Encephalitis ; metabolism ; pathology ; Microglia ; metabolism ; pathology ; Receptors, Leukotriene ; metabolism ; physiology

OBJECTIVETo investigate the expression of vascular cell adhesion molecule-1(VCAM-1) in lung slices from antigen -sensitized rats and the modulation by drugs.

METHODSIn isolated lung slices from ovalbumin(OVA)-sensitized rats, the relative expression of VCAM-1 was determined after drug treatment and OVA challenge.

RESULTThe expression of VCAM-1 was enhanced in the sensitized rat lungs,and OVA challenge did not further increase the expression. Glycocorticosteroid dexamethasone and leukotriene cysLT receptor antagonist ONO-1078 inhibited the expression,but tachykinin NK-1 receptor antagonist SR-140333 had no such effect.

CONCLUSIONVCAM-1 expression is enhanced in the sensitized rat lungs, and antigen challenge does not further up regulate the expression. Anti-inflammatory drugs have different effects on VCAM-1 expression. Dexamethasone and ONO-1078, but not SR-140333, can inhibit the expression.

Animals ; Chromones ; pharmacology ; Dexamethasone ; pharmacology ; Female ; In Vitro Techniques ; Lung ; chemistry ; Male ; Ovalbumin ; immunology ; Piperidines ; pharmacology ; Quinuclidines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Vascular Cell Adhesion Molecule-1 ; analysis

Animals ; Arachidonate 5-Lipoxygenase ; metabolism ; Brain Diseases ; enzymology ; metabolism ; Disease Models, Animal ; Histamine ; metabolism ; Humans ; Membrane Proteins ; metabolism ; Receptors, Histamine ; metabolism ; Receptors, Leukotriene ; metabolism

0.05).Conclusion Indexes of oxygen function may become criteria of early diagnosing NRDS,observing effect of treatment and guidance of ventilation weaning.

Biotechnology is one of the important areas of Beijing’s high-technology industry. Steadily progress had been obtained after 1995. Beijing has predominance in this area, such as research and development, talents, clinic, and so on. The development of Beijing biotechnology industry in recent years was focused, and the main challenges and relative suggestions were proposed.

OBJECTIVETo determine the effect of cysteinyl receptor agonist leukotriene D(4) (LTD(4)) and its antagonists on rat primary neurons.

METHODSIn the primarily cultured rat cortical neurons, the neuron injury was evaluated by measuring intracellular calcium, 3-(4, 5-dimethylthiazol-2yl)-2, 5-diphenyl tetrazolium bromide (MTT) reduction, and propidium iodide (PI) and Hoechst 33258 staining. The in vitro ischemic injury was induced by oxygen-glucose deprivation (OGD) for 1.5 h and reperfusion for 24 h.

RESULTLTD(4) (0.01-1 micromol/L) did not induce the elevation of intracellular calcium, neuron viability changes and neuron death. OGD-induced injury was not significantly ameliorated by the CysLT(1) receptor antagonists, pranlukast (0.2-10 micromol/L) and montelukast (0.2-10 micromol/L), as well as by the CysLT(1)/CysLT(2) receptor non-selective antagonist, BAY u9773 (0.02-1 micromol/L).

CONCLUSIONNeither agonist nor antagonists of cysteinyl receptors have the effects on the viability and ischemic-like injury in rat primary neurons.

Acetates ; pharmacology ; Animals ; Animals, Newborn ; Calcium ; metabolism ; Cell Hypoxia ; Cell Survival ; drug effects ; Cells, Cultured ; Cerebral Cortex ; cytology ; Chromones ; pharmacology ; Glucose ; pharmacology ; Leukotriene Antagonists ; pharmacology ; Leukotriene D4 ; pharmacology ; Neurons ; cytology ; drug effects ; metabolism ; Quinolines ; pharmacology ; Rats ; Receptors, Leukotriene ; agonists

OBJECTIVE: To evalute the effects of TAK-147, a novel acetylcholinesterase inhibitor on rat spatial memory deficit using the Morris water maze. METHODS: Morris water maze was used to measure spatial memory in rats, and open field test was used to analysis locomotor activity. RESULTS: Scopolamine (0.4mg/kg,IP) significantly increased the latency period in memory acquisition. Intraperitoneal TAK-147 injection ameliorated scopolamine-induced deficit in a dose-related manner. A significant effect was obtained at doses of 0.3 and 1.0 mg/kg. Both TAK-147 (0.3 and 1.0 mg/kg) and tacrine (3 and 5 mg/kg) significantly reversed scopolamine (1.5 mg/kg) increased latency in memory retrieval. However, TAK-147 had a more potent effect than tacrine. In the locomotor test, TAK-147 created no appreciable change, compared with scopolamine or saline. CONCLUSION: A novel acetycholinesterase inhibitor, TAK-147 ameliorates the scopolamine induced impaired spatial memory in rats.

OBJECTIVE: To develop a novel technique of optical recording and its validation for assessment of the neuroprotective effect of nimodipine, a L-type calcium channel blocker. METHODS: In vitro ischemia was induced by oxygen/glucose deprivation (OGD), the light transmittance (LT) of rat hippocampal slices undergoing OGD and reperfusion was quantitated using a simple apparatus relying on basic principles of light transmittance and a computerised image analysis system. RESULTS: OGD was associated with increased LT in the stratum radiatum of CA1 area and the dentate gyrus in hippocampal slices. Peak LT occurred (7.59 +/-1.42) min after OGD, followed by a marked decrease in LT (n=15 slices). Nimodipine administration (0.5 &mgr;mol/L, n=10 slices, 5 &mgr;mol/L, n=9 slices) appeared to protect the tissue from OGD damage by inhibiting elevation of LT, However, 50 &mgr;mol/L nimodipine resulted in increased LT (25.83 +/-6.32). min after administration (n=11 slices). CONCLUSION: LT signal measurement is a non-invasive, reliable method for determination of neuronal damage in ischemic rat brain slices Nimodipine is demonstrated opposite neuroprotective effects depending on its dose.

OBJECTIVE: To evaluate the feasibility of light transmission to measure focal cerebral ischemia in mice. METHODS: Persistent focal cerebral ischemia was induced by middle cerebral artey occlusion (MCAO) in mice. The brain were removed 24 h after MCAO and coronally dissected into 1 mm sections. Using a stereomicroscope, the brain section was illuminated with a halogen lamp and computerized images were stored. Next the brain sections were stained for 30 minutes with 0.5% TTC (2, 3, 5-triphenylterzolim chloride) at 37 degrees C. Using an image analyzer (AnalyPower 1.0), the infarct volumes obtained by light transmittance and TTC staining were calculated. Integrated gray scales of sections of both hemispheres were calculated by Photoshop 5.0. RESULTS: A close correlation existed between cerebral infarct volume measured by light transmission and TTC staining (r=0.81). The mean gray scales measured by both techniques of the ischemic hemispheres as well as those of the cortex, subcortex and hippocampus were siginificantly higher than those of non-ischemic hemispheres and of control mouse hemispheres (P <0.001). Further there were no significant difference between the two hemispheres of control mice and between hemispheres of control mice and non-ischemic hemispheres of the MCAO mice. CONCLUSION: Light transmission can be used for qualitative analysis of focal cerebral ischemia.