DHA与婴幼儿神经发育

大量科学证实大脑和神经系统的发育会受到遗传、环境、教育、营养与疾病等许多因素的影响.人每日摄入的营养素量,80%用于神经系统的发展和大脑活动.妊娠期母亲的营养摄入和婴儿出牛后早期的营养对婴幼儿神经系统的发育具有极其苇要的意义.许多研究结果显示,DHA在婴幼儿脑发育和视觉功能发育当中具有重要的作用.近年来,关于DHA对婴幼儿神经发育的影响已成为儿童保健学与营养学界关注的热点.     

消炎利胆散镇痛作用的初步研究

用热板法、扭体法实验测痛表明,消炎利胆敞有显著的镇痛作用。正连续给药一周后,消炎利胆散对小鼠痛阈提高率为121％(P<0.001),对小鼠扭体反应抑制率为50％(P<0.01)。动物实验结果与临床镇痛疗效基本相符。     

碱提类肝素对大鼠血浆脂质的调整作用及机理

碱提类肝素及其组分1和组分2能有效地预防和治疗高脂饲料诱发的大鼠血脂紊乱,包括降低血清TC,降低LDL-ch和VLDL-ch水平,提高HDL-ch/LDL-ch比值。这一作用可能主要是通过促进血管壁脂蛋白脂酶的释放,提高血浆脂蛋白脂酶活性而发挥的。     

Pathological and biochemical alterations of astrocytes in ovariectomized rats injected with D-galactose:A potential contribution to Alzheimer's disease processes

Astrocytes are implicated in the pathological changes of Alzheimer's disease. Our previous studies have demonstratedthat estrogen deprivation and oxidative stress act synergistically to accelerate0 the progress of Alzheimer's disease. Long-term D-galac-tose injection combined with ovariectomy may serve as a rodent model for Alzheimer's disease. To address the potential contributionof astroglia to the Alzheimer's disease pathogenesis, we investigated pathological and biochemical alterations of astrocytes under thisanimal model. Ovadectomized rats injected with D-galactose for 2 weeks showed extensive localization of glial fibrillary acidic proteinimmunoreactive astrocytes and slightly elevated glutathione levels in the hippocampus without significant impairments in the watermaze test and deficits of the cholinergic analyses, compared to the saline-injected rats. Ovariectomized rats injected with D-galactosefor 6 weeks, however, exhibited degeneration of astrocytes and decreased glutathione levels in the hippocampus, accompanied withsevere dysfunction of behavioral test and deficiency of cholinergic terminals. Electron microscopy further confirmed the pathologicalchanges of astrocytes, especially in the aggregated area of synapse and brain microvessels. Consistent with degeneration of perivascu-lar astrocytic endfeet, analysis of the horseradish peroxidase demonstrated an impairment of the blood-brain barrier permeability.These findings indicate that biochemical and pathological alterations of astrocytes may partially contribute to exacerbating neuronaldeficits in the course of Alzheimer's disease. Restoring neuroprotective potential of astrocytes may be a useful therapeutic target forAlzheimer's disease and other neurodegenerative diseases.     

Pathological and biochemical alterations of astrocytes in ovariectomized rats injected with D-galactose:A potential contribution to Alzheimer's disease processes

Astrocytes are implicated in the pathological changes of Alzheimer's disease. Our previous studies have demonstrated that estrogen deprivation and oxidative stress act synergistically to accelerate the progress of Alzheimer's disease. Long-term D-galactose injection combined with ovariectomy may serve as a rodent model for Alzheimer's disease. To address the potential contribution of astroglia to the Alzheimer's disease pathogenesis, we investigated pathological and biochemical alterations of astrocytes under this animal model. Ovadectomized rats injected with D-galactose for 2 weeks showed extensive localization of glial fibrillary acidic protein immunoreactive astrocytes and slightly elevated glutathione levels in the hippocampus without significant impairments in the water maze test and deficits of the cholinergic analyses, compared to the saline-injected rats. Ovariectomized rats injected with D-galactose for 6 weeks, however, exhibited degeneration of astrocytes and decreased glutathione levels in the hippocampus, accompanied with severe dysfunction of behavioral test and deficiency of cholinergic terminals. Electron microscopy further confirmed the pathological changes of astrocytes, especially in the aggregated area of synapse and brain microvessels. Consistent with degeneration of perivascular astrocytic endfeet, analysis of the horseradish peroxidase demonstrated an impairment of the blood-brain barrier permeability. These findings indicate that biochemical and pathological alterations of astrocytes may partially contribute to exacerbating neuronal deficits in the course of Alzheimer's disease. Restoring neuroprotective potential of astrocytes may be a useful therapeutic target for Alzheimer's disease and other neurodegenerative diseases.     

利凡诺注射用粉针的制备及安全试验研究

本文报道注射用Riv粉针的制备及其由化学品精制成药用品的安全性试验。Riv按200、400和1200mg/kg(小鼠耐受量分别相当于人用剂量的100、200和600倍)给小鼠分别以羊膜腔、腹腔及肌肉注射。结果:孕鼠耐受量相当于人用剂量100倍,羊膜腔给药母鼠无一死亡,安全试验合格;孕鼠耐受最为人用剂量200及600倍,在观察期内也出现显著毒性反应成死亡。后两种给药途径,达不到供临床使用的最低安全标准(100倍)。提示本品由化学品精制成药用品,安全性试验须摸拟临床中、晚期妊娠引产之方法—孕鼠羊膜腔给药,方能达标。此法可供有关医疗单位借鉴。     

K-ATP channel openers facilitate glutamate uptake by GluTs in rat primary cultured Astrocytes

Increasing evidence, including from our laboratory, has revealed that opening of ATP sensitive potassium channels(K-ATP channels) plays the neuronal protective roles both in vivo and in vitro. Thus K-ATP channel openers(KCOs) have been proposed as potential neuroprotectants. Our previous studies demonstrated that K-ATP channels could regulate glutamate uptake activity in PC12 cells as well as in synaptosomes of rats. Since glutamate transporters(GluTs) of astrocytes play crucial roles in glutamate uptake and KATP channels are also expressed in astrocytes, the present study showed whether and how KATP channels regulated the function of GluTs in primary cultured astrocytes. The results showed that nonselective KCO pinacidil, selective mitochondrial KCO diazoxide, novel, and blood-brain barrier permeable KCO iptakalim could enhance glutamate uptake, except for the sarcolemmal KCO P1075. Moreover pinacidil, diazoxide, and iptakalim reversed the inhibition of glutamate uptake induced by 1-methyl-4-phenylpyridinium(MPP+). These potentiated effects were completely abolished by mitochondrial K-ATP blocker 5-hydroxydecanoate. Furthermore, either diazoxide or iptakalim could inhibit MPP+-induced elevation of reactive oxygen species (ROS) and phosphorylation of protein kinases C(PKC). These findings are the first to demonstrate that activation of K-ATP channel, especially mitochondrial K-ATP channel, improves the function of GluTs in astrocytes due to reducing ROS production and downregulating PKC phosphorylation. Therefore, the present study not only reveals a novel pharmacological profile of KCOs as regulators of GluTs, but also provides a new strategy for neuroprotection.