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991.
Effects of hypomagnetic field on noradrenergic activities in the brainstem of golden hamster 总被引:1,自引:0,他引:1
Previous studies found that elimination of the geomagnetic field (GMF) interferes with the normal brain functions, but the underlying mechanism remains unknown. The present study examined the effects of long-term exposures to a near-zero magnetic environment on the noradrenergic activities in the brainstem of golden hamsters. Both the content of norepinephrine (NE) and the density of NE-immunopositive neurons in the tissue decreased significantly after the treatment, and the effects could be progressive with time. These variations may substantially contribute to behavioral and mood disorders reported in other studies when animals are shielded from the GMF. 相似文献
992.
993.
大鼠脑微血管内皮细胞培养及其药物转运体Oatp2和P-gp的表达 总被引:1,自引:0,他引:1
贴块法培养脑微血管内皮细胞(BMECs),倒置显微镜动态观察细胞生长及形态,Ⅷ因子相关抗原、CD34免疫细胞化学联合鉴定细胞并确定纯度。免疫细胞化学和Western印迹法检测药物转运体有机阴离子转运多肽亚型2(Oatp2)及P-糖蛋白(P-gp)在培养内皮细胞上的表达。结果显示,获得的BMECs呈多角形或铺路石形,单层贴壁生长;培养细胞Ⅷ因子相关抗原免疫细胞化学、CD34免疫荧光染色均为阳性,细胞纯度90%;培养细胞有Oatp2及P-gp表达,且二者均主要表达于BMECs细胞膜。提示贴块法可获得原代培养BMECs,方法简便易行,细胞纯度较高。原代培养的BMECs上有药物转运体Oatp2及P-gp的表达,为血脑屏障上药物转运体的体外研究提供了可能途径。 相似文献
994.
Doh-ura K Tamura K Karube Y Naito M Tsuruo T Kataoka Y 《Cellular and molecular neurobiology》2007,27(3):303-316
1. As an extension of our previous study of quinacrine and its derivatives, chelating chemicals were screened to obtain more
effective, better brain-permeable antiprion compounds using either prion-infected neuroblastoma cells or brain capillary endothelial
cells.
2. Eleven chemicals were found to have antiprion activity. Most of them shared a common structure consisting of benzene or
naphthalene at either end of an azo bond. Structure–activity data suggest that chelating activity is not necessary but might
contribute to the antiprion action.
3. Chrysoidine, a representative compound found here, was about 27 times more effective in the antiprion activity and five
times more efficiently permeable through the brain capillary endothelial cells than quinacrine was.
4. These chemicals might be useful as compounds for development of therapeutics for prion diseases. 相似文献
995.
An Inhibitory Role of Nitric Oxide in the Dynamic Regulation of the Blood-Brain Barrier Function 总被引:1,自引:0,他引:1
Yamauchi A Dohgu S Nishioku T Shuto H Naito M Tsuruo T Sawada Y Kataoka Y 《Cellular and molecular neurobiology》2007,27(3):263-270
1. The present study aimed at elucidating the effect of nitric oxide (NO) on blood-brain barrier (BBB) function with mouse
brain capillary endothelial (MBEC4) cells.
2. Histamine (20–100 μM) evoked NO production (1.6–7 μM) in MBEC4 cells in a dose-dependent manner.
3. The permeability coefficient of sodium fluorescein for MBEC4 cells and the cellular accumulation of rhodamine 123 in MBEC4
cells were increased dose-dependently by the addition of NO solutions (14 and 28 μM) every 10 min during a 30-min period.
4. The present study demonstrated that NO increased the permeability and inhibited the P-glycoprotein efflux pump of brain
capillary endothelial cells, suggesting that NO plays an inhibitory role in the dynamic regulation of the BBB function. 相似文献
996.
997.
Diniz PH Silva JH Gomez MV Guatimosim C Gomez RS 《Cellular and molecular neurobiology》2007,27(6):757-770
Experimental data suggest that halothane anesthesia is associated with significant changes in dopamine (DA) concentration
in some brain regions but the mechanism of this effect is not well known. Rat brain cortical slices were labeled with [3H]DA to further characterize the effects of halothane on the release of this neurotransmitter from the central nervous system.
Halothane induced an increase on the release of [3H]DA that was dependent on incubation time and anesthetic concentration (0.012, 0.024, 0.048, 0.072 and 0.096 mM). This effect
was independent of extracellular or intracellular calcium. In addition, [3H]DA release evoked by halothane was not affected by TTX (blocker of voltage-dependent Na+ channels) or reserpine (a blocker of vesicular monoamine transporter). These data suggest that [3H]DA release induced by halothane is non-vesicular and would be mediated by the dopamine transporter (DAT) and norepinephrine
transporter (NET). GBR 12909 and nomifensine, inhibitors of DAT, decreased the release of [3H]DA evoked by halothane. Nisoxetine, a blocker of NET, reduced the release of [3H]DA induced by halothane. In addition, GBR 12909, nisoxetine and, halothane decrease the uptake of [3H]DA into rat brain cortical slices. A decrease on halothane-induced release of [3H]DA was also observed when the brain cortical slices were incubated at low temperature and low extracellular sodium, which
are known to interfere with the carrier-mediated release of the neurotransmitter. Ouabain, a Na+/K+ ATPase pump inhibitor, which induces DA release through reverse transport, decreased [3H]DA release induced by halothane. It is suggested that halothane increases [3H]DA release in brain cortical slices that is mediated by DAT and NET present in the plasma membrane. 相似文献
998.
González Ramírez M Orozco Suárez S Salgado Ceballos H Feria Velasco A Rocha L 《Cellular and molecular neurobiology》2007,27(2):211-227
Effects of hyperthermia-induced seizures (HS) on GABAA and benzodiazepine (BDZ) receptor binding in immature rat brain were evaluated using in vitro autoradiography. HS were induced
in 10-days-old rats by a regulated stream of moderately heated air directed 50 cm above the animals. Rats were killed 30 min,
24 h or 20 days after HS and their brains were used for in vitro autoradiography experiments to determine GABAA and BDZ receptor binding. GABAA binding was significantly enhanced in all brain areas evaluated 30 min after HS, an effect that endures 24 h and 20 days
after seizures. Concerning BDZ receptor binding, a significant increase was detected in entorhinal and perirhinal cortices
and decreased in basolateral amygdala 30 min following HS. One day after HS, animals demonstrated enhanced BDZ binding in
the cingulate, frontal, posterior parietal, entorhinal, temporal and perirhinal cortices; striatum, accumbens, substantia
nigra pars compacta and amygdala nuclei. Twenty days after HS enhanced BDZ binding was restricted in the cingulated, frontal,
anterior and posterior parietal cortices, as well as in substantia nigra pars reticulata, whereas decreased values were found
in accumbens nucleus and substantia nigra pars compacta. Our data indicate differential effects of HS in GABAA and BDZ binding in immature brain. HS-induced GABAA and BDZ changes are different from those previously described in experimental models of temporal lobe epilepsy in adult animals. 相似文献
999.
Adameová A Kuzelová M Andelová E Faberová V Pancza D Svec P Ziegelhöffer A Ravingerová T 《Molecular and cellular biochemistry》2007,295(1-2):129-136
Both, diabetes mellitus (DM) and hypercholesterolemia (HCH) are known as risk factors of ischemic heart disease, however,
the effects of experimental DM, as well as of HCH alone, on ischemia/reperfusion-induced myocardial injury are not unequivocal.
We have previously demonstrated an enhanced resistance to ischemia-induced arrhythmias in rat hearts in the acute phase of
DM. Our objectives were thus to extend our knowledge on how DM in combination with HCH, a model that is relevant to diabetic
patients with altered lipid metabolism, may affect the size of myocardial infarction and susceptibility to arrhythmias. A
combination of streptozotocin (STZ; 80 mg/kg, i.p.) and the fat–cholesterol diet (1% cholesterol, 1% coconut oil; FCHD) was
used as a double-disease model mimicking DM and HCH simultaneosly occurring in humans. Following 5 days after STZ injection
and FCHD leading to increased blood glucose and cholesterol levels, anesthetized open-chest diabetic, diabetic–hypercholesterolemic
(DM–HCH) and age-matched control rats were subjected to 6-min ischemia (occlusion of LAD coronary artery) followed by 10 reperfusion
to test susceptibility to ventricular arrhythmias in the in vivo experiments and to 30-min ischemia and subsequent 2-h reperfusion for the evaluation of the infarct size (IS) in the Langendorff-perfused
hearts. The incidence of the most life-threatening ventricular arrhythmia, ventricular fibrillation, was significantly increased
in the DM–HCH rats as compared with non-diabetic control animals (100% vs. 50%; p<0.05). Likewise, arrhythmia severity score (AS) was significantly higher in the DM–HCH rats than in the controls (4.9±0.2
vs. 3.5±0.5; p<0.05), but was not increased in the diabetic animals (AS 3.7±0.9; p>0.05 vs. controls). Diabetic hearts exhibited a reduced IS (15.1±3.0% of the area at risk vs. 37.6±2.8% in the control hearts;
p<0.05), however, a combination of DM and HCH increased the size of myocardial infarction to that observed in the controls.
In conclusion, HCH abrogates enhanced resistance to ischemia-reperfusion injury in the diabetic rat heart. 相似文献
1000.
Gnanapragasam A Yogeeta S Subhashini R Ebenezar KK Sathish V Devaki T 《Molecular and cellular biochemistry》2007,294(1-2):55-63
Generation of reactive oxygen species and mitochondrial dysfunction has been implicated in adriamycin induced cardiotoxicity.
Mitochondrial dysfunction is characterized by the accumulation of oxidized lipids, proteins and DNA, leading to disorganization
of mitochondrial structure and systolic failure. The present study was aimed to evaluate the efficacy of Centella asiatica on the mitochondrial enzymes; mitochondrial antioxidant status in adriamycin induced myocardial injury. Adriamycin (2.5 mg/kg
body wt., i.p.) induced mitochondrial damage in rats was assessed in terms of decreased activities (p< 0.05) of cardiac marker enzymes (lactate dehydrogenase, creatine phosphokinase, amino transferases), TCA cycle enzymes (isocitrate
dehydrogenase, α-ketoglutarate dehydrogenase, malate dehydrogenase, respiratory marker enzymes (NADH-dehydrogenase, cytochrome-C-oxidase),
mitochondrial antioxidant enzymes (GPx, GSH, SOD,CAT) and increased (p< 0.05) level of lipid peroxidation. Mitochondrial damage was confirmed by transmission electron microscopic examination.
Pre-co-treatment with aqueous extract of Centella asiatica (200 mg/kg body wt, oral) effectively counteracted the alterations in mitochondrial enzymes and mitochondrial defense system.
In addition, transmission electron microscopy study confirms the restoration of cellular normalcy and accredits the cytoprotective
role of Centella asiatica against adriamycin induced myocardial injury. Our results demonstrated elevated oxidative stress and mitochondrial dysfunction
in adriamycin treated rats. Moreover, on the basis of our findings it may be concluded that the aqueous extract of C. asiatica not only possesses antioxidant properties but it may also reduce the extent of mitochondrial damage 相似文献