Observation on the Effect of Parental Participation in Nursing Under the IMCHB Model in Neonatal Hypoxic-Ischemic Encephalopathy

Objective:To investigate the clinical effects of parental participation in nursing under the Interaction Model of Client Health Behavior(IMCHB)model in neonatal hypoxic-ischemic encephalopathy(HIE).Methods:The First Affiliated Hospital of Gannan Medical University included 46 newborns with HIE admitted from October 2021 to October 2023 into the study population.They were divided into a control group and an observation group according to the random number table method,with the control group adopting routine nursing,and the observation group implementing parental participation in nursing under the IMCHB model.The indicators of physical,intellectual,and psychomotor development of the two groups were compared before and after nursing.Results:The physical,intellectual,and psychomotor development of the observation group was higher than that of the control group after 3 months of nursing,and the difference was statistically significant(P<0.05).Conclusion:The implementation of the IMCHB model of parental participation in the clinical care of HIE neonates can further promote their physical,intellectual,and psychomotor development.

Changes in hippocampal neurons and memory function during the developmental stage of newborn rats with hypoxic-ischemic encephalopathy

BACKGROUND: Under the normal circumstance, there exist some synapses with inactive functions in central nervous system (CNS), but these functions are activated following nerve injury. At the early stage of brain injury, the abnormal functions of brain are varied, and they have very strong plasticity and are corrected easily. OBJECTIVE: To observe the changes of neuronal morphology in hippocampal CA1 region and memory function in newborn rats with hypoxic-ischemic encephalopathy(HIE) from ischemia 6 hours to adult. DESIGN: Completely randomized grouping, controlled experiment. SETTING: Taian Health Center for Women and Children; Taishan Medical College. MATERIALS: Altogether 120 seven-day-old Wistar rats, of clean grade, were provided by the Experimental Animal Center, Shandong University of Traditional Chinese Medicine. Synaptophysin (SYN) polyclonal antibody was provided by Maixin Biological Company, Fuzhou. METHODS: This experiment was carried out in the Laboratory of Morphology, Taishan Medical College between October 2000 and December 2003. ① The newborn rats were randomly divided into 2 groups: model group and control group, 60 rats in each group. Five rats were chosen from each group at postoperative 6 hours, 24 hours, 72 hours, 7 days, 2 weeks and 3 weeks separately for immunohistochemical staining. Fifteen newborn rats were chosen from each group at postoperative 4 weeks and 2 months separately for testing memory ability (After test, 5 rats from each group were sacrificed and used for immunohistochemical staining)② The right common carotid artery of newborn rats of model group was ligated under the anesthetized status. After two hours of incubation, the rats were placed for 2 hours in a container filled with nitrogen oxygen atmosphere containing 0.08 volume fraction of oxygen, thus, HIE models were created; As for the newborn rats in the control group, only blood vessels were isolated, and they were not ligated and hypoxia-treated. ③ Thalamencephal tissue sections of newborn rats of two groups were performed DAB developing and haematoxylin slight staining. Cells with normal nucleous in 250 μm-long granular layer which started from hippocampal CA1 region were counted with image analysis system under high-fold optical microscope (×600), and the thickness of granular layer was measured. The absorbance (A) of positive reactant of SYN in immunohistochemically-stained CA1 region was measured. Learning and memory ability were measured with step through test 3 times successively. ④ t test and paired t test were used for comparing intergroup and intragroup difference of measurement data respectively, and Chi-square for comparing the difference of enumeration data. MAIN OUTCOME MEASURES: Comparison of cytological changes in hippocampal CA1 region and memory ability at different postoperative time points between two groups. RESULTS: Totally 120 newborn rats were involved in the result analysis. ① Cell morphological changes in hippocampal CA1 region: In the control group, with aging, perikaryon, nucleus and nucleolus in cortex of parietal lobe were significantly increased, Nissl body was compacted, the amount of neurons was declined, but the A of SYN positive reactant was relatively increased. In the model group, at postoperative each time point, neurons were seriously shrunk and dark-stained, nucleus was contracted, chromatin was condensed, nucleolus was unclear, even cells disappeared, especially the cells in 6 hours and 24 hours groups. The amount of neurons with normal morphology in hippocampal CA1 region and granular layer thickness in the model group at postoperative each time point were significantly less or smaller than those in the control group at postoperative 6 hours respectively (t =3.002-1.254, P < 0.01). The A value of SYN positive reactant at postoperative 2, 3 and 4 weeks was significantly higher than that at previous time point (t =2.011-2.716,P < 0.05-0.01). ② Test results of learning and memory ability: In the first test, there was no significant difference in the ratio of rats which kept memory ability between two groups (P > 0.05); In the third test, the ratio of rats which kept memory ability in the model group was significantly lower than that in the control group at postoperative 4 weeks and 2 months[53%(8/15),100%(15/15);60%(9/15),93%(14/15),χ 2=2.863,2.901,P < 0.01]. CONCLUSION: The destroyed hippocampal structure induces the decrease of learning and memory ability of developmental rats. Early interference can increase the quality of neurons and also promote functional development of the nervous system.

Can we further optimize therapeutic hypothermia for hypoxic-ischemic encephalopathy?

Perinatal hypoxic-ischemic encephalopathy is a leading cause of neonatal death and disability.Therapeutic hypothermia significantly reduces death and major disability associated with hypoxic-ischemic encephalopathy;however,many infants still experience lifelong disabilities to movement,sensation and cognition.Clinical guidelines,based on strong clinical and preclinical evidence,recommend therapeutic hypothermia should be started within 6 hours of birth and continued for a period of 72 hours,with a target brain temperature of 33.5 ±0.5℃ for infants with moderate to severe hypoxic-ischemic encephalopathy.The clinical guidelines also recommend that infants be re warmed at a rate of 0.5℃ per hour,but this is not based on strong evidence.There are no randomized controlled trials investigating the optimal rate of rewarming after therapeutic hypothermia for infants with hypoxic-ischemic encephalopathy.Preclinical studies of rewarming are conflicting and results were confounded by treatment with sub-optimal durations of hypothermia.In this review,we evaluate the evidence for the optimal start time,duration and depth of hypothermia,and whether the rate of rewarming after treatment affects brain injury and neurological outcomes.

Hyperbaric oxygen treatment promotes neural stem cell proliferation in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage

Hyperbaric oxygen therapy for the treatment of neonatal hypoxic-ischemic brain damage has been used clinically for many years, but its effectiveness remains controversial. In addition, the mechanism of this potential neuroprotective effect remains unclear. This study aimed to investigate the influence of hyperbaric oxygen on the proliferation of neural stem cells in the subventricular zone of neonatal Sprague-Dawley rats （7 days old） subjected to hypoxic-ischemic brain damage. Six hours after modeling, rats were treated with hyperbaric oxygen once daily for 7 days. Immunohistochemistry revealed that the number of 5-bromo-2＇-deoxyuridine positive and nestin positive cells in the subventricular zone of neonatal rats increased at day 3 after hypoxic-ischemic brain damage and peaked at day 5. After hyperbaric oxygen treatment, the number of 5-bromo-2＇- deoxyuddine positive and nestin positive cells began to increase at day 1, and was significantly higher than that in normal rats and model rats until day 21. Hematoxylin-eosin staining showed that hyperbaric oxygen treatment could attenuate pathological changes to brain tissue in neonatal rats, and reduce the number of degenerating and necrotic nerve cells. Our experimental findings indicate that hyperbaric oxygen treatment enhances the proliferation of neural stem cells in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage, and has therapeutic potential for promoting neurological recovery following brain injury.

Estrogen inhibits lipid peroxidation after hypoxic-ischemic brain damage in neonatal rats

Sprague-Dawley neonatal rats within 7 days after birth were used in this study. The left common carotid artery was occluded and rats were housed in an 8% O2 environment for 2 hours to establish a hypoxic-ischemic brain damage model. 17β-estradiol （1 × 10-5 M） was injected into the rat abdominal cavity after the model was successfully established. The left hemisphere was obtained at 12, 24, 48, 72 hours after operation. Results showed that malondialdehyde content in the left brain of neonatal rats gradually increased as modeling time prolonged, while malondialdehyde content of 17β-estrodial-treated rats significantly declined by 24 hours, reached lowest levels at 48 hours, and then peaked at 72 hours after injury. Nicotinamide-adenine dinucleotide phosphate histochemical staining showed the nitric oxide synthase-positive cells and fibers dyed blue/violet and were mainly distributed in the cortex, hippocampus and medial septal nuclei. The number of nitric oxide synthase-positive cells peaked at 48 hours and significantly decreased after 17β-estrodial treatment. Our experimental findings indicate that estrogen plays a protective role following hypoxic-ischemic brain damage by alleviating lipid peroxidation through reducing the expression of nitric oxide synthase and the content of malondialdehyde.

Reperfusion after hypoxia-ischemia exacerbates brain injury with compensatory activation of the antiferroptosis system:based on a novel rat model

Hypoxic-ischemic encephalopathy,which predisposes to neonatal death and neurological sequelae,has a high morbidity,but there is still a lack of effective prevention and treatment in clinical practice.To better understand the pathophysiological mechanism underlying hypoxic-ischemic encephalopathy,in this study we compared hypoxic-ischemic reperfusion brain injury and simple hypoxic-ischemic brain injury in neonatal rats.First,based on the conventional RiceVannucci model of hypoxic-ischemic encephalopathy,we established a rat model of hypoxic-ischemic reperfusion brain injury by creating a common carotid artery muscle bridge.Then we performed tandem mass tag-based proteomic analysis to identify differentially expressed proteins between the hypoxic-ischemic reperfusion brain injury model and the conventional Rice-Vannucci model and found that the majority were mitochondrial proteins.We also performed transmission electron microscopy and found typical characteristics of ferroptosis,including mitochondrial shrinkage,ruptured mitochondrial membranes,and reduced or absent mitochondrial cristae.Further,both rat models showed high levels of glial fibrillary acidic protein and low levels of myelin basic protein,which are biological indicators of hypoxic-ischemic brain injury and indicate similar degrees of damage.Finally,we found that ferroptosis-related Ferritin(Fth1)and glutathione peroxidase 4 were expressed at higher levels in the brain tissue of rats with hypoxic-ischemic reperfusion brain injury than in rats with simple hypoxic-ischemic brain injury.Based on these results,it appears that the rat model of hypoxic-ischemic reperfusion brain injury is more closely related to the pathophysiology of clinical reperfusion.Reperfusion not only aggravates hypoxic-ischemic brain injury but also activates the anti-ferroptosis system.

Electroencephalography studies of hypoxic ischemia in fetal and neonatal animal models

Alongside clinical achievements,experiments conducted on animal models (including primate or non-primate) have been effective in the understanding of various pathophysiological aspects of perinatal hypoxic/ ischemic encephalopathy (HIE).Due to the reasonably fair degree of flexibility with experiments,most of the research around HIE in the literature has been largely concerned with the neurodevelopmental outcome or how the frequency and duration of HI seizures could relate to the severity of perinatal brain injury,following HI insult.This survey concentrates on how EEG experimental studies using asphyxiated animal models (in rodents,piglets,sheep and non-human primate monkeys) provide a unique opportunity to examine from the exact time of HI event to help gain insights into HIE where human studies become difficult.

链脲佐菌素诱导糖尿病脑病大鼠模型的构建及评价

背景:目前研究较成熟的糖尿病脑病模型主要有链脲佐菌素诱导模型、高糖高脂饮食诱导模型和自发性动物模型。建立简便易行、周期短、安全有效的糖尿病脑病模型对其发病机制的深入探讨和治疗药物的筛选有重要的作用。目的:进一步验证链脲佐菌素诱导糖尿病脑病大鼠模型的方法并对其进行评价。方法:将20只SD大鼠随机分为对照组(n=10)和模型组(n=10),模型组大鼠左下腹腔一次性注射45 mg/kg链脲佐菌素建立糖尿病实验动物模型,对照组大鼠用等量的柠檬酸缓冲液代替注射。实验期间监测大鼠体质量、饮食量、饮水量和血糖,8周后检测葡萄糖耐量和氧化应激水平,并比较脑组织病理变化及凋亡蛋白的表达情况。结果与结论:①与对照组相比,模型组大鼠饮食量、饮水量、脑指数、血糖和血糖曲线下面积显著升高、体质量明显下降(P<0.01);②脑组织病理学显示,模型组大鼠存活神经细胞数量明显减少(P<0.01),神经细胞病理损伤明显高于对照组;③模型组大鼠较对照组血清超氧化物歧化酶、过氧化氢酶和谷胱甘肽活力均明显降低(P<0.01),氧化活性丙二醛的浓度明显升高(P<0.05);④脑组织中凋亡相关蛋白Bax和Caspase-3表达水平增加,Bcl-2表达水平降低(P<0.01);⑤结果说明,注射45 mg/kg链脲佐菌素8周后可以使糖尿病大鼠脑组织有明显的病理损伤,成功构建糖尿病脑病大鼠模型。

足月儿全脑缺氧缺血性脑病模型的建立

目的建立一种简单稳定、适宜临床研究的足月儿全脑缺氧缺血性脑病(HIBD)大鼠模型并探讨该模型的评价方法。方法将10日龄SD大鼠82只,随机分为假手术组(Sham,n=22)和模型组(HIBD,n=60)。通过结扎10日龄SD大鼠双侧颈总动脉,缺血1.5 h,缺氧30 min后给予血管再通的方法,制备足月儿全脑HIBD大鼠模型;假手术组不做缺血和缺氧处理。(1)病理相关检测:术后3 d,进行TTC染色、HE与尼氏染色,海马区电镜检测,观察脑组织病理结构变化;脑干湿比重法测脑含水量评估脑水肿情况。(2)行为学评价:术后12 h进行惊厥评估,术后3 d进行Longa评分,术后10 d进行悬吊实验,术后3周进行Morris水迷宫实验。结合术后一般情况与行为学实验结果进行HIBD分级。结果与假手术组相比,HIBD组TTC切片染色可见双侧白色梗死灶;HE与尼氏染色可见海马区神经元排列紊乱、坏死脱失;电镜检测可见海马区神经元细胞水肿,线粒体空泡化,自噬溶酶体增多;脑含水量显著升高(P<0.01)。与假手术组相比,HIBD组大鼠早期可有惊厥发作伴不同程度运动神经功能障碍,远期可出现发育迟缓、学习认知能力降低(P<0.01)。结论结扎10日龄大鼠双侧颈总动脉,缺氧后再通,能较稳定地复制出中重度足月儿全脑HIBD大鼠模型,可为进一步探索HIBD发病机制与治疗用药提供理想的动物模型。

Hippocampus hypoxia-inducible factor-1 alpha and heme oxygenase-1 expression in the delayed encephalopathy after acute carbon monoxide poisoning rat model

Objective To research the expression of hypoxia-inducible factor-1 alpha(HIF-1α)and heme oxygenase-1(HO-1)in hippocampus of rats with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP)and its functions.Methods One hundred and fiftysix rats were selected and randomly divided into

乌司他丁对大鼠胰性脑病保护作用的实验研究

目的 :探讨乌司他丁对大鼠急性出血坏死性胰腺炎时对脑组织损害的保护作用 ,为胰性脑病的治疗提供实验依据。方法 :将 90只SD大鼠随机分为正常对照组 ,急性出血坏死性胰腺炎诱导组和乌司他丁处理组 ,经胰胆管逆行注射 5%牛磺胆酸钠建立大鼠ANP模型 ,12h后处死动物 ,测定血清TNFα水平 ,并检测脑组织含水量、脑微血管内白细胞聚集及附壁现象。结果 :经乌司他丁处理后 ,血清中乌司他丁水平、脑组织含水量、脑组织MDA含量、脑微血管内白细胞聚集及附壁现象显著降低(P <0 .0 1)。结论

两种新生儿缺血缺氧性脑病模型建模方法的比较

目的比较两种新生儿缺血缺氧性脑病(HIE)模型建模方法的差异,探讨麻醉和动物缺血缺氧间期对HIE动物模型的影响。方法采用7d龄SD乳鼠建立HIE模型。传统组动物乙醚麻醉后结扎左侧颈总动脉,休息2～3h,同时入37℃水溶闭缺氧箱,持续充以8%氧+92%氮的混合气体,气流量1L/min,维持2.5h。改进组动物动脉结扎手术前动物不予麻醉,且术后动物不作休息立即进行缺氧。比较建模过程中两组动物的存活情况;光镜下观察建模后3d两组动物左侧大脑半球的病理变化情况,并比较两组动物病理总评分的差异。结果改进组建模过程中所有动物未见死亡,传统组建模过程中6只动物死亡(P<0.025)。建模后3d,改进组动物脑组织变性、坏死显著,病理总评分550分,传统组大部分动物脑组织未见明显病变,总评分130分(P<0.01)。结论传统HIE建模方法动物在建模过程中死亡率高,而存活的模型动物病理变化却不确切。改进的HIE建模方法模型动物个体之间均衡性好,脑部病变确切,建模过程中动物死亡率低,值得推广。

幼年大鼠缺氧缺血性脑病动物模型的研究

目的探讨建立幼年大鼠缺氧缺血性脑病(HIE)动物模型的可靠方法。方法结扎幼年wistar大鼠(1月龄左右)左颈总动脉两端,置于8%浓度的低氧环境中2.5 h,观察大鼠行为;经心脏灌流4%多聚甲醛固定取脑,观察脑部外观变化,采用HE染色及光镜技术观察其脑组织结构改变。结果造模后幼鼠行为表现符合经典缺氧缺血性脑病动物模型的行为改变;缺氧缺血后3 h左侧大脑出现轻度脑损伤,24 h病变明显,4 d出现胶质细胞增生,18 d神经元大量坏死、丢失,多部位形成胶质瘢痕。病理变化与幼儿HIE相似。结论本方法建立的大鼠缺氧缺血性脑病动物模型快速、可靠,可用于实验研究。

丙二醛、超氧化物歧化酶及肿瘤坏死因子-α在大鼠实验性胰性脑病中的作用

目的探讨丙二醛(MDA)、超氧化物歧化酶(SOD)及肿瘤坏死因子-α(TNF-α)在大鼠实验性胰性脑病中对脑组织的作用,为揭示胰性脑病的发病机理和治疗提供实验依据。方法将36只Wistar大鼠按拆信封法随机分为对照组(n=6)和胰性脑病组(n=30)。对照组经颈内动脉注入生理盐水;胰性脑病组经颈内动脉注入磷脂酶A2,复制大鼠胰性脑病模型。对照组大鼠于制模后第1d处死,胰性脑病组分别于造模后第1、3及7d各处死10只动物,检测脑组织含水量,观察脑微血管内白细胞聚集及附壁现象、脑细胞和神经纤维变化,检测大鼠脑组织匀浆中TNF-α、MDA含量及SOD活性变化。结果随时间延长,胰性脑病组大鼠脑微血管内白细胞聚集及附壁数目显著增加,神经元细胞水肿及神经纤维脱髓鞘改变明显,脑组织含水量、MDA及TNF-α的含量明显增加,SOD活性明显降低(P<0.05,P<0.01)。结论大鼠胰性脑病模型中,MDA、SOD及TNF-α对胰性脑病时脑损害的发生和发展有重要作用。

新生鼠缺血缺氧性脑病中神经干细胞的形态学观察

【目的】建立新生鼠缺血缺氧性脑病动物模型,探讨HIE病程中神经干细胞(neuralstemcells,NSCs)的形态学改变。【方法】210只新生7dSD乳鼠随机分为正常对照组、单纯缺氧组及缺血缺氧组。每组70只。每组又根据处死时间点随机分成3h,6h,1d,3d,7d,14d,21d等7个小组。每小组10只。缺血缺氧组结扎新生7dSD大鼠左颈总动脉,置于8%氧浓度的低氧环境中2.5h。单纯缺氧组缺氧2.5h。采用HE染色、免疫组织化学染色以及光镜技术分别对3组SD大鼠脑组织中的NSCs形态学进行检测。【结果】缺血缺氧组缺血缺氧后3h出现轻度脑损伤,1d病变最严重,3d、7d胶质细胞增生,14d、21d出现脑萎缩。3组SD鼠在7个时间点脑组织均存在NSCs,且细胞呈单一的圆形,突起不超过1个,阳性NSCs呈明显的区域性分布,神经球集落样存在的NSCs较多,单纯缺氧组在每一时间点NSCs的表达明显高于缺血缺氧组及正常对照组。在6h时间点,处于增殖状态的NSCs增多,尤其是室下区。1d和3d时间点,坏死脑组织中仍可见NSCs及其神经球。3d时间点后病侧脑组织的NSCs逐渐下降。【结论】成功建立了缺血缺氧性脑病动物模型;HIE发病中早期NSCs增殖;NSCs随着病情的演变开始减少;低氧有利于NSCs的增殖;早期采用NSCs干预治疗有希望成为临床治疗HIE的重要途径。

四氯化碳诱导大鼠肝性脑病模型的制备

目的建立肝性脑病(HE)动物模型。方法应用四氯化碳联合酒精自饮法制作慢性肝功能衰竭引起HE发生的模型,进行迷宫试验、脑电图、血液生化、形态学、行为活动观察等检测。结果 1.肉眼下可见模型组肝脏普遍肿大,表面较粗糙,有较粗的颗粒,暗红色;正常组肝脏未见异常。模型组肝内有大量纤维增生,肝细胞溶解,弥漫性大片坏死,残留肝细胞成片气球样变。2.与对照组大鼠比较,造模组第九周水迷宫测试逃避潜伏期明显延长,以潜伏期延长超过正常x+2.5 s为标准,本实验有14/20(55%)只大鼠水迷宫潜伏期明显延长;3.HE模型组血氨浓度明显高于正常对照组,组间比较差异有显著性(P<0.01);4.正常组脑电图以α波为主,无明显异常;模型组出现肝性脑病变化。结论 1.建立了肝硬化合并肝性脑病较为理想的动物模型;2.水迷宫测试联合检测更易检出HE。

肿瘤坏死因子α抗体对大鼠胰性脑病保护作用的实验研究(英文)

目的 探讨肿瘤坏死因子α(TNFα)抗体在大鼠急性出血坏死性胰腺炎时对脑组织损害的保护作用,从而为胰性脑病的治疗提供实验依据。方法 将60只SD大鼠随机分为正常对照组,急性出血坏死性胰腺炎诱导组和TNFα抗体处理组,经胰胆管逆行注射5%牛磺胆酸建立大鼠ANP模型,测定血的TNFα水平,12h后处死动物,检查胰腺组织形态学变化,并检测脑组织含水量、脑微血管内白细胞聚集及附壁现象。结果 经TNFα抗体处理后,血清中TNFα水平、脑组织含水量、脑微血管内白细胞聚集及附壁现象显著降低(P<0.05),胰腺组织病理损害程度减轻。结论 TNFα抗体可以减轻急性出血坏死性胰腺炎时脑损害的发生和发展。

杜仲木脂素对糖尿病脑病大鼠的治疗作用及机制研究

目的探讨杜仲木脂素对糖尿病脑病(DE)大鼠的治疗作用及核因子E2相关因子2(Nrf2)/血红素氧化酶1(HO-1)信号通路的影响。方法构建DE大鼠模型,将建模成功的48只大鼠随机分为模型组、杜仲木脂素低剂量组(200mg/kg)、杜仲木脂素高剂量组(400mg/kg)、二甲双胍组(200mg/kg),每组12只。另选取12只健康大鼠作为对照组。各组每天给予相应药物干预1次,连续6周。检测大鼠认知和记忆能力、血清白细胞介素6(IL-6)、TNF-α、丙二醛、超氧化物歧化酶(SOD)、脑组织海马区中Nrf2、HO-1信使RNA(mRNA)和蛋白表达水平;并观察脑组织海马区病理学变化。结果与对照组比较,模型组大鼠逃避潜伏期、血清IL-6、TNF-α、丙二醛水平显著升高,经过原平台位置次数、原平台象限停留时间、血清SOD水平、脑组织海马区中Nrf2、HO-1mRNA和蛋白表达水平显著降低(P<0.05);与模型组比较,杜仲木脂素低、高剂量组大鼠逃避潜伏期、血清IL-6、TNF-α、丙二醛水平显著降低,经过原平台位置次数、原平台象限停留时间、血清SOD水平、脑组织海马区中Nrf2、HO-1mRNA和蛋白表达水平显著升高(P<0.05)。与杜仲木脂素低剂量组比较,杜仲木脂素高剂量组大鼠逃避潜伏期、血清IL-6、TNF-α、丙二醛水平显著降低(P<0.05);杜仲木脂素高剂量组经过原平台位置次数、原平台象限停留时间、血清SOD水平、脑组织海马区中Nrf2、HO-1mRNA表达水平显著高于杜仲木脂素低剂量组[(6.07±0.70)次vs(4.76±0.52)次、(30.96±2.96)svs(23.49±2.60)s、(77.02±6.51)U/mlvs(61.71±6.75)U/ml、(0.69±0.06)vs(0.49±0.05)、(0.74±0.07)vs(0.57±0.06),P<0.05]。结论杜仲木脂素能改善DE大鼠认知能力,提升其抗氧化能力并抑制炎性反应,保护大鼠脑组织海马区,其机制可能与激活Nrf2/HO-1信号通路有关。

电针治疗对缺氧缺血性脑病模型大鼠mTOR表达的影响

【目的】观察电针对缺氧缺血性脑病模型大鼠雷帕霉素靶蛋白(m TOR)表达的干预作用。【方法】选择7日龄SD大鼠,随机分为3组:假手术组、模型组、电针组。每组又以1、3、7、21 d分为4个亚组,采用苏木精—伊红(HE)染色观察缺氧缺血侧脑组织的形态学变化,Western blot法检测m TOR的蛋白表达。【结果】HE染色显示:电针组在21 d时,神经细胞界限清楚,排列有序,细胞肿胀变轻,细胞轮廓及核仁清晰,可见胶质细胞增生。模型组m TOR蛋白的表达均在第1天开始增加,第3、7、21天持续增加,与假手术组比较,差异均有统计学意义(P<0.05)。电针组在1、3、7、21 d 4个时间点与模型组比较,差异均有统计学意义(P<0.05)。【结论】电针能够促进m TOR蛋白水平的表达,对缺氧缺血性脑损伤大鼠可起到脑保护作用。

环孢素A在实验性大鼠胰性脑病中的保护作用

目的:探讨环孢素(cyclosporine A,CsA)对大鼠胰性脑病脑组织损害的保护作用,为胰性脑病的治疗提供实验依据。方法:将60只Wister大鼠随机分为对照组和CsA治疗组,两组大鼠均经颈内动脉注射精制胰磷脂酶A2(PLA2),建立大鼠胰性脑病模型,CsA治疗组在造模前5min腹腔注射CsA(30mg/kg),之后每天同时间腹腔注射CsA(30 mg/kg),直至处死,对照组用等容积生理盐水代替。对照组和CsA治疗组分别于造模后1、3及7d各处死动物10只,测定大鼠脑组织匀浆TNF-α、IL-10水平,并检测脑组织含水量、脑组织的组织学改变、中枢神经系统脱髓鞘改变。结果:经CsA处理后,大鼠脑组织匀浆TNF-α水平、脑组织含水量较对照组显著降低(P<0.05),而IL-10则较对照组升高(P<0.05),CsA治疗组脑组织神经细胞水肿较轻,脱髓鞘改变轻微。结论:CsA可以减轻胰性脑病脑损害的发生和发展。