EFFECTS OF CEREALS FROM KASHIN－BECK DISEASE ENDEMIC AREA ON FIBRILLOGENESIS IN VITRO OF CARTILAGE COLLAGEN TYPE Ⅱ IN RATS

ＥＦＦＥＣＴＳＯＦＣＥＲＥＡＬＳＦＲＯＭＫＡＳＨＩＮ－ＢＥＣＫＤＩＳＥＡＳＥＥＮＤＥＭＩＣＡＲＥＡＯＮＦＩＢＲＩＬＬＯＧＥＮＥＳＩＳＩＮＶＩＴＲＯＯＦＣＡＲＴＩＬＡＧＥＣＯＬＬＡＧＥＮＴＹＰＥⅡＩＮＲＡＴＳＦｕＺｈｉｈｏｕ；ＺｈａｎｇＳｈｉｙｕａｎ（...     

大脑皮层神经细胞原代培养及其缺氧性损害模型

用２ｄ龄的ＳＤ大鼠大脑皮层进行分散神经细胞原代培养，经氰化钠阻断细胞呼吸链，模拟了大脑皮层神经细胞急性缺氧损害模型。模型中缺氧细胞形态不典型，膜流动性降低，乳酸脱氢酶漏出增多，类似整体动物脑缺氧后神经细胞变化。此模型可用于研究缺氧皮层神经细胞的损伤、损伤后恢复及药物的保护作用。     

EFFECT OF MELATONIN AGAINST GLUTAMATE-INDUCED EXCITOTOXICITY ON CULTURED CEREBRAL CORTICAL NEURONS

Melatonin(MT) is a kind of very importantpineal hormone.Besides its sedative,hypnotic andanalgetic effects,in recent years,many researchershave suggested that it may be used in the treat-ment of many acute and chronic central nervoussystem diseases,for example,brain trauma,epilepsy,Alzheimer s disease,and so on[1～ 3 ] .　However,its mechanism of resisting diseases isstill unclear.In the present research,an isolatedpattern of excitotoxic neuron injury was induced byglutamate.On the basis of …     

卡马西平对培养皮层神经细胞毒性的研究

在对体外新生大白鼠（0～1d）大脑皮层神经细胞进行原代培养的基础上，分别加入不同浓度卡马西平（Carbamazepine，CBZ），继续培养3d。检测乳酸脱氨酶（LDH）释出率双膜流动性。结果显示：高浓度的CBZ（24mg／L）可导致神经细胞LDH释出率明显升高（P<0．01）、膜流动性明显降低（P＜0．01）。提示高浓度卡马西平对神经细胞存在有毒性作用。     

EFFECT OF MILD HYPOTHERMIA ON ACTIVITY NITRIC OXIDE SYNTHASE IN CORTICAL NEURONS AND GLYCEMIA LEVELS OF NEONATAL RATS WITH HYPOXIC ISCHEMIC BRAIN DAMAGE

EFFECT OF MILD HYPOTHERMIA ON ACTIVITY NITRIC OXIDE SYNTHASE IN CORTICAL NEURONS AND GLYCEMIA LEVELS OF NEONATAL RATS WITH HYPOXIC ISCHEMIC BRAIN DAMAGE     

亚低温对新生大鼠缺氧缺血性脑损伤大脑皮质神经元一氧化氮合酶表达及血糖水平的影响

通过亚低温对新生鼠缺氧缺血性脑损伤（ＨＩＢＤ）大脑皮质神经元一氧化氮合酶（ＮＯＳ）及血糖水平影响的研究,探讨亚低温对缺氧缺血性脑损伤的保护作用机制。建立新生鼠缺氧缺血性脑病（ＨＩＥ）标准化动物模型,将其随机分为对照组、３１℃亚低温和３４℃亚低温干预组并设立假手术组,应用免疫组化染色观察大脑皮质区ＮＯＳ阳性神经元数目,并利用微量血糖监测仪测定血糖。结果表明,缺血缺氧后１２ｈ、２４ｈ,亚低温干预组大脑皮质ＮＯＳ阳性神经元数均显著低于对照组,血糖水平均显著高于对照组。３１℃和３４℃亚低温干预两组间各个时期大脑皮质区ＮＯＳ阳性神经元数目及血糖水平无显著差异。亚低温可通过抑制神经元内ＮＯＳ活性,减少过量ＮＯ的生成,以及提高血糖水平,对缺氧缺血性脑损伤鼠大脑神经细胞起到保护作用     

THE EFFECT OF LIGUSTRAZINE ON NEUROGENESIS IN CORTEX AFTER FOCAL CEREBRAL ISCHEMIA IN RATS

Objective To explore the effect of Ligustrazine on neurogenesis in cortex after focal cerebral ischemia in rats. Methods Focal cerebral ischemia was induced by left middle cerebral artery occlusion with a suture. Two hours later, injection of Ligustrazine （80 mg/kg, 1 time/d） was performed peritoneally. Four hours after the ischemia, 5-bromodeoxyuridine （BrdU） （50 mg/kg, 1 time/d） was injected peritoneally. At 7 d, 14 d and 21 d after ischemia, BrdU positive cells in the cortex were observed by cal staining. Results In ischemic model group, at 7 day, sparsely-distributed BrdU positive cells were observed in the Ⅱ-- Ⅵ layers of the ipsilateral cortex, with a bandlike distribution in ischemic penumbra. With the prolongation of ischemia, the number of BrdU positive cells increased. In Ligustrazine group, BrdU positive cells were also observed in theⅡ-- Ⅵ layers of the cortex, with an intense distribution in ischemic penumbra. The numbers of BrdU positive cells at 7 d, 14 d and 21 d were more than those in ischemic model group respectively. Conclusion Ligustrazine increases the proliferated cells in cortex after focal cerebral ischemia in rats. The results suggest that it may be useful for promoting self-repair after ischemia.     

THE EFFECT ON PROTEOGLYCAN METABOLISM OF DEOXYNIVALENOL AND SELENIUM IN THE CULTURED HUMAN FETAL CHONDROCYTES IN VITRO

Kashin BeckDisease(KBD)isasevere,en demicosteoarthrosis,butitspathogenesisisstilla pendentproblem.Withregardtoetiologyanalysis,mycotoxinhypothesisandlow seleniumhypothesis havebeenstudiedmoreinChina[1].Thepathologi calfeaturesofKBDarethedegenerationandnec…     

培养中的下丘脑神经元的形态学研究

取新生大鼠下丘脑分散培养１、３、７、１４ｄ的细胞，应用免疫细胞化学、电镜和图像分析等技术研究下丘脑神经元。结果显示：培养的下丘脑神经元可表达神经丝蛋白和神经元特异性烯醇化酶；某些神经元突起可见串珠样膨体，突起末端有生长锥；电镜下，神经元胞质含丰富的蛋白质合成细胞器；神经元培养１～３ｄ生长最快；７ｄ，胞体面积和突起长度均达高峰值，１４ｄ时基本维持在７ｄ水平。     

在培养心肌细胞上测定细胞跨膜电位

利用固定微电极技术和倒置显微镜装置,在培养心肌细胞上记录细胞跨膜电位获得成功,电位振幅可达80mv左右。此方法具有内环境影响因素少、敏感性高等特点,可广泛用于生理、病理生理及药理等心血管方面的研究。     

STUDY ON THE EFFECT OF T-2 TOXIN AND SELENIUM ON CD44 EXPRESSION IN THE CULTURED HUMAN FETAL CHONDROCYTES IN VITRO

KBD (Kashin BeckDisease)isasevere ,en demicosteoarthrosisandthepathogenesisofitisstillapendentproblem[1] .WiththestudyofetiologyofKBD ,thehypothesisofselenium deficiencyinthesurroundingandfoodcontaminatedbyfungaltoxinisanoticeableone .The pathologicalfeaturesofKBDarethedegenerationandnecrosisofthearticu larcartilage ,disorderofmetabolismofcartilagematrix .Thestudyontheosteoarthrosissuggeststhatthereductionoftheaggregationandincreaseofdeg radationofaggrecanareinitialaffairsifcartilagehasdeg…