in no change in MT-I/-II expression. This suggests that MT induction was specifically elicited by neuronal injury. Based upon recent reports indicating that MT-I/-II are major neuroprotective proteins within the brain, our results provide further evidence that MT-I/-II plays an important role in the cellular response to neuronal injury.     

Noninvasive monitoring of citrate, acetate, lactate, and renal medullary osmolyte excretion in urine as biomarkers of exposure to ischemic reperfusion injury

Injury during the transplant process affects the alloantigen-dependent factors and the alloantigen-independent processes of "chronic" rejection. Consequently, the determination of reliable parameters for the assessment of ischemic damage is essential for the prediction of renal changes after ischemia/reperfusion injury. The aim of this study was to assess the ability of (1)H NMR spectroscopy to predict the early graft dysfunction in an ischemia/reperfusion model after preservation in two standard preservation solutions, Euro-Collins (EC) and University of Wisconsin (UW). The second aim was to specify the role of the UW solution in preventing renal medullary injury. Urine and plasma samples from three experimental groups were examined during 2 weeks: control group (n = 5), EC group (cold flushed and 48-h cold storage of kidney in EC and autotransplantation, n = 12), and UW group (cold flushed and 48-h cold storage of kidney in UW and autotransplantation; n = 12). We also examined these kidneys 30-40 min after implantation and on the sacrifice day. Creatinine clearance was significantly reduced in the EC group during the second week. Fractional excretion of sodium and urine N-acetyl-beta-d-glucosaminidase activity were improved but not significantly different in the preserved groups. Urinary concentrations of the alpha-class glutathione S-transferase were significantly greater in the EC group during the first week after transplantation. The most relevant resonances for evaluating renal function after transplantation determined by (1)H NMR spectroscopy were those arising from citrate, dimethylamine (DMA), lactate, and acetate in urine and trimethylamine-N-oxide (TMAO) in urine and plasma. These findings suggest that graft dysfunction is associated with damage to the renal medulla determined by TMAO release in urine and plasma associated with DMA and acetate excretion. Citrate is also a urinary marker that can discriminate kidneys with a favorable evolution. Our results suggest that (1)H NMR spectroscopy is an efficient technique for detecting ischemic damage when accurate and precise data on graft injury is required. In addition, this study outlines the specific impact of the UW solution against injury to the renal medulla.     

牛磺酸对大鼠肢体缺血/再灌注后肺组织损伤的保护作用

目的:观察大鼠肢体缺血再灌注(LIR)后肺组织形态学的变化及牛磺酸对其影响.方法:Wistar大鼠随机分为3组,对照组(control)、缺血/再灌注组(LIR)、牛磺酸 缺血/再灌注组(Tau LIR),各组动物通过大体、光镜和透射电镜观察肺组织形态学变化,并测定肺系数和肺通透指数及肺组织活性氧和MDA含量.结果:大鼠LIR后肺组织出现以肺泡毛细血管膜通透性增加为特征的组织细胞损伤,光镜下显示毛细血管扩张充血、血管周围间隙增大、肺泡腔中有大量蛋白渗出物,电镜下可见肺泡上皮细胞之间、毛细血管内皮之间的紧密连接松解;肺系数和肺通透指数升高;肺组织活性氧及MDA含量增加.提前给予外源性牛磺酸可使肺组织损伤变化减轻.结论:牛磺酸对大鼠LIR后肺损伤有保护作用,其保护机理之一与其抗氧化,保护细胞之间的紧密连接有关.     

缺血预适应对大鼠肢体缺血/再灌注后肺损伤的影响

目的:观察肢体缺血预适应对大鼠肢体缺血/再灌注(I/R)后肺损伤的影响并探讨其机制。方法:将雄性Wistar大鼠随机分为4组(n=8):对照组(C),肢体缺血/再灌注组(LI/R),缺血预适应组(IPC)和L-NAME组。各组大鼠均于肢体缺血4h再灌注4h处死,分别测定其动脉血氧分压(PaO2)和二氧化碳分压(PaCO2),血浆及肺组织丙二醛(MDA)、一氧化氮(NO)、内皮素(ET)含量,计算血浆NO/ET比值;以及肺湿干比(W/D)、肺系数(LI),肺组织髓过氧化物酶(MPO)含量。结果:大鼠LI/R后4h,PaO2明显降低;W/D、LI、血浆及肺组织的MDA、NO、ET和肺组织MPO活性均明显增加,而血浆NO/ET比值明显减小。与LI/R组比较,IPC组各项损伤指标明显减轻,NO水平升高,血浆NO/ET比值明显增大。与对照组和IPC组比较,L-NAME处理组,各项损伤指标数值明显增加,NO水平降低;血浆NO/ET比值明显减小,差异均具有显著性。各组大鼠PaCO2的变化无显著性。结论:缺血预适应对肢体缺血/再灌注后肺损伤具有保护作用,其机制可能与内源性NO合成增加有关。     

Influence of rapidly successive head impacts on brain strain in the vicinity of bridging veins

Acute subdural hematoma due to a bridging vein rupture is a devastating but rare injury. There has to date been no satisfactory biomechanical explanation for this infrequent but costly injury. We surmise that it may be associated with multiple head impacts. Though numerical models have been used to estimate vein strains in single impact events, none to date have examined the influence on localized brain strain of rapidly consecutive impacts. Using the Simulated Injury Monitor, we investigated the hypothesis that such double impacts can increase strain beyond that created by any single impact. Input to our parametric study comprised hypothetical biphasic rotational head accelerations producing a maximum angular velocity of 40 rad./s. In each of 19 simulations, two identical angular inputs are applied at right angles to each other but with time separations varying from 0 to 40 ms. For these double impacts, it has been generally found that strain in the region of the bridging veins is different, than what would be associated with any corresponding single impact. In some cases, the effect is to actually reduce the tissue strain. In others, the strain in the region of the bridging veins is increased markedly. The mechanistic explanation for the strain increase is that the tissue strain from the first impact has not diminished fully when strain from the second impact is initiated. Rapidly consecutive impacts could be a potential mechanism leading to vein rupture that warrants further investigation.     

脉冲1 064 nm激光视网膜损伤动物模型的建立

目的:建立脉冲1 064 nm Nd:YAG激光致视网膜出血性损伤及非出血性损伤动物模型,为治疗药物评价提供技术基础.方法:应用自由振荡脉冲及调Q脉冲1 064 nm激光照射青紫蓝灰兔视网膜,通过在光路中加人透镜获得直径200μm眼底光斑,加入衰减片改变角膜入射激光能量.照射即刻对损伤应用检眼镜进行实时观察,并用眼底相...     

Eupatilin alleviates inflammatory response after subarachnoid hemorrhage by inhibition of TLR4/MyD88/NF-κB axis

Early brain injury (EBI) is associated with the adverse prognosis of subarachnoid hemorrhage (SAH) patients. The key bioactive component of the Chinese herbal medicine Artemisia asiatica Nakai (Asteraceae) is eupatilin. Recent research reports that eupatilin suppresses inflammatory responses induced by intracranial hemorrhage. This work is performed to validate whether eupatilin can attenuate EBI and deciphers its mechanism. A SAH rat model was established by intravascular perforation in vivo. At 6 h after SAH in rats, 10 mg/kg eupatilin was injected into the rats via the caudal vein. A Sham group was set as the control. In vitro, BV2 microglia was treated with 10 μM Oxyhemoglobin (OxyHb) for 24 h, followed by 50 μM eupatilin treatment for 24 h. The SAH grade, brain water content, neurological score, and blood-brain barrier (BBB) permeability of the rats were measured 24 h later. The content of proinflammatory factors was detected via enzyme-linked immunosorbent assay. Western blot analysis was conducted to analyze the expression levels of TLR4/MyD88/NF-κB pathway-associated proteins. In vivo, eupatilin administration alleviated neurological injury, and decreased brain edema and BBB injury after SAH in rats. Eupatilin markedly reduced the levels of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α), and suppressed the expression levels of MyD88, TLR4, and p-NF-κB p65 in the SAH rats' cerebral tissues. Eupatilin treatment also reduced the levels of IL-1β, IL-6, and TNF-α, and repressed the expression levels of MyD88, TLR4, and p-NF-κB p65 in OxyHb-induced BV2 microglia. Additionally, pyrrolidine dithiocarbamate or resatorvid enhanced the suppressive effects of eupatilin on OxyHb-induced inflammatory responses in BV2 microglia. Eupatilin ameliorates SAH-induced EBI via modulating the TLR4/MyD88/NF-κB pathway in rat model.     

NOGO-A immunolabeling is present in glial cells and some neurons of the recovering lumbar spinal cord in lizards

The transected lumbar spinal cord of lizards was studied for its ability to recover after paralysis. At 34 days post-lesion about 50% of lizards were capable of walking with a limited coordination, likely due to the regeneration of few connecting axons crossing the transection site of the spinal cord. This region, indicated as “bridge”, contains glial cells among which oligodendrocytes and their elongation that are immunolabeled for NOGO-A. A main reactive protein band occurs at 100–110 kDa but a weaker band is also observed around 240 kDa, suggesting fragmentation of the native protein due to extraction or to physiological processing of the original protein. Most of the cytoplasmic immunolabeling observed in oligodendrocytes is associated with vesicles of the endoplasmic reticulum. Also, the nucleus is labeled in some oligodendrocytes that are myelinating sparse axons observed within the bridge at 22–34 days post-transection. This suggests that axonal regeneration is present within the bridge region. Immunolabeling for NOGO-A shows that the protein is also present in numerous reactive neurons, in particular motor-neurons localized in the proximal stump of the transected spinal cord. Ultrastructural immunolocalization suggests that NOGO is synthesized in the ribosomes of these neurons and becomes associated with the cisternae of the endoplasmic reticulum, probably following a secretory pathway addressed toward the axon. The present observations suggest that, like for the regenerating spinal cord of fish and amphibians, also in lizard NOGO-A is present in reactive neurons and appears associated to axonal regeneration and myelination.