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

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

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.

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

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

BACKGROUNDEdaravone had been validated to effectively protect against ischemic injuries. In this study, we investigated the protective effect of edaravone by observing the effects on anti-apoptosis, regulation of Bcl-2/Bax protein expression and recovering from damage to mitochondria after OGD (oxygen-glucose deprivation)-reperfusion.

METHODSViability of PC12 cells which were injured at different time of OGD injury, was quantified by measuring MTT (2-(4,5-dimethylthia-zol-2-yl)-2,5-diphenyltetrazolium bromide) staining. In addition, PC12 cells' viability was also quantified after their preincubation in different concentration of edaravone for 30 min followed by (OGD). Furthermore, apoptotic population of PC12 cells that reinsulted from OGD-reperfusion with or without preincubation with edaravone was determined by flow cytometer analysis, electron microscope and Hoechst/PI staining. Finally, change of Bcl-2/Bax protein expression was detected by Western blot.

RESULTS(1) The viability of PC12 cells decreased with time (1 - 12 h) after OGD. We regarded the model of OGD 2 h, then replacing DMEM (Dulbecco's Modified Eagle's Medium) for another 24 h as an OGD-reperfusion in this research. Furthermore, most PC12 cells were in the state of apoptosis after OGD-reperfusion. (2) The viability of PC12 cells preincubated with edaravone at high concentrations (1, 0.1, 0.01 micromol/L) increased significantly with edaravone protecting PC12 cells from apoptosis after OGD-reperfusion injury. (3) Furthermore, edaravone attenuates the damage of OGD-reperfusion on mitochondria and regulated Bcl-2/Bax protein imbalance expression after OGD-reperfusion.

CONCLUSIONNeuroprotective effects of edaravone on ischemic or other brain injuries may be partly mediated through inhibition of Bcl-2/Bax apoptotic pathways by recovering from the damage of mitochondria.

Animals ; Antipyrine ; analogs & derivatives ; pharmacology ; Apoptosis ; drug effects ; Flow Cytometry ; Ischemia ; prevention & control ; Microscopy, Electron ; Mitochondria ; drug effects ; Neuroprotective Agents ; pharmacology ; PC12 Cells ; Proto-Oncogene Proteins c-bcl-2 ; analysis ; Rats ; bcl-2-Associated X Protein ; analysis

OBJECTIVETo evaluate the inhibitive effect of C-21 steroidal glycosides from the root of Cynanchum auriculatum (CGB) on rat glioma C6 cells.

METHODSC6 cells were treated with CGB for 24, 48,72 h at concentration of 30, 60, 120 mg/L, respectively. MTT assay was used for evaluating cell viability; fluorescence-activated cell sorting analysis after Annexin V/propidium iodide staining or single propidium iodide staining was used to test cell apoptosis and cell cycle.

RESULTSCGB at 30, 60, 120 mg/L concentration-dependently decreased C6 cell viability (P<0.001). CGB at 60 and 120 mg/L induced C6 cell apoptosis and cell cycle arrest. The fraction of G0/G1 cells was increased (P<0.05) and that of S phase cells was decreased (P<0.01).

CONCLUSIONCGB can inhibit the growth of rat glioma C6 cells, and induce apoptosis and G0/G1 cell cycle arrest.

Animals ; Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cynanchum ; chemistry ; Glioma ; pathology ; Monosaccharides ; pharmacology ; Rats ; Steroids ; pharmacology

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.