ABSTRACT
AIM: To investigate the protective effects of the total paeony glycoside(TPG) on the focal cerebral ischemia and regional cerebral blood flow(rCBF) in rats. METHOD: The rat model of focal cerebral ischemia was made by middle cerebral artery occlusion(MCAO) with nylon suture.TPG was injected into every group rats once a day before 48 h,and injected before MCAO 30 min and after 4 h,12 h.After 24 h the effects of the drug were studied about neurological deficit,the water content of brain tissue,the cerebral infarcted zone,under microscopic examination,as well as rCBF on each rat with laser Doppler fiowmeter(LDF). RESULTS: The sympton of brain ischemia was obvious in model rats by contrast to the sham rats,and the model rats rCBF decreased markedly after MCAO.50 mg/kg and 100 mg/kg TPG injection could obviously promote neurological deficit,decrease the water content of brain tissue and the cerebral infarcted zone.And the pathological slices also proved its protective effect on neuron.The laser Doppler flowmeter detected result indicated that 100 mg/kg TPG inject could greatly increase MCAO rats rCBF. CONCLUSIONS: TPG injection has a marked prospective activity on rat focal brain ischemia in rats,and the increase of rCBF may be one of the protection mechanism.
ABSTRACT
Aim To investigate the effects of Breviscapine(BE)on intracellular Ca2+ concentration in human umbilical vein endothelial cells(HUVECs). Methods HUVECs were incubated with the calcium ion-sensitive fluorescent indicator fluo-3/AM, and then a laser confocal microscope was applied to measure changes of fluorescence intensity under different agonists to investigate the effects of Breviscapine on intracellular Ca2+ concentration in HUVECs. Results ①BE induced Ca2+ transients in the buffer with or without Ca2+;②The Ca2+ transients induced by BE could be overlapped by cyclopiazonic acid (CPA);③Pretreatment of BE inhibited Ca2+ influx caused by KCl.④ BE had no evident effect on the calcium influx in- duced by the restoration of extracellular Ca2+ after the depletion of intracellular Ca2+ stores.Conclusion BE depletes CPA-sensitive intracellular Ca2+ stores and inhibits Ca2+ influx through voltage-dependent Ca2+ channels, and BE has no evident effect on the calcium influx induced by the restoration of extracellular Ca2+ after the depletion of intracellular Ca2+ stores.