Autophagy induces mitochondrial dysfunction in neurons from neonatal rats with hypoxic ischemic encephalopathy

AIM: To explore the influence of autophagy on the induction of mitochondrial dysfunction in the neurons in a neonatal rat hypoxic ischemic encephalopathy (HIE) model. METHODS: Ten-day-old rat pups (n=30) were randomly divided into sham group and model group. The rats in the latter group were subject to hypoxia-ischemia treatment via unilateral common carotid artery ligation. The rats were sacrificed for brain pathological examination, and the protein levels of cleaved caspase-3 and LC3B-II were detected by immunohistochemical analysis. For the in vitro experiments, the autophagy of primarily cultured rat neurons was observed after hypoxia, and Western blot and mitochondrial function testing were also performed. RESULTS: Compare with sham group, the hypoxia-ischemia treatment caused atrophy and apoptosis of neurons, and ventricular area enlargement of rat brains. Immunohistochemical results demonstrated significantly higher levels of apoptosis- and autophagy-associated proteins, such as cleaved caspase-3 and LC3B-II (P<0.01). In vitro experiments demonstrated that hypoxia induced autophagy and apoptosis in the neurons. Compared with sham group, there were higher levels of reactive oxygen species and mitochondrial superoxide, and lower mitochondrial membrane potential in the model group (P<0.01). CONCLUSION: In neonatal HIE rat model, the hypoxia-induced mitochondrial dysfunction is related to apoptosis and autophagy. It will provide a new idea for administration of autopahgy inducer agents in treatment of HIE.     

Neuroprotective effect of methanolic extracts of Allium cepa on ischemia and reperfusion-induced cerebral injury

The present study is designed to investigate the effect of methanolic extract of outer scales and edible portions of Allium cepa bulb on ischemia and reperfusion-induced cerebral injury. Global cerebral ischemia was induced by bilateral carotid artery occlusion for 10 min followed by reperfusion for 24 h. Pretreatment with methanolic extract of outer scales (100 mg/kg and 200 mg/kg) and edible portions (100 mg/kg and 200 mg/kg) of A. cepa bulb markedly reduced cerebral infarct size and attenuated impairment in short-term memory and motor coordination. The protective effect of methanolic extract of outer scales and edible portions of A. cepa bulb was accompanied by a marked decrease in mitochondrial TBARS.     

Effects of noninvasive delayed limb ischemic preconditioning on prognosis of myocardial infarction

AIM: To study the effects of noninvasive delayed limb ischemia preconditioning (NDLIP) on animal cardiac function, myocardial morphology and myocardial apoptosis after myocardial infarction (MI). METHODS: Healthy SD male rats[n=45, weighing (250±10) g] were randomly divided into 3 groups:MI group:the animal model of MI was established by surgical ligation of left anterior descending artery (LAD) after 2 weeks; NDLIP group:after the success of the MI animal model, NDLIP was carried out every other day until the 4th, 6th and 8th weeks; sham group:as the negative control group, the animals were taken heart LAD threading but no ligation. All rats were fed conventionally. At the end of the 4th, 6th and 8th weeks, all rats were made ventricular intubation, and then the hemodynamic parameters were recorded. The blood samples were withdrawn from the abdominal aorta and the serum was separated via centrifugation. The serum contents of Bcl-2 and Bax were measured by ELISA. Left ventricular anterior wall was homogenized. The mitochondrial respiratory chain complexes Ⅰ, Ⅱ, Ⅲ and Ⅳ in the myocardial tissues were detected by ELISA. RESULTS: At the end of the 4th, 6th and 8th weeks, compared with MI group, left ventricular systolic pressure in NDLIP group was significantly increased, while left ventricular end-diastolic pressure in NDLIP group was significantly decreased (both P<0.05). Mitochondrial respiratory chain complexesⅠ, Ⅱ, Ⅲ and Ⅳ in NDLIP group were significantly increased (P<0.05). The serum level of Bcl-2 in NDLIP group was significantly increased and Bax level was reduced remarkably (both P<0.01). CONCLUSION: NDLIP improves the hemodynamic indexes, promotes the mitochondrial respiratory function and inhibits cell apoptosis, thus improving the prognosis of MI.     

二甲醚发动机的研究与开发

介绍了二甲醚作为代用燃料的性能优势,二甲醚发动机的结构、原理和排放应对措施     

四冲程汽油机缸内斜轴涡流研究

利用双特征角气道稳流试验台,对一款二气门四冲程单缸试验机的3种不同进气道方案进行了不同测试平面的气流运动试验和分析.结果表明,提高原气道涡流强度来改善燃烧的同时会降低气道的流通能力,但适度提高滚流强度的同时还可以提高流通能力.利用测得的无因次涡流比和滚流比,提出了一个简便的斜轴涡流特征参数计算公式,并通过试验数据给予了有效性证明.另外对特征角α=60°时的无因次涡流比和利用涡流与滚流合成的无因次斜轴涡流比进行了线性回归分析,3种方案数据的相关系数分别是0.96、0.97、0.97,因此,通过稳流气道试验台测取某一特征角度下的无因次涡流比可以评价进气道斜轴涡流的性能.     

PC12细胞诱导的神经缺血细胞Smad7-siRNA及沉默效果的检测

目的探讨诱导PC12细胞分化的神经细胞靶向沉默Smad7基因特性,同时进行沉默效果检测．方法以Smad7基因为靶目标,设计合成3条siRNA序列,进行细胞转染,利用Rea1time—PCR和Westernblot技术检测沉默效果,筛选出最有效的干扰序列,同时检测出最佳的转染浓度和转染时间．结果针对Smad7基因设计合成及筛选出靶向沉默Smad7基因的干扰序列（siRNA1）;siRNA1的最佳转染浓度是4μg／mL;siRNA1的最佳转染时间是24h;siRNA1对Smad7的抑制效果优于其他干扰序列．结论siRNA1能有效沉默Smad7基因;lipofecta—mineTM2000可成功将siRNA1转染至神经细胞,转染效率较高;利用siRNA技术能有效抑制神经细胞．     

避免渔船螺旋桨被流刺网绞缠的试验

流刺网是影响船舶航行安全的因素之一,本试验利用渔船的冲程使渔船冲过流刺网,从而使渔船驾驶员掌握渔船航行中避免螺旋桨被流刺网绞缠的方法,确保渔船航行生产的安全。     

脑活素治疗新生大鼠缺血缺氧性脑病机理的研究

7日龄Wister大鼠结扎左侧颈总动脉后吸入氧氮混合气体（8％O2和92％N2）2h,制成缺血缺氧性脑病动物模型,测定大鼠脑组织中丙二醛（MDA）的含量和超氧化物歧化酶（SOD）的活性。结果显示,缺血缺氧后6h,缺血缺氧组MDA含量显著升高,24h达到高峰,以后逐渐下降,96h与对照组比较无统计学差异;缺血缺氧脑活素治疗组MDA含量于缺血缺氧后6h已经显著下降,72h与对照组比较无统计学差异。缺血缺氧组SOD活力值在缺血缺氧后6h已经下降,24h降到最低点,以后逐渐回升,96h与对照组比较无统计学差异;缺血缺氧脑活素治疗组SOD活力值在缺血缺氧后6h明显提高,于缺血缺氧后96h与对照组比较无统计学差异。结果提示,缺血缺氧引起新生大鼠脑组织的氧化-抗氧化系统失衡,氧自由基大量产生,参与了新生大鼠缺血缺氧性脑病脑损伤过程;脑活素能够抑制氧自由基的生成,提高SOD的活力值,对缺血缺氧性脑病具有神经保护作用。