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Er-Qing Wei

Publications and source records attributed to Er-Qing Wei.

12 recordsLinked to original sources
PubMed2003

Effects of endogenous histamine on seizure development of pentylenetetrazole-induced kindling in rats.

This study was performed to investigate whether or not endogenous histamine can protect seizure development of pentylenetetrazole (PTZ)-induced kindling in rats. An intracerebroventricular (i.c.v.) injection with clobenpropit (5 and 10 microg), a representative H(3)-antagonist, significantly prolonged the onset of kindling and inhibited the seizure stages in a dose-dependent manner. Its action was significantly reversed by both immepip (2 microg, i.c.v.), an H(3)-agonist, and alpha-fluoromethylhistidine (alpha-FMH, 10 microg, i.c.v.), a selective histidine decarboxylase inhibitor. alpha-FMH (20 microg, i.c.v.) and pyrilamine (1 and 5 mg/kg i.p.), a classical H(1)-antagonist, markedly augmented the severity of seizure development of PTZ-induced kindling. Therefore, these results indicate that brain endogenous histamine plays a certain protective role on seizure development of PTZ-induced kindling in rats, and that its protective roles are mediated by H(1)-receptors.

Animals↗
PubMed2002

[Novel quantitative method for evaluating oxygen/glucose deprivation-induced injury of hippocampal slices]

OBJECTIVE: To establish a simple, sensitive in vitro method to evaluate oxygen/glucose deprivation (OGD)-induced injury of brain hippocampal slices in rats. METHODS: Rat hippocampal slices were incubated in 2% 2, 3, 5-triphenyltetrazolium chloride (TTC) solution after oxygen/glucose deprivation. They were then soaked in a measured volume of ethanol and dimethylsulfoxide (50:50) to extract the TTC formazan Product which was then measured by spectrophotometry. OGD induced LDH release was simultaneously measured. RESULTS: Progressive prolongation of OGD induced hippocampal injury resulted in decreased formazan coloration as determined by spectrophotometry. There was a parallel increase in LDH release, thus a negative correlation in these two products was noted. (r=-0.933,P <0.01). The injury was attenuated in the brain slices pre-treated with nimodipine, dexamethasone, and ketamine, but not ONO-1078. CONCLUSION: Solvent extraction and spectrophotometric quantification of formazan represents an objective measurement of OGD-induced injury of rat hippocampal slices.

Journal Article↗
PubMed2002

[Light transmission measurement of focal ischemic cerebral infarction in mice]

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.

Journal Article↗
PubMed2002

[Optical recording method for evaluation of neuronal damage in rat hippocampal slices during ischemia and reperfusion]

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.

Journal Article↗
PubMed2002

[Effects of TAK-147, a novel acetylcholinesterase inhibitor, on spatial memory deficit as evaluated by Morris water maze of rats]

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.

Journal Article↗
PubMed2002

VCAM-1 expression, eosinophil infiltration, and pharmacological modulation in rat allergic airway inflammation.

AIM: To determine vascular cell adhesion molecule-1 (VCAM-1) expression and eosinophil infiltration in the lungs of the rats with allergic airway inflammation, and their possible modulation by dexamethasone and neurokinin-1 receptor antagonist SR140333. METHODS: Sensitized rats were challenged with inhalation of 1 % ovalbumin aerosol. Protein expression of VCAM-1 in the lungs and eosinophil infiltration around bronchi in different groups were determined 24 h after challenge. SR140333 (0.01 and 0.10 mg/kg) and dexamethasone (0.50 mg/kg) were injected ip, twice a day, for 3 d before challenge. RESULTS: The expression of VCAM-1 was increased in the sensitized rat lungs as compared with the non-sensitized rats (P<0.05). The increment was inhibited by pretreatment with dexamethasone (P<0.05), but not with SR140333 (P>0.05). On the other hand, antigen challenge in sensitized rats evoked eosinophil infiltration (P<0.05) but no further increase in VCAM-1 expression (P>0.05). Furthermore, SR140333 inhibited eosinophil infiltration (P<0.05) but had no effect on VCAM-1 expression (P>0.05), whereas dexamethasone inhibited both responses (P<0.05). CONCLUSION: The expression of VCAM-1 increases during antigen sensitization in rat lungs, and dexamethasone and SR140333 may inhibit allergic airway inflammation in different mechanisms.

Animals↗
PubMed2002

Reversal of scopolamine-induced spatial memory deficits in rats by TAK-147.

AIM: To evaluate effect of TAK-147 on spatial memory deficit induced by scopolamine. METHODS: Morris water maze was used to measure spatial memory in rats and open field test was used to analyse locomotor activity. RESULTS: In the acquisition memory process, scopolamine (0.4 mg/kg, ip) markedly increased the escape latency to the platform. Ip injection of both TAK-147 and donepezil ameliorated scopolamine-induced deficit, dose-related and significant effect was obtained at doses of 0.1-1.0 mg/kg. In the memory retrieval process, increased latency induced by scopolamine (1.5 mg/kg, ip) was also significantly reversed by treatment with TAK-147 (0.1, 0.3, and 1.0 mg/kg), donepezil (0.3 and 1.0 mg/kg), and tacrine (3 and 5 mg/kg), respectively. TAK-147 has a little potent efficacy to donepezil, and was more potent than tacrine. In the locomotor test, both TAK-147 and donepizil created no appreciable change of locomotor activities, compared with scopolamine or saline. CONCLUSION: TAK-147 plays an important role in spatial cognition, and this result provides additional evidence that TAK-147 is an ideal AChE inhibitor and is useful for the treatment of Alzheimer's disease.

Animals↗
PubMed2002

Effects of histidine, a precursor of histamine, on pentylenetetrazole-induced seizures in rats.

AIM: The effect of histidine on pentylenetetrazole-induced seizures was investigated in rats. METHODS: Chemical kindling was elicited by repeated ip injection a subconvulsant dose of pentylenetetrazole (35 mg/kg) once every 48 h until the occurrence of seizure stages 4-5, and seizure activity of kindling was recorded for 30 min. RESULTS: In the kindling development process, ip injection of histidine (200, 500 mg/kg), a precursor of histamine, prolonged latency for the onset of myoclonic jerks and the clonic generalized seizure, and inhibited seizure stage in a dose-dependent manner. In the kindling challenge process, histidine (500, 1000 mg/kg) and H3 antagonist thioperamide (10, 20 microg) al so showed a significant anticonvulsant effect. The inhibitory action of histidine was enhanced significantly by thioperamide (5 microg), however, was antagonized by both alpha fluoromethylhistidine (20 microg), a selective histidine decarboxylase inhibitor and H1 ant agonist pyrilamine (2, 5 mg/kg), dose-dependently and significantly. In addition, H2 antagonist zolantidine appeared no appreciable effect, even at a dose of 10 mg/kg. CONCLUSION: These results indicated that brain endogenous histamine may play certain important role in protect against generalized clonic seizures, its action may via presynaptic H3-receptors and postsynaptic H1-receptors.

Animals↗
PubMed2002

[Trends in the post-genomic pharmacological research].

With the advent of post-genome era, pharmacogenomics will be a new field in pharmacological sciences. In parallel, high-throughput screening, in silico research, as well as lots of visualization techniques are emerging as novel approaches in pharmacological researches. Some progress in the implementation of aforementioned new idea and methods in pharmacodynamics and pharmacokinetics research are also introduced in this review.

Genome, Human↗
PubMed2002

Neuroprotective effect of ONO-1078, a leukotriene receptor antagonist, on focal cerebral ischemia in rats.

AIM: To determine whether ONO-1078 (pranlukast), a potent leukotriene receptor antagonist, has neuroprotective effect on focal cerebral ischemia in the rat. METHODS: Focal cerebral ischemia was induced by 30 min of middle cerebral artery (MCA) occlusion and followed by 24 h reperfusion. ONO-1078 (0.003-1.0 mg/kg) or vehicle (saline 1 mL/kg) was ip injected 30 min before MCA occlusion and 2 h after reperfusion. The neurological score, infarct volume, neuron density (in cortex, hippocampus, and striatum), brain edema, and albumin exudation around the vessels were determined 24 h after reperfusion. RESULTS: ONO-1078 slightly improved the neurological deficiency, and dramatically decreased infarct volume and neuron loss which showed a bell shaped dose response effect with highest effect at doses of 0.01-0.3 mg/kg. Enlargement of the ischemic hemisphere and albumin exudation were inhibited at doses of 0.01-1.0 mg/kg. CONCLUSION: ONO-1078 has the protective effect on focal cerebral ischemia in rats, which is partially attributed to the inhibition of brain edema. This may represent a novel approach to the treatment of acute cerebral ischemia with cysteinyl leukotriene receptor antagonists.

Animals↗
PubMedDate not supplied

Green tea catechins evoke a phasic contraction in rat aorta via H2O2-mediated multiple-signalling pathways.

1. The contractile effects of tea polyphenols (TP) and its four principle catechins, namely (-)-epicatechin (EC), (-)-epicatechin-3-gallate (ECG), (-)-epigallocatechin (EGC) and (-)-epigallocatechin-3-gallate (EGCG), on rat aorta contractility were investigated using the isometric tension recording technique. 2. At concentrations of 5-100 mg/L, TP evoked phasic contraction of rat aorta in a concentration-dependent but endothelium-independent manner. Of the four catechins tested, EGCG and EGC (3-300 micromol/L), but not EC and ECG, mimicked the contractile response to TP, suggesting that the epigallol moiety in the B ring may be associated with the contractile effect. 3. Contractions in response to EGCG and EGC were not affected by several endogenous vasoconstrictor receptor antagonists, but could be abolished by 10 micro mol/L BAPTA-AM, a membrane-permeable Ca2+ chelator, or attenuated by removal of extracellular Ca2+, suggesting the involvement of both intracellular and extracellular Ca2+ in evoking the contraction. 4. Pretreatment with non-selective Ca2+ channel antagonists mefenamic acid (10 micro mol/L), tetrandrine (30 micro mol/L) and SKF 96365 (30 micromol/L), but not nifedipine (1 micromol/L), the selective inhibitor of voltage-dependent Ca2+ channels, inhibited the contractile responses to EGC and EGCG, indicating the involvement of Ca2+ influx via non-voltage dependent Ca2+ channels. 5. Several intracellular Ca2+ channel modulators, including procaine (5 mmol/L), dantrolene (30 micromol/L) and 2-amino ethoxydiphenyl borate (50 micromol/L; an inositol 1,4,5-trisphosphate receptor inhibitor), also inhibited EGCG- and EGC-induced contractions, thus suggesting a role of intracellular Ca2+ release in these contractions. 6. Both EGCG- and EGC-induced contractions were depressed, to different degrees, by inhibitors of several receptor-coupled enzymes, including phospholipase C, protein kinase C, phospholipase A2 and tyrosine kinase. Furthermore, both EGCG- and EGC-induced contractions were completely abolished by catalase, but not by superoxide dismutase or mannitol/dimethyl sulphoxide. 7. Taken together, these data show, for the first time, that TP and its related catechins that contain an epigallol structure in the B ring, as in EGCG and EGC, exert direct contractile effects on rat aortic smooth muscle via a H2O2-mediated pathway.

Animals↗