Objective To boserve the effects of sophoridine on central nervous system in mice. Methods Behavioral methodology was employed to observe the effect of sophoridine on the normal mouse autonomic activities, and sleeping latency and sleep-lasting time of mice under threshold dosage of pentobarbital sodium. And to observe the synergistic effects of inducing convulsion between sophoridine and pentylenetetrazol, nicotin, strychine, isoniazid, and picrotoxin by subthreshold dosage. Results Sophoridine ip administrated (10 and 20 mg/kg) made the autonomic activities of mice suppressed by the rate of 66.9% and 76.6%, the sleeping latency of mice given pentobarbital sodium (40 mg/kg) prolonged, and sleeping time shortened (P

Aim Tostudytheanalgesiceffectofoxyso-phoridine (OSR)on GABA transporter-1 (GAT-1 )mR-NA expression and its influence on GAT-1 expression inmice.Methods Formalintestwasusedtodetectthe analgesic effect of OSR(iv).Immunohistochemis-try was taken to inspect the expression of GAT-1 in cerebral cortex and thalamus in mouse brain. The quantitative real-time PCR method was used to inspect the influence of OSR on GAT-1 mRNA expression of braininmice.Results OSR(500,250,125mg· kg-1 ,iv ) could significantly increase the foot-licking latency.OSR(500 mg·kg-1,ip)could significantly decrease the number of GAT-1 immuopositive cells incerebral cortex and thalamus in mouse brain,and re-duce GAT-1 mRNA expression in brain(P<0. 01,P<0.05)intheformalintest.Conclusion OSRhasa significant analgesic effect,and its analgesic mecha-nism is related to the GAT-1 expression in mouse brain.

Objective Complex of oxymatrine(OMT)-carbenoxolone sodium(CS)was prepared,and the acute toxicity of the OMT-CS complex and their protective effects on injured liver induced by carbon tetrachloride(CCl_4)were also studied.Methods The OMT-CS complex was formed after preparing OMT and CS solutions individually then mixing them in ratio,the constant was detemined by UV-vis,the complex was characterized by powder X-ray diffraction,IR,and NMR.The sequence method was employed to test LD_50 of the complex by iv injection.The aspartate transaminase(AST)and alanine aminotransferase(ALT)in serum were measured in acute hepatic injuried models by CCl_4 proportionally im injected the complex in mice.Results The ratio of OMT and CS in the complex appeared to be 1∶1.The results of powder X-ray diffraction measurement indicated that a novel crystalline structure of complex was formed.The acute toxicities of LD_50 of the complexes in 1∶1,and 2∶1 were lower than that of both OMT and CS only.Compared with the model group by CCl_4,AST and ALT levels in serum were lower than that in the complex at 1∶1 and 2∶1 ratios.Conclusion The toxicity of the complex in different proportions on acute hepatic injuried mice by CCl_4 decreases obviously,compared with their precursor drugs.

.This study is to investigate the analgesic effect produced by intrathecal injection (ith) of oxysophoridine (OSR) and the mechanism of GABAA receptor. Warm water tail-flick test was used to detect the analgesic effect of OSR (12.5, 6.25, and 3.13 mg.kg-1 ith) and to observe the influence of GABA (gamma aminobutyric acid) agonist or antagonist on the analgesic effect of OSR in mice. Immunohistochemistry method were used to detect the influence of OSR (12.5 mg.kg-1, ith) on the GABAARalpha1 protein expression in spinal cord. The results obtained covers that OSR (12.5 and 6.25 mg.kg-, ith) alleviates pain significantly with the warm water tail-flick test (P<0.05, P<0.01), the rate of pain threshold increases by 68.45%; GABA and muscimol (MUS) produces analgesic synergism together with the OSR, picrotoxin (PTX) and bicuculline (BIC) antagonize the analgesic effect of OSR; OSR (12.5 mg.kg-1, ith) significantly increase the positive number of GABAARalpha1 nerve cell in spinal cord (P<0.01) and significantly decrease the average grey levels (P<0.01). In conclusion, OSR intrathecal injection has significant analgesic effect. And GABAA receptor in spinal cord is involved in the analgesic mechanism.

Objective To investigate the effects of valproic acid (VPA) on acute lung injury induced by Lipopolysaccharide in rats. Method The rat model of acute lung injury was made by intravenous injection of lipopolysaccharide (LPS). The pathological changes of lung were observed under light microscope and inflammatory cytokines in serum detected by using ELISA to judge whether the model was successfully done or not. All rats were divided into three groups as per the different intervention agents employed. Rats in control group were treated with intravenous injection of NS in dose of 5 ml/kg, rats in LPS group were exposed to LPS with dosage of 10 mg/kg and model rats in LPS + VPA group were treated with VPA in dose of 300 mg/kg. The rats were sacrificed 6 h after LPS or NS administration. The blood PaO2 ,A-aDO2 and blood lactic acid (Lac) were measured, the lungs were removed for observing the histopathological changes and determination of wet/dry lung weight (W/D) ratio and myeloperoxidase (MPO) activity as well as albumin concentration in broncho-alveolar lavage fluid (BALF) . Seurm was collected to determine the concentrations of tumor necrosis factor-a (TNF-α) and interleukin-1β( IL-1 β) by using LISA 6 h later. All data were presented in ((x)±s). One-way ANOVA was used for comparing differences between groups. Results Compared with acute lung injury group, the blood PaO2 (94. 50 ± 4.38 ) in rats of LPS + VPA group was higher, whereas A-aDO2 ( 13.50 ± 4.77 ) and blood lac( 2.13 ± 1. 02 ) in LPS + VPA group were lower. VPA significantly lowered W/D (5.33 ±0. 12) ratio and MPO activity (4.38 ±0. 42) in the lung. Albumin concentration ( 1. 260 ± 0. 039 ) in BALF, and the levels of TN F-α( 2 410 ±320 )and IL-1β( 1 220 ± 162 )in serum were lower in LPS + VPA group. The histological changes of lung injury were lessened by VPA. Conclusions Valproic acid has protective effects against lipopolysaccharide-induced acute lung injury in rats.

Objective To study the effects of two types of crystalloids on postoperative inflam-matory reaction during the process of cesarean section.Methods Sixty patients undergoing cesarean section were randomly divided into Ringer lactate solution group (RL)and Ringer acetate solution group (RA)with 30 cases in each group.Before anesthesia,10 ml/kg crystal solution was infused, the infusion rate was 1 5-20 ml·kg-1 ·h-1 .The patients were performed epidural anesthesia in left lateral position.Crystal solution was infused to maintain the blood pressure during the operation.Ve-nous blood was drawn at the beginning of the operation (T1 ),the end of the operation (T2 ),four hours after operation (T3 ),twenty-four hours after operation (T4 )in order to measure the blood plasma value of IL-6,TNF-α,CRP.Results The blood plasma value of IL-6,TNF-α,CRP had no significant differences at T1 ,T4 ;but the value of group RA was significantly higher than that of group RL (P <0.05)at T2 ,T3 .Conclusion Ringer acetate solution causes more significant postop-erative inflammatory cytokine release than Ringer lactate solution does during the process of cesarean section.

Aim To investigate the protective effect of lipoxin A4(LXA4)on ischemic brain injury in a rat model of permanent focal cerebral ischemia.Methods Adult male Sprague-Dawley rats weighing 200～250 g were used and rats were randomly divided into four groups:sham group,ischemia alone group,LXA4 10 ng group and LXA4 100 ng group.Permanent focal cerebral ischemia was induced by improved thread occlusion of right middle cerebral artery.Approximately 10 mm of nylon surgical thread was inserted into the right internal carotid artery in the rats of sham group.After the middle cerebral artery occlusion,the same volume of LXA4(5 ?l)or isotonic Na chloride(5 ?l)was injected respectively into the right lateral ventricle of the rat in 10 minutes.After 24 h of ischemia,the neurological deficit and the infarct volume were assessed by the method of Longa's score and 2,3,5-triphenyltetrazolium chloride(TTC)staining;the levels of malondialdehyde(MDA)and actvities of myeloperoxidase(MPO)in the ischemia cortex were measured by spectrophotometer;the contents of tumor necrosis factor-?(TNF-?)and interleukin-1?(IL-1?)were assayed by ELISA method.The histopathological change was observed after HE staining.Results Treatment with LXA4 10 ng or 100 ng significantly improved functional recovery,reduced relative infarction volume,inhibited MPO activity,decreased MDA,TNF-? and IL-1? levels,and improved histopathological injury.Moreover,the effects of neurological recovery and decreasing TNF-? level in LXA4 100 ng group were better than those in 10 ng group.Conclusion Treatment with LXA4 protects against permanent focal cerebral ischemia injury in rats.

Aim To study the analgesic action of oxysophoridine and its effect on the expression of protein kinase C?(PKC?) in dorsal horn of spinal cord(it should be expressed as in dorsal horn of the spinal),cerebral cortex and thalamus of the mice.Methods Hot plate test was used to observe and analyze the analgesic strength and action position of OSR through iv and icv approaches,immunohistochemistry(SABC) was taken to inspect the expression of PKC? in dorsal horn of spinal cord(it should be expressed as in dorsal horn of the spinal),cerebral cortex and thalamus of the mice after administrating OSR.Results The foot-licking latencies of mice were prolonged both iv OSR(500、250、125 mg?kg-1)and icv OSR(100,50,25 mg?kg-1)in the hot plate test(P

Aim To observe the effect of oxysophori-dine( OSR) on the EEG changes and its power spectrums of cerebral frontal cortex in anaesthetized rats. Methods With the equipment of brain stereotactic apparatus,electrode was implanted into frontal lobe of cerebral cortex in rats. Unipolar lead and computerized FFT technique were employed to record the index of EEG,power spectrum and frequency distributions to analyze the effect of OSR on the bioelectricity altera-tions of frontal lobe in cerebral cortexi in rats. Results Administrated( icv) with OSR at the dose of 2. 5,5, 10 mg/rat in rats,the EEG of frontal lobe of cerebral cortex was mainly featured by low amplitude and slow waves accompanied by spindle-formed sleeping waves with a significant decrease of total power of EEG( P