海带多糖在高脂血症大鼠中的降血脂和抗氧化作用

目的 探讨海带多糖对高脂血症大鼠血脂的调节作用机制. 方法 健康雌性Wistar大鼠32只,应用高脂饲料喂养方法建立高脂血症动物模型,海带多糖干预治疗.血生化法检测大鼠血清甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白(HDL)水平,硝酸还原酶法检测血清和肝组织一氧化氮(NO)含量,黄嘌呤氧化酶法测定血清和肝组织超氧化物歧化酶(SOD)活性,酶联免疫吸附法检测血清和肝组织中氧化低密度脂蛋白(ox-LDL)水平,免疫组织化学技术检测肝细胞SOD和诱导性一氧化氮合酶(iNOS)表达. 结果 海带多糖治疗后,大鼠血清TG、TC和LDL水平较模型组显著下降,而HDL显著升高(P<0.05).肝组织匀浆ox-LDL和NO水平较模型组显著降低,而SOD活性显著升高.肝细胞iNOS表达较模型组显著降低,SOD表达显著增强(P<0.05). 结论 海带多糖可通过抗氧化机制而发挥调节血脂水平的作用.     

羊栖菜对高脂血症大鼠降血脂和抗氧化作用研究

目的探讨羊栖菜在高脂血症大鼠中的抗氧化作用机制。方法健康雌性Wistar大鼠40只,应用高脂饲料喂养方法建立高脂血症动物模型,羊栖菜粉饲料喂养干预治疗。氧化酶法检测大鼠血清三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)和高密度脂蛋白(HDL)水平,硫代巴比妥酸法检测血清脂质过氧化物丙二醛(MDA)水平,硝酸还原酶法检测血清一氧化氮(NO)含量,黄嘌呤氧化酶法测定血清超氧化物歧化酶(SOD)活性,化学比色法检测血清谷胱甘肽过氧化物酶(GSH-PX)的活性。结果辛伐他汀组和羊栖菜治疗组动物血清TG、TC和LDL水平较模型对照组显著下降而HDL水平显著高于模型对照组(P<0.05)。辛伐他汀组和羊栖菜治疗组动物血清MDA和NO水平较模型对照组均显著下降(P<0.05),而血清SOD和GSH-PX活性均显著高于模型对照组(P<0.05)。但羊栖菜治疗组与辛伐他汀组比较,上述指标均无明显差异(P>0.05)。结论羊栖菜活性成分可能通过增强SOD和GSH-PX的活性,发挥抗氧化作用而影响脂质代谢。     

持续肌肉泵注镇痛液用于晚期癌症镇痛的临床观察

１临床资料慢性前列腺炎分为两组，观察组１８０例，年龄２３～６０岁，平均３４．８岁；已婚１４４例，未婚３６例；病程３个月～１０年，平均２．４年。对照组６９例，年龄２４～６２岁，平均３４．７岁；已婚５１例，未婚１８例；病程４个月～１１年，平均２．５年。两组临床表现均有不同程度的会阴部疼痛、腰骶部疼痛或不适、睾丸疼、排尿阻力增加及尿路刺激症状、失眠、情绪波动等神经官能症状，性功能丧失或减退。直肠指诊：前列腺不同程度触痛，硬度不等。B型超声显示前列腺大小约（４．３±０．６）cm×（３．５±０．５）cm×（２…     

胡黄连苷Ⅱ治疗脑缺血损伤最佳剂量和时间窗的研究

目的 研究胡黄连苷Ⅱ治疗大鼠脑缺血损伤的最佳剂量和时间窗.方法 应用双侧颈内动脉结扎法建立大鼠前脑缺血模型,按照正交试验设计分组,经腹腔注射胡黄连苷Ⅱ于预治疗,酶联免疫吸附法检测血清神经元特异性烯醇化酶（NSE）、神经胶质细胞标志蛋白S100B、髓鞘碱性蛋白（MBP）的含量,综合评价胡黄连苷Ⅱ在脑缺血损伤中的疗效.结果 据血清NSE、S100B和MBP含量分析,胡黄连苷Ⅱ治疗脑缺血损伤的最佳治疗时机和剂量分别为脑缺血1.5 h、腹腔注射20 mg/kg.结论 从治疗时间窗最大化和用药剂量最小化原则综合分析,在脑缺血损伤治疗中,在脑缺血1.5 h腹腔注射胡黄连苷Ⅱ20 mg/kg体重疗效最好.     

神经调节素对实验性痴呆大鼠神经元凋亡的影响

阿尔采末病(Alzheimer′s disease,AD)多发于老年人,以近期记忆障碍为主要临床症状,脑海马区神经元凋亡是AD的重要发病机制之一[1].实验证实[2],NRG1β具有抑制神经元凋亡的作用.本实验利用单侧侧脑室一次性注射可溶性大片段淀粉样蛋白β1-40(Aβ1-40)复制痴呆大鼠模型,探讨NRG1β对拟痴呆大鼠的保护作用及机制.     

Therapeutic time window of picroside on cerebral ischemia reperfusion injury in rats

BACKGROUNG: Cerebral schemia may result in cerebral edema and neuronal injury by activating some endogenous mechanisms. It has been confirmed that picrosideⅡ could protect neuronal damage in vitro an ex vitro. OBJECTIVE: The aim of the present study is to explore the neuroprotective effects and the perfect treatment window of picrosideⅡ on brain insult in rats following middle cerebral artery occlusion and reperfusion (MCAO/R). DESIGN, TIME AND SETTING: A randomized, controlled animal experiment was performed at Institute of Cerebrovascular Diseases, Qingdao University Medical College from September 2008 to May 2009. MATERIALS AND METHODS: One hundred and sixty-five adult healthy male Wistar rats were randomly divided into a sham-operation group (n=15), a control group (n=75) and a treatment group (n=75). Rats in the control group and the treatment group were experimented surgery operation of MCAO/R with an intraluminal monofilament suture from left external-internal carotid artery. Those in the treatment group were injected 1.0％ picrosideⅡat a single dosage of 10mg/kg from the tail vein. We evaluated neurological function score by Longa’s method, cerebral infarction volume with tetrazolium chloride (TTC) stain. Then we compared cell apoptosis by terminal deoxynucleotidyl transference-mediated biotinylated deoxyuridine triphosphate nick end labeling technique (TUNEL), and determined the expression alternation of aquaporin-4 (AQP-4) via fluorescence labeling analysis and RT-PCR technique. RESULTS: After MCAO/R, neurological function scores were decreased, and a small infarction focus could be detected in ischemic cortex in the control group at ischemic 0.5h, along with the increased number of positive-apotosis cells and the elevated expression of AQP-4 mRNA and its protein. With the duration of ischemia, neurological scores and infarction sizes obviously increased in the control group during ischemic 1.0h-2.0h. A great deal of positive-apoptotic cells were widespread in the cortex and the striatum in the ischemic ipsilateral. Simultaneously, the expression of AQP-4 mRNA and its protein increased to some extent. PicrosideⅡ treatment significantly improved the loss of neurological function, decreased the infarction volume, and elevated the expression levels of AQP-4 mRNA and its protein compared with those in the control group. The therapeutic effect of picrosideⅡ was notable, especially in the ischemic 1.0h subsection. CONCLUSION: These results demonstrate that picrosideⅡ played a neuroprotective effect on cerebral ischemic reperfusion by inhibiting apoptosis and regulating the expression of AQP-4 mRNA and its protein. The best therapeutic window is at ischemic 1h after MCAO.     

胡黄连苷Ⅱ对大鼠脑缺血/再灌注损伤NF-κB和I-κB的干预作用

目的研究胡黄连苷Ⅱ对大鼠脑缺血/再灌注后核转录因子κB(NF-κB)和NF-κB抑制因子(I-κB)表达的影响。方法应用线栓法建立大鼠大脑中动脉闭塞再灌注模型,经尾静脉注射胡黄连苷Ⅱ(10mg·kg-1)和丹参素钠(10mg·kg-1)干预治疗,原位TUNEL检测神经细胞凋亡,免疫组化检测NF-κB和I-κB的表达,ELISA法检测脑组织匀浆NF-κB和I-κB的含量。结果假手术组大鼠皮质、纹状体和海马区脑组织NF-κB和I-κB弱表达,TUNEL阳性细胞数量较少,散在分布。阴性对照组大鼠各区脑组织TUNEL阳性细胞数量较假手术组均增多,NF-κB和I-κB表达增强,脑组织匀浆NF-κB和I-κB增高(P<0.05)。阳性对照组和胡黄连苷组各区脑组织TUNEL阳性细胞数量,NF-κB和I-κB表达(A值)及脑组织匀浆NF-κB和I-κB含量均低于阴性对照组(P<0.05),阳性对照组与胡黄连苷组比较,各指标差异均无显著性(P>0.05)。结论胡黄连苷Ⅱ可能通过下调NF-κB和I-κB的表达,抑制脑缺血/再灌注损伤的炎症反应导致的神经细胞凋亡。