Tissue or organic injuries(especially induced by ischemia/reperfusion) are often followed by inflammatory response characterized with neutrophil infiltration.Neutrophils exacerbate tissue or organic injuries by releasing elastase.Since brain injuries induced by cerebral ischemia/reperfusion,intracerebral hemorrhage,cerebral trauma also accompany infiltration of neutrophil,and elastase derived from neutrophil probably plays an important role in brain injury.

Aim To study the effects of sodium magnesium fructose diphosphate (SMFD) on free calcium concentration and nitric oxide synthase activity of ischemic synaptosome, so as to explore the protective mechanisms of SMFD on cerebral ischemia. Methods The synaptosomes from normal rat brain were prepared by phase partition and cultured with oxygen-glucose deprivation to establish ischemic synaptosome model. The intrasynaptosomal free calcium concentration and nitric oxide synthase activity were detected separtately after the synaptosomes were co-incubated with SMFD (1.3 mmol*L-1) or fructose-1,6-diphosphate (FDP, 4.0 mmol*L-1) for 60 min. Results SMFD decreased the free calcium concentration and reduced the activity of nitric oxide synthase (NOS) of ischemic synaptosomes. Its effects were more powerful than those of FDP. Conclusion SMFD may protect neurons from ischemic injury by preventing intracellular Ca2+ overload and inhibiting the activity of nitric oxide synthase.

OBJECTIVE:To study the protective effects of sodium magnesium fructose diphosphate(FDPM)on brain damage induced by ischemiareperfusion in rats.METHODS:Rats were subjected to cerebral ischemia-reperfusion induced by inserting a nylon thread into internal carotid artery to block the origin of middle cerebral artery and removing the thread for recirculation.After1h ischemia,FDPM(400mg/kg),fructose-1,6-diphosphate(FDP,400mg/kg)or magnesium sulfate(MgSO 4 ,30mg/kg)was administrated10min after the onset of ischemia.Neurological scale was scored after1h ischemia and after2h,5h and23h recirculation,and infarction area,MDA content and histopathological change of brain tissue were studied after1h ischemia and after23h recirculation.RESULTS:Compared with model group,400mg/kg FDPM decreased neurological scale,diminished infarction area,reduced MDA content and relieved pathomorphological changes of brain tissue subjected to ischemia-reperfusion in rats.These effects were more powerful than those of FDP(400mg/kg)or MgSO 4 (30mg/kg).CONCL_ USION:FDPM(400mg/kg)could markedly prevent rats from brain damage after cerebral ischemia-reperfusion,and its effects were more potent than those of FDP(400mg/kg)or MgSO 4 (30mg/kg).

AIM: To study the analgesic effect and toxicity of Weifu qitong Capsule (Rhizoma Corydalis, cortex Magnoliae Officinalis, Radix Aucklandiae, etc.) to provide experimental data for its clinical application. METHODS: The analgesic effect of Weifu qitong Capsule was assessed by hot-plate test and writhing test, its acute and subacute toxicity studies were also conducted. RESULTS: Taking high dose of Weifu qitong Capsule, after 4.5 h (6.249 g/kg) WFQC could increase pain threshold in hot-plate test. Taking low, middle or high dose of WFQC after 2 h, WFQC could significantly extend writhing latent period and decrease writhing frequency (P