Dynamic changes in proprotein convertase 2 activity in cortical neurons after ischemia/reperfusion and oxygen-glucose deprivation

In this study, a rat model of transient focal cerebral ischemia was established by performing 100 minutes of middle cerebral artery occlusion, and an in vitro model of experimental oxygen-glucose deprivation using cultured rat cortical neurons was established. Proprotein convertase 2 activity gradually decreased in the ischemic cortex with increasing duration of reperfusion. In cultured rat cortical neurons, the number of terminal deoxynucleotidyl transferase-mediated 2＇-deoxyuridine 5＇-triphosphate-biotin nick end labeling-positive neurons significantly increased and proprotein convertase 2 activity also decreased gradually with increasing duration of oxygen-glucose deprivation. These experimental findings indicate that proprotein convertase 2 activity decreases in ischemic rat cortex after reperfusion, as well as in cultured rat cortical neurons after oxygen-glucose deprivation. These changes in enzyme activity may play an important pathological role in brain injury.

Autologous transplantation with fewer fibers repairs large peripheral nerve defects

Peripheral nerve injury is a serious disease and its repair is challenging. A cable-style autologous graft is the gold standard for repairing long peripheral nerve defects; however, ensuring that the minimum number of transplanted nerve attains maximum therapeutic effect remains poorly understood. In this study, a rat model of common peroneal nerve defect was established by resecting a 10-mm long right common peroneal nerve. Rats receiving transplantation of the common peroneal nerve in situ were designated as the in situ graft group. Ipsilateral sural nerves（10–30 mm long） were resected to establish the one sural nerve graft group, two sural nerves cable-style nerve graft group and three sural nerves cable-style nerve graft group. Each bundle of the peroneal nerve was 10 mm long. To reduce the barrier effect due to invasion by surrounding tissue and connective-tissue overgrowth between neural stumps, small gap sleeve suture was used in both proximal and distal terminals to allow repair of the injured common peroneal nerve. At three months postoperatively, recovery of nerve function and morphology was observed using osmium tetroxide staining and functional detection. The results showed that the number of regenerated nerve fibers, common peroneal nerve function index, motor nerve conduction velocity, recovery of myodynamia, and wet weight ratios of tibialis anterior muscle were not significantly different among the one sural nerve graft group, two sural nerves cable-style nerve graft group, and three sural nerves cable-style nerve graft group. These data suggest that the repair effect achieved using one sural nerve graft with a lower number of nerve fibers is the same as that achieved using the two sural nerves cable-style nerve graft and three sural nerves cable-style nerve graft. This indicates that according to the ‘multiple amplification＇ phenomenon, one small nerve graft can provide a good therapeutic effect for a large peripheral nerve defect.

硫酸镁对大鼠脑缺血再灌注损伤后神经功能的保护作用

目的：验证硫酸镁对脑缺血再灌注损伤后神经功能的保护作用。方法：２２只ＳＤ大鼠随机分为对照组、缺血组和硫酸镁治疗组。参照Ｐｕｌｓｉｎｅｌｉ和Ｂｒｉｅｒｌｅｙ的方法建立脑缺血再灌注动物模型，并观察动物神经行为学和病理学的改变。结果：与对照组和缺血组相比，硫酸镁能改善神经行为异常和减轻脑组织病理损害，且对血压无明显影响。结论：硫酸镁能明显减轻缺血再灌注后脑组织病理形态学的损害程度。

常压氧疗治疗缺血性脑卒中的实验研究

[目的]研究常压氧疗对缺血性脑卒中的作用和机制。[方法]将30只健康雄性SD大鼠随机分为3组:假手术组(S组),缺血再灌注组(I/R组),常压氧疗治疗组(NBO组)。I/R组和NBO组采用线栓法阻塞大鼠右侧大脑中动脉制备局灶性脑缺血再灌注模型,缺血2h后拔出线拴行再灌注,其中NBO组于缺血后15min给予3h的NBO(100%氧)。再灌注24h时进行神经功能缺陷评分、测定脑梗死体积,并检测脑组织中超氧化物歧化酶(SOD)和谷胱苷肽过氧化物酶(GSH-PX)活性以及丙二醛(MDA)、肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)含量。[结果]与S组比较,I/R组大鼠神经功能缺陷评分、脑梗死体积、TNF-α、IL-1β和MDA含量均增加(P<0.05),SOD和GSH-PX活性降低(P<0.05);与I/R组比较,NBO组神经功能缺陷评分、脑梗死体积、TNF-α、IL-1β和MDA含量均降低(P<0.05),SOD和GSH-PX活性升高(P<0.05)。[结论]常压氧疗对大鼠脑缺血再灌注损伤具有保护作用,能改善神经功能,减小梗死体积,其作用机制可能与通过减轻氧化应激及抑制炎性反应有关。

早期康复护理干预对颅脑损伤术后偏瘫患者的影响

目的:探讨对颅脑损伤术后偏瘫患者进行早期康复护理干预的临床效果。方法:35例颅脑损伤术后偏瘫患者在常规治疗和一般护理基础上,采用避免患侧输液、功能位摆放、按摩活动患肢、音乐疗法、心理疏导、指导日常生活能力训练等康复护理干预,并与35例常规护理组做对照。结果:4周后观察到干预组患者在日常生活能力、神经功能缺损程度等方面优于对照组。结论:对颅脑损伤术后偏瘫患者进行早期康复护理干预,可明显减少并发症和残疾程度,有利于患者早日恢复日常生活能力,回归家庭和社会。

早期颅骨修补治疗脑外伤的临床应用优势

目的 探讨早期颅骨修补治疗脑外伤的临床应用优势。方法 选取我院2013年5月-2015年5月收治的100例脑外伤患者,采用抽签分组方式将其分为两组,每组50例患者,对照组采用晚期颅骨修补术治疗,观察组采用早期颅骨修补治疗。比较两组患者的治理效果、临床各项评分、不良事件发生率。结果 观察组患者治疗效果、神经功能缺损评分、格拉斯哥评分、功能状态评分、不良事件发生率均优于对照组[100.00%vs 92.00%（10.76±1.54）分vs（19.65±1.78）分,（12.75±1.86）分vs（9.73±1.75）分,（92.36±2.43）分vs（72.43±1.32）分,2.00%vs 24.00%],差异有统计学意义（P〈0.05）。结论 早期颅骨修补治疗脑外伤患者效果显著。

通络Ⅳ号联合西药治疗脑梗死急性期随机平行对照研究

[目的]观察通络Ⅳ号联合西药治疗脑梗死急性期疗效。[方法]使用随机平行对照方法,将80例住院患者按随机数字表法随机分为两组。对照组40例血栓通注射液175mg+生理盐水250mL,静滴,1次/d;胞二磷胆硷钠注射液0.5g+生理盐水250mL中,静滴,1次/d;阿司匹林肠溶片100mg,1次/d。颅内高压20%甘露醇125mL,静滴,1～4次/d,随颅内高血压缓解逐渐减量至停用;合并高血压、糖尿病、冠心病对症治疗。治疗组40例通络Ⅳ号[①黄芪30kg,杜仲15kg,当归12kg,桑寄生15kg,第1次10倍水量浸泡30min后煎煮2h,第2次8倍水量煎煮1.5h,合并2次煎液,30目筛网滤过,滤液浓缩至密度为1.02～1.08(80°C)备用。②水蛭1kg,丹参15kg研磨成细粉,过120目筛,拌匀。③将丹参、水蛭粉加入浓缩液中拌匀,泛成小丸,80℃干燥,分装6g/袋],6g/次,3次/d,必要时鼻饲给药。西药治疗同对照组。连续治疗14d为1疗程。观测神经功能缺损评分、谷氨酸(Glu)、S100β蛋白、不良反应。连续治疗1疗程,判定疗效。[结果]神经功能缺损评分均有改善(P<0.05),治疗组改善优于对照组(P<0.05);Glu变化均有改善(P<0.05),治疗组改善优于对照组(P<0.05);S100β蛋白变化均有改善(P<0.05),治疗组改善优于对照组(P<0.05)。[结论]通络Ⅳ号联合西药治疗脑梗死急性期,减少了缺血再灌注损伤,有较好的脑保护作用。

L-3-n-butylphthalide protects against vascular dementia via activation of the Akt kinase pathway

As a neuroprotective drug for the treatment of ischemic stroke, 3-n-butylphthalide, a celery seed ex- tract, has been approved by the State Food and Drug Administration of China as a clinical therapeutic drug for ischemic stroke patients. L-3-n-butylphthalide possesses significant efficacy in the treatment of acute ischemic stroke. The activated Akt kinase pathway can prevent the death of nerve cells and exhibit neuroprotective effects in the brain after stroke. This study provides the hypothesis that I-3-n- butylphthalide has a certain therapeutic effect on vascular dementia, and its mechanism depends on the activation of the Akt kinase pathway. A vascular dementia mouse model was established by cere- bral repetitive ischemia/reperfusion, and intragastrically administered I-3-n-butylphthalide daily for 28 consecutive days after ischemia/repedusion, or 7 consecutive days before ischemia/reperfusion. The Morris water maze test showed significant impairment of spatial learning and memory at 4 weeks after operation, but intragastric administration of I-3-n-butylphthalide, especially pretreatment with I-3-n- butylphthalide, significantly reversed these changes. Thionine staining and western blot analylsis showed that preventive and therapeutic application of I-3-n-butylphthalide can reduce loss of pyrami- dal neurons in the hippocampal CA1 region and alleviate nerve damage in mice with vascular demen- tia. In addition, phosphorylated Akt expression in hippocampal tissue increased significantly after I-3-n- butylphthalide treatment. Experimental findings demonstrate that I-3-n-butylphthalide has preventive and therapeutic effects on vascular dementia, and its mechanism may be mediated by upregulation of phosphorylated Akt in the hippocampus.

依达拉奉对脑缺血再灌注损伤患者神经功能、氧化应激和炎性反应的影响

目的观察依达拉奉对脑缺血再灌注损伤患者神经功能、氧化应激和炎性反应的影响。方法选择2017年9月—2019年9月辽宁省金秋医院神经内科治疗脑缺血再灌注损伤患者170例作为研究对象,随机数字表法分成观察组(85例)和对照组(85例)。对照组患者行常规治疗方案,观察组患者在对照组基础上加用依达拉奉治疗。治疗2周后,比较2组治疗效果及治疗前后神经功能(NIHSS、ADL评分)、氧化应激(血清MDA、SOD)和炎性反应因子(TNF-α、IL-6、NSE、S-100β)蛋白水平变化。结果治疗后,观察组患者的总有效率为94.1%,高于对照组的80.0%(χ^2=7.518,P=0.006);NIHSS评分低于对照组,ADL评分高于对照组(t=9.427、7.603,P<0.01);血清MDA水平低于对照组,SOD水平高于对照组(t=14.660、18.524,P均<0.01);血清TNF-α、IL-6水平低于对照组(t=12.369、9.333,P均<0.01);血清NSE、S-100β蛋白水平低于对照组(t=13.110、6.185,P均<0.01)。结论依达拉奉应用于脑缺血再灌注损伤治疗中能够提高患者治疗效果,改善神经功能,控制炎性反应,改善患者预后。