基于BPL算法的AC-(LCC)DC系统全电磁暂态快速仿真方法

对AC-(LCC)DC混联电网的全电磁暂态仿真计算,数值积分过程中将面临频繁的间断现象。现有的电磁暂态仿真计算主要是采用隐式梯形积分方法,但隐式类积分方法在面临间断问题时计算效率很低。为解决此问题,该文将Borel-Padé-Laplace(BPL)算法引入AC-(LCC)DC系统的全电磁暂态数值仿真计算,提出一类新的全电磁暂态计算方法。与传统的数值积分类方法不同,BPL算法是将Borel-Laplace变换与经典的Padé逼近相结合的一类新的渐近数值方法。采用含2条LCC-HVDC输电线路的3机9节点AC/DC系统作为算例系统,以PSCAD/EMTDC的仿真结果为基准,对提出的新方法进行测试。算例测试结果表明:基于BPL算法的全电磁暂态计算方法可以避免传统隐式类积分方法所面临的问题,在计算效率上具有明显的优势。

Tongqiao Huoxue Decoction combined with butylphthalide in the treatment of acute ischemic stroke and its effect on VEGF

Objective:To study the effect of Tongqiao Huoxue Decoction combined with butylphthalide soft capsules on acute ischemic stroke and its effect on serum vascular endothelial growth factor(VEGF).Methods:There are 76 patients with acute ischemic stroke(Acute Ischemic Stroke,AIS),including 38 cases in the control group and the observation group.All patients were treated with conventional treatment methods for this disease.On this basis,the control group was given butylphthalide soft capsules orally,0.2g/time,3 times a day,and the observation group was given Tongqiaohuoxue Decoction on the basis of oral butylphthalide soft capsules.One dose a day,two times in the morning and evening.All patients were treated for 20 days as a course of treatment.The clinical efficacy of the two groups of patients were compared,the collateral circulation rate before and after treatment,NIHSS,MoCA and MMSE,hemorheology(plasma viscosity,fibrinogen,whole blood high and low shear viscosity),VEGF levels and the occurrence of adverse reactions.Results:The effective rate of the two groups was 92.1%in the observation group and 73.7%in the control group,which was significantly different(P<0.05).The collateral circulation patency rate was 86.8%in the observation group and 57.9%in the control group,which was significantly different(P<0.05).After treatment,the MoCA,MMSE scores and VEGF levels of the observation group were significantly higher than those before the treatment and the control group,with significant differences(P<0.05).The NIHSS score and hemorheology were improved compared with those before the treatment and the control group.There are significant differences(P<0.05).Conclusion:Tongqiao Huoxue Decoction combined with butylphthalide soft capsules can significantly improve collateral circulation,hemorheology,neurological and cognitive functions in patients with acute ischemic stroke.The mechanism may be related to the increase of VEGF levels and the promotion of neovascularization.

Effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction

Objective: To study the effect of Butylphthalide combined with Urinary Kallidinogenase on the pathological course of nerve damage in patients with massive cerebral infarction. Methods:The patients with massive cerebral infarction who received treatment in our hospital between January 2016 and December 2017 were selected and randomly divided into the group A receiving Butylphthalide treatment, the group B receiving Urinary Kallidinogenase treatment and the group C receiving Butylphthalide combined with Urinary Kallidinogenase treatment on the basis of conventional treatment. 14 d after treatment, serum levels of nerve markers, coagulation indexes, growth factors and oxidative stress indexes were determined. Results:After treatment, visinin-like protein-1 (VILIP-1), neuron-specific enolase (NSE), S100B protein (S100B), thromboxane A2 (TXA2), lysophosphatidic acid (LPA), D-dimer (D-D), 8-isoprostanes F2α (8-iso-PGF2α) and malondialdehyde (MDA) levels of 3 groups significantly decreased whereas nitric oxide (NO), nitric oxide synthase (NOS), vascular endothelial growth factor (VEGF), brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I), superoxide dismutase (SOD) and total antioxidant capacity (T-AOC) levels significantly increased, and VILIP-1, NSE, S100B, TXA2, LPA, D-D, 8-iso-PGF2α and MDA levels of the group C after treatment were significantly lower than those of the group A and group B whereas NO, NOS, VEGF, BDNF, IGF-I, SOD and T-AOC levels were significantly higher than those of the group A and group B. Conclusion: Butylphthalide combined with Urinary Kallidinogenase is better than monotherapy in improving the pathological course of nerve damage in patients with massive cerebral infarction.

Chinese herbal extract dl-3n-butylphthalide A commonly used drug for the treatment of ischemic stroke as a novel therapeutic approach to treat neurodegenerative diseases

DI-3n-butylphthalide is the active component isolated from the seeds of Apium graveolens Linn. A number of pharmacological and clinical studies have proven that dl-3n-butylphthalide is highly potent and multi-targeted with low toxicity and has a long time-window for the treatment of ischemic cerebrovascular disease. The mechanisms underlying dl-3n-butylphthalide include improving mitochondrial function and microcirculation, inhibiting apoptosis and reducing oxidative stress. Furthermore, dl-3n-butylphthalide may also be promising for the treatment of neurodegenerative diseases, such as Alzheimer＇s disease, vascular dementia and Parkinson＇s disease.

Hypoxia inducible factor-1alpha mediates protection of DL-3-n-butylphthalide in brain microvascular endothelial cells against oxygen glucose deprivation-induced injury

Studies have demonstrated that DL-3-n-butylphthalide can significantly alleviate oxygen glucose deprivation-induced injury of human umbilical vein endothelial cells at least partly associated with its enhancement on oxygen glucose deprivation-induced hypoxia inducible factor-1α expression.In this study,we hypothesized that DL-3-n-butylphthalide can protect against oxygen glucose deprivation-induced injury of newborn rat brain microvascular endothelial cells by means of upregulating hypoxia inducible factor-1α expression.MTT assay and Hoechst staining results showed that DL-3-n-butylphthalide protected brain microvascular endothelial cells against oxygen glucose deprivation-induced injury in a dose-dependent manner.Western blot and immunofluorescent staining results further confirmed that the protective effect was related to upregulation of hypoxia inducible factor-1α.Real-time RT-PCR reaction results showed that DL-3-n-butylphthalide reduced apoptosis by inhibiting downregulation of pro-apoptotic gene caspase-3 mRNA expression and upregulation of apoptosis-executive protease bcl-2 mRNA expression;however,DL-3-n-butylphthalide had no protective effects on brain microvascular endothelial cells after knockdown of hypoxia inducible factor-1α by small interfering RNA.These findings suggest that DL-3-n-butylphthalide can protect brain microvascular endothelial cells against oxygen glucose deprivation-induced injury by upregulating bcl-2 expression and downregulating caspase-3 expression though hypoxia inducible factor-1α pathway.

THE STUDY ON IN VITRO METABOLISM OF BUTYLPHTHALIDE BY GAS CHROMATOGRAPHY-MASS SPECTROMETRY

The in vitro metabolism o. butylphthalide (HBP) by rat liver microsomes was studied in this paper. Capillary GC/MS and BSTFA/1%TMCS derivatization were used for the separation and structure identification of the six metabolites. 3-Hydroxylation and r-hydroxylation have been proved to be the main metabolism pathways of HBP by rat liver microsomes.

Effect of butylphthalide soft capsule on the anti-inflammatory effect and plaque stability in patients with ischemic cerebrovascular disease and carotid atherosclerosis

Objective:To explore the effect of butylphthalide soft capsule on the serum hs-CRP, MMP-9, and TNF-α in patients with ischemic cerebrovascular disease in order to evaluate the the therapeutic effect in the treatment of carotid atherosclerosis.Methods:According to the carotid ultrasound results, the patients were divided into the stable plaque group (control group) and the vulnerable plaque group. The patients in the vulnerable plaque group were randomized into the intervention 1 group and intervention 2 group. The patients in the two subgroups were given bayaspirin and atorvastatin. On this basis, the patients in the intervention 1 group were given butylphthalide soft capsules. The serum hs-CRP, MMP-9, and TNF-αbefore treatment and 6 months after treatment in each group were detected. The color Doppler ultrasound was used to measure and evaluate IMT, Crouse score, and plaque echo change. Results: The serum hs-CRP, MMP-9, and TNF-α levels before treatment between the two subgroups were significantly higher than those in the control group, but the comparison between intervention 1 group and intervention 2 group was not statistically significant. The serum hs-CRP, MMP-9, and TNF-α levels 6 months after treatment in the two subgroups were significantly reduced when compared with before treatment. The serum hs-CRP, MMP-9, and TNF-α levels after treatment in the intervention 1 group were significantly lower than those in the intervention 2 group. IMT 6 months after treatment in the two subgroups was significantly reduced when compared with before treatment. The reduced degree of IMT after treatment in the intervention 1 group was significantly greater than that in the intervention 2 group. Crouse score after treatment in the two subgroups was significantly reduced when compared with before treatment, but the comparison between the two groups was not statistically significant. The unstable plaque number after treatment in the two subgroups was significantly reduced when compared with before treatment. The unstable plaque number after treatment in the intervention 1 group was significantly lower than that in the intervention 2 group.Conclusions:Butylphthalide soft capsule can resist the inflammation, reverse the prolieration of carotid intima, stabilize the vulnerable plaque, and remove the non-atherosclerotic plaque.

Effects of L-3-n-butylphthalide on caspase-3 and nuclear factor kappa-B expression in primary basal forebrain and hippocampal cultures after beta-amyloid peptide 1-42 treatment

BACKGROUND： L-3-n-butylphthalide （L-NBP） can inhibit phosphorylation of tau protein and reduce the neurotoxicity of beta-amyloid peptide 1-42 （Aβ1-42）. OBJECTIVE： To observe the neuroprotective effects of L-NBP on caspase-3 and nuclear factor kappa-B （NF- K B） expression in a rat model of Alzheimer＇s disease. DESIGN, TIME AND SETTING： A cell experiment was performed at the Central Laboratory of Provincial Hospital affiliated to Shandong University between January 2008 and August 2008. MATERIALS： L-NBP （purity 〉 98%） was provided by Shijiazhuang Pharma Group NBP Pharmaceutical Company Limited. Aβ1-42, 3-[4,5-dimethylthiazolo-2]-2,5 iphenyltetrazolium bromide （MTT）, and rabbit anti-Caspase-3 polyclonal antibody were provided by Cell Signaling, USA; goat anti-choactase and rabbit anti-NF- kB antibodies were provided by Santa Cruz, USA. METHODS： Primary cultures were generated from rat basal forebrain and hippocampal neurons at 17 or 19 days of gestation. The cells were assigned into five groups： the control group, the Aβ1-42 group （2 μmol/L）, the Aβ1-42 ＋ 0.1 μmol/L L-NBP group, the Aβ1-42 ＋ 1 μ mol/L L-NBP group, and the Aβ1-42 ＋ 10μmol/L L-NBP group. The neurons were treated with Aβ1-42 （2 μmol/L） alone or in combination with L-NBP （0.1, 1, 10 μmol/L） for 48 hours. Cells in the control group were incubated in PBS. MAIN OUTCOME MEASURES： Morphologic changes were evaluated using inverted microscopy, viability using the M-I-I- method, and the changes in caspase-3 and NF- k B expression using Western blot. RESULTS： Induction with Aβ1-42 for 48 hours caused cell death and soma atrophy, and increased caspase-3 and NF- K B expression （P 〈 0.05）. L-NBP blocked these changes in cell morphology, decreased caspase-3 and NF- k B expression （P 〈 0.05）, and improved cell viability, especially at the high dose （P 〈 0.05）. CONCLUSION： AI3^-42 is toxic to basal forebrain and hippocampal primary neurons; L-NBP protects against this toxicity and inhibits the induction of caspase-3 and NF- K B expression.

Effect of dl-3-n-butylphthalide on infarction volume in animal models of ischemic stroke:A meta-analysis

BACKGROUND Ischemic stroke is a frequently-occurring disease in the elderly and characterized by high morbidity and mortality.Dl-3-n-butylphthalide(NBP),a synthetic compound based on natural celery seeds,has potential therapeutic effects on cerebral ischemia,brain trauma,memory impairment,and epilepsy.AIM To evaluated the effect of NBP on infarct volume in experimental ischemic stroke.METHODS Twenty one relevant literatures were included from the PubMed,EMBASE,Web of Science,Chinese National Knowledge Infrastructure,VIP information database,and Wanfang database,and data on the effect of dl-3-n-butylphthalide on infarction volume in the middle cerebral artery occlusion model were extracted.Statistical analysis was performed using standard mean difference with random effects model of Revman 5.3.RESULTS The data of meta-analysis of the 21 studies had suggested that NBP reduced the cerebral infarction volume of middle cerebral artery occlusion model animals compared to the control group significantly[SMD:-3.97,95%CI:-4.71 to-3.23,P<0.01;heterogeneity:χ2=59.09,df=20(P<0.01);I2=66%].CONCLUSION NBP was effective in experimental ischemic stroke.

3-N-Butylphthalide mitigates high glucose-induced injury to Schwann cells:association with nitrosation and apoptosis

A high glucose state readily causes peripheral axon atrophy, demyelination, loss of nerve fiber function, and delayed regeneration. However, few studies have examined whether nitration is also critical for diabetic peripheral neuropathy. Therefore, this study investigated the effects of high glucose on proliferation, apoptosis, and 3-nitrotyrosine levels of Schwann cells treated with butylphthalide. In addition, we explored potential protective mechanisms of butylphthalide on peripheral nerves. Schwann cells were cultured in vitro with high glucose then stimulated with the peroxynitrite anion inhibitors uric acid and 3-n-butylphthalide for 48 hours. Cell Counting Kit-8 and flow cytometry were used to investigate the effects of uric acid and 3-n-butylphthalide on proliferation and apoptosis of Schwann cells exposed to a high glucose environment. Effects of uric acid and 3-n-butylphthalide on levels of 3-nitrotyrosine in Schwann cells were detected by enzyme-linked immunosorbent assay. The results indicated that Schwann cells cultured in high glucose showed decreased proliferation, but increased apoptosis and intracellular 3-nitrotyrosine levels. However, intervention with uric acid or 3-n-butylphthalide could increase proliferation of Schwann cells cultured in high glucose, and inhibited apoptosis and intracellular 3-nitrotyrosine levels. According to our data, 3-n-butylphthalide may inhibit cell nitrification and apoptosis, and promote cell proliferation, thereby reducing damage to Schwann cells caused by high glucose.

Effects of butylphthalide on bronchial asthma in guinea pigs and involvement of endothelin

Objective: To study the effects of butylphthalide on bronchial asthma in guinea pigs, and investigate the involvement of endothelin. Methods: In guinea pigs, bronchial asthma was induced by injection of ovalbumin(OVA) and provoked by inhalation of OVA, and the effects of butylphthalide on asthma were evaluated through the changes it induced by OVA, pulmonary function, endothelin-1(ET-1) contents and activity of endothelin converting enzyme-1(ECE-1) in bronchoalveolar lavage fluid(BALF), serum and lung tissue, and the gene expression of ET-1 in lung tissue. Results: Butylphthalide significantly improved pulmonary function, lowered asthmatic behavior score, inhibited the activity of ECE-1, and reduced ET-1 gene expression level in lung tissue. Conclusion: Butylphthalide has an anti-asthma effect and the mechanisms involve inhibition of ECE-1 activity and lowering of ET-1geng expression.

L-3-n-butylphthalide protects against vascular dementia via activation of the Akt kinase pathway

As a neuroprotective drug for the treatment of ischemic stroke, 3-n-butylphthalide, a celery seed ex- tract, has been approved by the State Food and Drug Administration of China as a clinical therapeutic drug for ischemic stroke patients. L-3-n-butylphthalide possesses significant efficacy in the treatment of acute ischemic stroke. The activated Akt kinase pathway can prevent the death of nerve cells and exhibit neuroprotective effects in the brain after stroke. This study provides the hypothesis that I-3-n- butylphthalide has a certain therapeutic effect on vascular dementia, and its mechanism depends on the activation of the Akt kinase pathway. A vascular dementia mouse model was established by cere- bral repetitive ischemia/reperfusion, and intragastrically administered I-3-n-butylphthalide daily for 28 consecutive days after ischemia/repedusion, or 7 consecutive days before ischemia/reperfusion. The Morris water maze test showed significant impairment of spatial learning and memory at 4 weeks after operation, but intragastric administration of I-3-n-butylphthalide, especially pretreatment with I-3-n- butylphthalide, significantly reversed these changes. Thionine staining and western blot analylsis showed that preventive and therapeutic application of I-3-n-butylphthalide can reduce loss of pyrami- dal neurons in the hippocampal CA1 region and alleviate nerve damage in mice with vascular demen- tia. In addition, phosphorylated Akt expression in hippocampal tissue increased significantly after I-3-n- butylphthalide treatment. Experimental findings demonstrate that I-3-n-butylphthalide has preventive and therapeutic effects on vascular dementia, and its mechanism may be mediated by upregulation of phosphorylated Akt in the hippocampus.

To investigate the effects of butylphthalide on reducing neuronal apoptosis in rats with cerebral infarction by inhibiting the JNK/P38 MAPK signaling pathway

Objective:To investigate the effects of butylphthalide on reducing neuronal apoptosis in rats with cerebral infarction by inhibiting the JNK/P38 MAPK signaling pathway.Methods:Forty-eight SD male rats were divided into DZ group(control group),CI group(model group)and NBP group(butylphthalide group).Rats in CI group and NBP group were used to establish cerebral infarction models.NBP group used NBP.The solution(80 mg/(kg?d))was administered orally,and the remaining two groups were administered with the same volume of peanut oil.After 14 consecutive days of treatment,the Zea Longa score was used to evaluate the neurological function of DZ,CI and NBP rats.Scoring,TTC staining was used to observe the cerebral infarction volume of rats in DZ group,CI group and NBP group,HE staining was used to observe the pathological morphology of brain tissue in DZ group,CI group and NBP group.Neuronal apoptosis,Western blot was used to detect the expression of p-JNK and p-p38MAPK in brain tissues of DZ group,CI group and NBP group.Results:The neurological function of the rats in the CI group was higher than that in the DZ group,and the difference was statistically significant(P<0.05).The neurological function score of the rats in the NBP group was reduced compared with the CI group,and the difference was statistically significant(P<0.05).The cerebral infarction volume in the group was 35.56%higher than that in the DZ group,and the difference was statistically significant(P<0.05).The minor infarct volume in the NBP group was 21.59%,which was less than that in the CI group,and the difference was statistically significant(P<0.05).Nerve cells are neatly sorted,with a large number.The gap between blood vessels and interstitial tissue in the CI group is enlarged,the cells are severely contracted,and the neuron structure is incomplete.Compared with the CI group,the NBP group has reduced neuron contraction and increased number;The dead nerve cells were brown.The apoptosis rate of nerve cells in the CI group was 79.65%higher than that in the DZ group was 5.82%.The difference was statistically significant(P<0.05).The nerve cell apoptosis rate in the NBP group was 30.23%.Compared with CI group,the difference was statistically significant(P<0.05);Western blot results showed that p-JNK and p-p38MAPK protein expression in CI group was higher than that in DZ group,and the difference was statistically significant(P<0.05).The levels of p-JNK and p-p38MAPK proteins in the NBP group were lower than those in the CI group.There was statistically significant(P<0.05).Conclusion:Butylphthalide can improve neurological damage,reduce apoptotic nerve cells,and reduce infarct volume in rats with cerebral infarction,which is related to the inhibition of JNK/P38 MAPK pathway expression.

Clinical Efficacy and Safety of Joint Butylphthalide and Human Albumin Treatment of PTCI

Objective:To observe the clinical efficacy and safety of butylphthalide joint human albumin in the treatment of the progress of type in acute cerebral infarction(PTCI).Methods:120 patients with PTCI in Department of Neurology of Shuyang People's Hospital were used to observe the efficacy.These patients were all treated by routine medicine including anti-platelet,statins,edaravone,ginkgo leaf extract and dipyridamole after admission.According to whether used butylphthalide and(or)human albumin in the treatment of PTCI,the patients were divided into A group 30 cases,B group 45 cases,and C group 45 cases.Patients of group C were given conventional treatment.Group B were given conventional treatment and human albumin injection(5 g,ivgtt,qd,3 days in a course);Group A were treated with butylphthalide(first,with butylphthalide and sodium chloride injection 100 ml,ivgtt,for 7 d,then with butylphthalide soft capsules 0.2 g,tid,for 21 d),human albumin(5 g,ivgtt,qd,for 3 d)and routine medicine.The change of NIHSS score,Barthel Index,and mRS of three groups respectively during progress,1 week,2 weeks and 90 days after progress were observed and analyzed.Results:NIHSS score,Barthel Index,and mRS of group A,group B and group C all showed no statistically significant(all p>0.05)on 1 week after treatment;NIHSS score and mRS of group A were both lower than group B and group C on 2 weeks and 90 days after treatment,and both of them showed statistically significant(p<0.05);Barthel Index of group A was higher than group B and group C on 90 days after treatment,it showed statistically significant(p<0.05);The total effective rate of group A(96.7%)>group B(88.9%)>group C(77.8%),showed statistically significant(p<0.05).Conclusions:Butylphthalide joint human albumin treatment of PTCI has good therapeutic effect and safety,it is useful to clinical promotion and further research.

Effect of Ginkgo Biloba extract combined with butylphthalide on serum biochemical indexes of patients with mild to moderate Alzheimer's disease

Objective: To study the effect of Ginkgo Biloba extract combined with butylphthalide on serum biochemical indexes of patients with mild to moderate Alzheimer's disease. Methods:The patients who were diagnosed with mild to moderate Alzheimer's disease for the first time in Weinan Central Hospital between March 2015 and December 2017 were selected as the research subjects and randomly divided into two groups, observation group received Donepezil Hydrochloride Tablets + Ginkgo Biloba Extract Tablets + Butylphthalide Soft Capsules treatment, and control group received Donepezil Hydrochloride Tablets treatment. The serum levels of metabolites, cytokines, oxidative stress mediators and other biochemical indicators were measured before treatment and 3 months after treatment. Results: 3 months after treatment, serum Hcy, IL-1β, TNF-α, HMGB1, MCP-1, MDA and Tau levels of both groups of patients were significantly lower than those before treatment whereas UA, VitB12, FA, VEGF, BDNF, GPX3, CAT and SOD levels were significantly higher than those before treatment, and serum Hcy, IL-1β, TNF-α, HMGB1, MCP-1, MDA and Tau levels of observation group after treatment were significantly lower than those of control group whereas UA, VitB12, FA, VEGF, BDNF, GPX3, CAT and SOD levels were significantly higher than those of control group. Conclusion: Ginkgo Biloba extract combined with butylphthalide treatment of mild to moderate Alzheimer's disease can significantly improve the substance metabolism and reduce the inflammatory stress response.

Effect of butylphthalide injection on inflammatory factors, neurological factors and hemorheology in patients with acute cerebral infarction

Objective: To investigate the effects of butylphthalide injection on inflammatory factors, neurological factors and hemorheology in patients with acute cerebral infarction. Methods:The patients in the observation group were treated with intravenous infusion of butyphthalide on the basis of the control group, 120 cases of acute cerebral infarction patients are randomly divided into control group (n=60) and observation group (n=60), patients in the control group were given conventional thraphy, on the basis of the thraphy of the control group, the observation group were treated with intravenous infusion of butyphthalide. Both groups were given sustainable treatment for 14 d, the levels of inflammatory factors, neurological factors and hemorheologywere compared before and after the treatment. Results: The levels of serum hs-CRP, TNF-α, NSE, MBP, S100B, whole blood viscosity, plasma specific viscosity, hematocrit and platelet aggregation rate in the two groups before treatment were no significant difference. After treatment, the levels of hs-CRP, TNF-α in the observation group and observation group were (4.98±1.14) mg/L, (5.54±1.29) ng/L and (7.54±0.93) mg/L, (8.32±1.31) ng/L, which were significantly lower than those in the same group before treatment, and the level of hs-CRP, TNF-α in the observation group were significantly lower than those in the control group;the levels of NSE, MBP, S100B in the observation group and observation group were (6.38±2.39) μg/L, (10.19±3.28) μg/L, (0.96±0.09) ng/L and (11.73±2.43) μg/L, (17.43±4.51) μg/L, (1.65±0.12) ng/L, which were significantly lower than those in the same group before treatment, and the observation group levels were significantly lower than those in the control group;the levels of whole blood viscosity, plasma specific viscosity, hematocrit and platelet aggregation rate in the observation group and observation group were(5.17±0.89) mPa?s,(1.32±0.22) mPa?s, (0.35±0.13)%, (0.32±0.08)% and (5.68±0.91) mPa?s, (1.63±0.24) mPa?s, (0.41±0.14)%, (0.40±0.11)%, which were significantly lower than those in the same group before treatment, and the observation group levels were significantly lower than those in the control group. Conclusion: On the basis of conventional treatment, the addition of butyphthalide can effectively reduce the level of serum inflammatory factors, promote the repair of nerve function, improve the level of hemorheology, which has important clinical value.

Asymmetric synthesis of 3-butylphthalide using isomannide and isosorbide as chiral auxiliaries

A new approach for asymmetric syntheses of （S） and （R）-3-n-butylphthalide （NBP） is presented. The diastereoselective addition of dibutylzinic to aromatic aldehyde 10 or 11 generated from isomannide- or isosorbide-derived chiral auxiliary afforded S-NBP or R-NBP in high optical yields.

EFFECT OF DL-3-N-BUTYLPHTHALIDE ON BRAIN EDEMA IN RATS SUBJECTED TO FOCAL CEREBRAL ISCHEMIA

The present study evaluated the effect of dl-3-n hutylphthalide(NBP),a novel brain protective agent,on brain edema in rats following focal ischemiet. Edema was induced by occluding the right middle cerchral artery (MCAO) ,producing permanent focal ischemia in the right eerehral hemlspheme,which developed ipsilateral brain edenaa reproduclbly. Edema was assessed 24 b after MCA occlusion by determining the brain water content from wet and dry weight measurements,and the sodium,potasslum concentrations with ionselective electrodas.In this model,NBP at the dose of 80,160 and 240 mg/kg po 15 min after MCAO prevented from brain edema in a dose-dependent manner. A significant reduction of sodium content and an increase in potassium level wee ohserved in all drug-treated groups. It showed that NBP strongly attenuated brain water entry ,sodium accumulation and potassium loss. Nimodlpine treatment (Smg/kg sc) also reduced brain edemo (P<0. 05). The mesults suggest that & strong anti-edema activity ot NBP may play an important role to contribute to the treatment ot ischemic damage.

Dl-3-butylphthalide-enhanced hematopoietic stem cell transplantation and endogenous stem cell mobilization for the treatment of cerebral infarcts

Exogenous stem cell transplantation and endogenous stem cell mobilization are both effective for the treatment of acute cerebral infarction. The compound dl-3-butylphthalide is known to improve microcirculation and help brain cells at the infarct loci. This experiment aimed to investigate the effects of dl-3-butylphthalide intervention based on the transplantation of hematopoietic stem cells and mobilization of endogenous stem cells in a rat model of cerebral infarction, following middle cerebral artery occlusion. Results showed that neurological function was greatly improved and infarct volume was reduced in rats with cerebral infarction. Data also showed that dl-3-butylphthalide can promote hematopoietic stem cells to transform into vascular endothelial cells and neuronal-like cells, and also enhance the therapeutic effect on cerebral infarction by hematopoietic stem cell transplantation and endogenous stem cell mobilization.

丁苯酞序贯疗法联合高压氧疗及糖皮质激素对急性一氧化碳中毒迟发性脑病的临床疗效研究

目的 评估丁苯酞序贯疗法(BST)辅助治疗对急性一氧化碳中毒迟发性脑病(DEACMP)的临床疗效。方法 选取延安市人民医院神经内科2018年1月至2023年6月就诊的DEACMP患者为研究对象。采用随机数字表法,将DEACMP患者随机分为高压氧治疗(HBOT)组、糖皮质激素(GC)组(GC联合HBOT)、BST组(HBOT、GC联合BST),均持续治疗30 d。观察并比较3组DEACMP治疗期间不良反应发生情况及治疗后临床疗效。比较3组治疗前后炎症指标、神经损伤指标、认知功能、神经功能和日常生活能力。结果 研究共纳入患者120例,每组各40例。治疗期间,3组患者均未观察到严重不良反应事件,无1例患者因不良反应而终止治疗。BST组治疗总有效率显著高于GC组和HBOT组,而GC组高于HBOT组(P<0.05)。治疗前,3组炎症指标、神经损伤指标、认知功能、神经功能和日常生活功能评分差异均无统计学意义(P> 0.05)。治疗后,3组血清脂蛋白磷脂酶(LP-PLA2)、全身炎症反应指数(SIRI)、肿瘤坏死因子-α(TNF-α)、中枢神经特异蛋白(S100-β)、神经元特异性烯醇化酶(NSE)水平均较治疗前下降(P<0.05),且BST组低于HBOT组和GC组,GC组低于HBOT组(P<0.05)。治疗后,3组简易智力状态检查量表(MMSE)、蒙特利尔认知评估量表(MoCA)、和Barthel指数(BI)评分均较治疗前升高(P<0.05),但美国国立卫生研究院卒中量表(NIHSS)评分下降(P<0.05)。此外,BST组MMSE、MoCA、和BI评分高于HBOT组和GC组(P<0.05),NIHSS评分低于HBOT组和GC组(P<0.05);GC组MMSE、MoCA、BI评分高于HBOT组,NIHSS评分低于HBOT组(P<0.05)。结论 与HBOT治疗和HBOT联合GC治疗比较,BST辅助治疗可提升DECAMP患者临床疗效,改善炎症状态、认知功能和日常生活能力。