Shenmai Injection (SMI), a traditional Chinese medicine with nourishing properties, has been explored for its therapeutic effects in ischemic stroke (IS). This study aimed to evaluate the protective effects of SMI in patients with IS who received intravenous thrombolysis and to elucidate its potential molecular mechanisms through laboratory investigations. Patients with IS were randomized to receive either SMI or a placebo for 10 days within 12 h post-intravenous thrombolysis. Clinical efficacy and safety were assessed. An IS cell model was induced using H2O2, followed by treatment with SMI to explore its therapeutic effects and underlying mechanisms. The modified Rankin Scale (mRS) score at 30 days was significantly lower in the SMI group (n = 35) compared to the placebo group (n = 35), indicating improved functional outcomes. No significant difference was observed in NIHSS scores between the groups. Adverse events and biochemical indices showed no significant differences, confirming the safety of SMI. In the H2O2-induced cell model, SMI enhanced cell viability, reduced apoptosis, and decreased the levels of malondialdehyde (MDA) and reactive oxygen species (ROS). It also improved ATP content and mitochondrial membrane potential. Mechanistic studies revealed that these protective effects were partially mediated through the AMPKα1. SMI significantly improves short-term outcomes in IS patients treated with rt-PA thrombolysis. Its protective effects are likely mediated through the AMPKα1, highlighting its potential as an adjunctive therapy for IS.

Background: Atherosclerosis is a chronic inflammatory disease that leads to ischemic cerebrovascular and cardiovascular diseases. Curcumin, known for its anti-inflammatory properties, may influence the development of atherosclerosis. This study aims to elucidate the effects of curcumin and its mechanisms on atherosclerosis progression. Methods: The proliferative ability, the angiogenesis capacity, and cell migration rate were assessed using cell counting kit-8 (CCK-8), 5-ethynyl-29-deoxyuridine (EdU), tube formation assays, and wound healing, respectively. Furthermore, the protein expression levels of proliferating cell nuclear antigen (PCNA), glycogen synthase kinase 3 beta (GSK3 beta), p-GSK3 beta, beta-catenin, and c-myc were determined utilizing western blot analysis. Results: Oxidized low-density lipoprotein (ox-LDL) significantly triggered cell damage by inhibiting cell proliferation, reducing the migration rate, and angiogenesis capacity in human umbilical vein endothelial cells (HUVECs) (p < 0.05). Curcumin treatment significantly alleviated ox-LDL-induced HUVECs injury (p < 0.05), as evidenced by elevating the proliferative ability (p < 0.05), cell migration (p < 0.05), and angiogenesis (p < 0.05). Moreover, the Wnt/beta-catenin pathway was substantially boosted following ox-LDL treatment (p < 0.05), which was suppressed by curcumin (p < 0.05). Additionally, SKL2001 significantly increased the levels of beta-catenin and c-myc (p < 0.05). The inhibitory effects of curcumin treatment on the Wnt/beta-catenin signaling pathway were reduced by SKL2001 (p < 0.05). Furthermore, the promoting effects of curcumin on ox-LDL-induced cell damage were hampered following SKL2001 treatment in HUVECs (p < 0.05). Conclusion: Curcumin elevated cell proliferation, migration, and angiogenesis of HUVECs to inhibit the development of atherosclerosis through inactivating the Wnt/beta-catenin pathway.

OBJECTIVE:To explore the neuroprotective effects and mechanism of Tanreqing Injection (TRQ) on treating ischemic stroke based on network pharmacology and in vivo experimental validation. METHODS:The chemical compounds of TRQ were retrieved based on published data, with targets retrieved from PubChem, Therapeutic Target Database and DrugBank. Network visualization and analysis were performed using Cytoscape, with protein-protein interaction networks derived from the STRING database. Enrichment analysis was performed using Kyoto Encyclopedia of Genes Genomes pathway and Gene Ontology analysis. In in vivo experiments, the middle cerebral artery occlusion (MCAO) model was used. Infarct volume was determined by 2,3,5-triphenyltetrazolium hydrochloride staining and protein expressions were analyzed by Western blot. Molecular docking was performed to predict ligand-receptor interactions. RESULTS:We screened 81 chemical compounds in TRQ and retrieved their therapeutic targets. Of the targets, 116 were therapeutic targets for stroke. The enrichment analysis showed that the apelin signaling pathway was a key pathway for ischemic stroke. Furthermore, in in vivo experiment we found that administering with intraperitoneal injection of 2.5 mL/kg TRQ every 6 h could significantly reduce the infarct volume of MCAO rats (P<0.05). In addition, protein levels of the apelin receptor (APJ)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) pathway were increased by TRQ (P<0.05). In addition, 41 chemical compounds in TRQ could bind to APJ. CONCLUSIONS:The neuroprotective effect of TRQ may be related to the APJ/PI3K/AKT signaling pathway. However, further studies are needed to confirm the findings.

目的 观察千山活血膏穴位贴敷人迎穴治疗颈动脉斑块的有效性及安全性.方法 纳入2019 年9 月—2020 年11 月就诊于北京中医药大学东方医院脑病科门诊的颈动脉斑块患者60 例,采用随机双盲安慰剂平行对照的设计方法将患者分为试验组与对照组各30 例.2 组均口服阿托伐他汀钙片,试验组同时给予千山活血膏贴敷人迎穴,对照组给予千山活血膏安慰剂贴敷人迎穴,2 组均治疗90 d.比较2 组患者治疗后中医证候疗效、单项症状疗效、颈动脉超声指标.结果 试验组27 例,对照组24 例完成研究.中医证候疗效,试验组总有效率为51.9%(14/27),对照组为16.7%(4/24),试验组明显高于对照组(P<0.05).单项症状疗效,试验组头痛的总有效率为75.0%(9/12),对照组为 16.7%(2/12),头晕的总有效率分别为 59.1%(13/22)和 21.1%(4/19),试验组均明显高于对照组(P均<0.05).双侧颈动脉内膜中层厚度(IMT)、右侧颈内动脉血流速度呈现试验组较前降低,对照组较前升高的趋势.2 组均未见严重不良反应.结论 千山活血膏穴位贴敷人迎穴可改善颈动脉斑块患者的症状,有降低双侧颈动脉IMT的趋势,且未发生严重不良反应.

Background Shenmai injection (SMI) has been used in the treatment of cerebrovascular diseases and cardiovascular diseases. However, the underlying mechanism of SMI for neuroprotection after acute ischemic stroke (AIS) remains unclear. This study aimed to explore the potential molecular mechanism of SMI in treating reperfusion injury after AIS and its protective effect on PC12 cells against oxidative stress through in vitro experiments based on network pharmacological predictions. Methods The network pharmacology method was used to collect the compounds in SMI and AIS damage targets, construct the “drug-disease” target interaction network diagram, screen the core targets, and predict the potential mechanism of SMI treatment of AIS. In addition, the oxidative stress model of PC12 cells was induced by H2O2 to evaluate the neuroprotective effect and predictive mechanism of SMI on PC12 cells. Results A component-targeted disease and functional pathway network showed that 24 components from SMI regulated 77 common targets shared by SMI and AIS. In PC12 cells damaged by H2O2, SMI increased cell survival, alleviated oxidative stress injury, prevented cell apoptosis, and increased the expression of APJ, AMPK, and p-GSK-3β. After Si-APJ silenced APJ expression, the above protective effect of SMI was significantly weakened. Conclusion SMI is characterized by multiple components, multiple targets, and multiple pathways and inhibits oxidative stress and alleviates nerve injury induced by H2O2 through regulating the APJ/AMPK/GSK-3β pathway.

Background: Acute ischemic stroke (AIS) and following reperfusion therapy-induced cerebral ischemia reperfusion (I/R) injury have been recognized as an important subject of cerebrovascular disease with high mortality. Oxidative stress is an important pathological process of cerebral I/R injury. microRNA-19a (miR-19a) is involved in I/R. As the organ protectant agent, Shenmai Injection (SMI) is widely used in the clinical treatment of cerebral infarction. Purpose: This study aims to explore whether SMI can reduce oxidative stress by regulating miR-19a, thereby treating I/R injury. Methods: The oxidative stress state of PC12 cells was induced by H 2 O 2 , and then the cells were cultured with SMI. The therapeutic effect of SMI was evaluated by detecting cellular superoxide dismutase (SOD), malondialdehyde (MDA) and other oxidative markers with the kit. Western blot, PCR, immunofluorescence and other techniques were used to elucidate the potential mechanism of SMI. Results: Cell viability assay results showed that SMI could improve the viability of PC12 cells stimulated by H 2 O 2 . Compared with the H 2 O 2 group, after SMI treatment, the contents of MDA and reactive oxygen species (ROS) were significantly reduced, while the activity of SOD was significantly increased, and SMI could reduce apoptosis by increasing the content of adenosine 5'-triphosphate (ATP) in cells and enhancing the mitochondrial membrane potential (∆Ψm). Western blot and qRT-PCR results showed that these effects were partially achieved through the AMPK/Sirt1/PGC-1α pathway. The level of miR-19a was significantly increased in H 2 O 2 group, and SMI could protect the cells by reducing miR-19a. Further investigated the target of miR-19a, and transfected cells with miR-19a mimic and inhibitor respectively. We found that AdipoR2 was a direct target of miR-19a, and miR-19a could inhibit AdipoR2/PI3K/Akt/mTOR pathway. Conclusion: SMI can activate AMPK/Sirt1/PGC-1α and AdipoR2/PI3K/Akt/mTOR pathways by reducing miR-19a levels, and protect PC12 cells stimulated by H 2 O 2 .

癫痫是神经系统常见疑难病,严重影响患者的生命、生活.五神脏理论是对五神与五脏关系的高度概括,是中医形神统一整体观念的重要体现:通过对五神亢盛调节可协调五脏功能,通过对五脏虚实调理亦可调节五神.癫痫发病特点与五神病变特点有高度相似之处,与五脏相关,且癫痫病因病机复杂,非独一脏一神可言尽,因此,在此基础上提出"五神-五脏-五痫"辨证体系,将神、脏病变特点与癫痫发作特点对应,五脏精准定位,以整体观为核心,调节五神盛衰、五脏虚实,以求保障机体阴阳平衡,有利于患者个体化治疗方案建立,指导癫痫辨证,为癫痫中医临床论治提供新的思路.

对于癫痫的临床诊疗,中、西医各有其优势和不足,因此,有必要从中西医结合的角度梳理癫痫的发作机制,进而探讨癫痫的治疗思路.中医学认为癫痫是由风、火、痰等病理因素影响五脏生理功能,通过经络传递系统作用脑部,使患者神机失常而发病;西医学则认为癫痫是由各种病理因素导致脑部病灶区的神经元电传导机制异常而引起.中、西医学均认为癫痫病位在脑,且两者均为传递信息通路的异常而导致癫痫发作,基于相通的发作机制理论,可借鉴西医学中对于癫痫病灶的定位来为中医治疗提供思路,具体可结合经络辨证,或与头针相结合的思路来进行中医的临床诊疗.

BACKGROUND:Acute ischemic stroke (AIS) is an important factor leading to adult death and disability globally. For AIS patients who meet certain conditions, recombinant tissue plasminogen activator (rt-PA) intravenous thrombolysis is an important method recommended by national guidelines to achieve vascular recanalization. However, complications such as hemorrhagic transformation and vascular reocclusion after thrombolysis are still unsolved problems in clinical. Several systematic reviews of clinical randomized controlled trials (RCTs) in the past have shown that Chinese herbal injections (CHIs) can improve the neurological function of patients, increase the tolerance of ischemic tissues to hypoxia, and inhibit platelet aggregation. Therefore, this study conducted a meta-analysis of AIS treatment with intravenous thrombolysis alone and compared it with the combined application of CHIs. To evaluate whether CHIs have a synergistic effect on thrombolytic therapy and provide a basis for clinical application.METHODS:The following databases will be searched until September 2020: ①English databases: PubMed, Cochrane Library, Embase; ②Chinese databases: CNKI, Wanfang database, Weipu database, SinoMed. RCTs will be included to compare the efficacy of thrombolysis combined with CHIs and thrombolysis alone in the treatment of AIS. Data extraction and risk of bias assessments will be carried out by 2 verifiers independently. The risk of bias will be evaluated through the Cochrane risk of bias tool. Review Manager software 5.3 will be used for statistical analysis.RESULTS:This study will provide comprehensive evidence for the treatment of AIS by CHIs combined with intravenous thrombolysis from multiple aspects.CONCLUSION:The conclusion of the meta-analysis will provide a basis for judging whether CHIs combined with intravenous thrombolysis is an effective measure for the treatment of AIS.ETHICS AND DISSEMINATION:Ethical approval is not needed because this study will be based on data that already published. We will publish the findings of this study in a peer-reviewed journal and related conferences.PROSPERO REGISTRATION NUMBER:CRD42020215546.

目的 借助于高效液相色谱(Ultra Performance Liquid Chromatography,UPLC)-串联质谱(Tandem mass spectrometry,MS/MS)技术以及气相色谱(Gas Chromatography,GC)-MS/MS技术确定大鼠灌服柴贝止痫汤后主要吸收入血成分,并计算其在大鼠体内的药代动力学特征.方法 采用Thermo Syncronis C18(2.1×100 mm,1.9μm)为色谱柱,乙腈-0.01％甲酸水为流动相,分析时间0～8分钟,进样量5μL,流速0.25 mL/min;电喷雾电离源ESI(+),监测模式为二级数据依赖性扫描;GC载气为He气,恒流模式,流速为1 mL/min,进样量1μL,气化室温度250℃,柱温为程序升温,起始温度为80℃,维持1分钟.雄性Wistar大鼠6只,给予中药柴贝止痫汤(生药8.125 g/kg)灌胃,分别于灌胃前及灌胃后各时间点眶静脉取血,样品处理后采用液质联用及气质联用技术检测17种单体成分在不同时间点大鼠血液中的浓度,采用DAS 2.0软件计算药代动力学参数:AUC(0-t)、AUC(0-∞)、MRT(0-t)、MRT(0-∞)、t1/2、Tmax、Cmax.结果 大鼠血浆中检测出15种单体成分,其含量由高到低排列依次为:天麻素、对羟基苯甲醛、胡芦巴碱、天麻苷元、原儿茶醛、柴胡皂苷A、香草醛、细辛醛、贝母素乙、α-细辛醚、茴香脑、β-细辛醚、柴胡皂苷C、贝母素甲、贝母辛,柠檬醛及柴胡皂苷D未检测出.柴贝止痫汤整体入血成分血药浓度在0.25～0.5小时达到高峰,半衰期平均值为4.28小时.结论 该方法日内精密度和日间精密度良好,回收率在标准范围内,符合定量检测要求;柴贝止痫汤灌胃后贝母素甲、贝母素乙等15种化合物可吸收入血,0.25～0.5小时入血成分浓度达到高峰,可作为复方含药血清最佳采血时间.

β细胞的功能缺陷是我国2型糖尿病的主要的发病机制之一.近年来大量研究表明β细胞去分化是β细胞功能缺陷的主要原因,而FOXO1是对β细胞的去分化有着重要影响的核转录因子,这方面的研究可以为糖尿病的治疗和研究提供新的思路和方向.本文针对FOXO1影响β细胞去分化的作用机制,以及能够抑制和逆转β细胞去分化的干预措施做了系统的总结和分析,发现减肥和饮食控制,以及早期使用胰岛素被证明可以有效抑制和逆转β细胞去分化,其他药物在此方面的作用尚需要进一步证实.

癫痫作为一种发作性脑部疾病,其发作具有短暂性、重复性和刻板性的特征,且发作期与间歇期交替,时发时止.对于癫痫发作的病机,历来并无统一说法.本文主要从伏邪致病、少阳枢机不利、中焦气机不畅、节律紊乱以及玄府病变五个角度论述癫痫发作的中医学病机,并探讨中西医发病机制间的联系,以期从病机的角度为癫痫的临床诊疗提供思路.

探讨颈动脉斑块的中医病机,可为指导临床治疗提供思路.根据现代医学对颈动脉斑块的认识,结合"虚气留滞"理论对其病机进行探讨,揭示了颈动脉斑块的病机在于元气虚衰,导致气滞、血瘀、痰凝等流动性物质郁滞而阻滞脉络.内皮损伤为颈动脉斑块的始动环节,此阶段以元气亏虚为主,内皮的屏障作用、内分泌作用及功能衰退与元气的功能与衰减规律一致;斑块形成阶段与因元气亏虚而致痰瘀留滞一致,斑块导致的血管狭窄与易损斑块脱落导致脑血管事件与痰瘀阻滞脉络导致中风相符.根据疾病的病机特点,其治则当以培补元气为主,佐以行气化痰、活血通络等,各阶段的病机重点不同,治则也应有所不同.

目的 观察柴贝止痫汤添加治疗对耐药性癫痫局灶性意识障碍发作的患者血清中炎症因子的影响.方法 采取自身前后对照的研究方法,通过利用炎症抗体芯片技术,观察耐药性癫痫局灶性意识障碍性发作患者服药前、服药3个月、服药6个月后血清中炎症因子的变化.结果 ①柴贝止痫汤添加治疗耐药性癫痫局灶性意识障碍性发作患者治疗3个月后具有下调血清中IL-1β、IL-4、IL-17、IL-1α、IL-15、IL-6、IL-11、I-309、MIG、GCSF、GM-CSF炎症因子的趋势.②柴贝止痫汤添加治疗6个月后与治疗前相比,血清中I-309、IL-11、MIG表达下降,且具有下调IL-1β、I-309、IL-1α、IL-15、IL-8、IL-17、IL-6、IL-11、IL-16、MIG、IL-1ra、GCSF、BCL、MIP-1β、MIP-1α、IL-12P40炎性因子的趋势.结论 柴贝止痫汤添加治疗耐药性癫痫局灶性意识障碍性发作患者6个月后可能具有改善患者血清炎症因子的作用,其KEGG通路可能与Toll样受体信号通路、细胞因子受体相互作用及细胞因子信号通路相关.

目的 旨在使用网络药理学的方法探讨柴贝止痫汤入血成分治疗癫痫的潜在机制.方法 通过检索相关数据库收集治疗癫痫的靶点以及柴贝止痫汤已鉴定的15个入血成分的作用靶点,构建柴贝止痫汤入血成分治疗癫痫的靶点网络图,并检索靶点间的蛋白-蛋白相互作用.使用Cytoscape构建网络图、分析网络.并将共有靶点使用clusterProfiler包进行GO富集分析和KEGG富集分析.结果 柴贝止痫汤中的入血成分具有125个治疗癫痫的靶点,原儿茶醛具有较多的癫痫治疗靶点,碳酸酐酶是柴贝止痫汤入血成分的主要治疗靶点,AKT1是治疗癫痫的关键靶点.治疗靶点富集于3744个生物过程,295个细胞组分,431个分子功能和253个KEGG通路.主要作用于神经元突触和神经元胞体,在氧化应激、神经细胞死亡、神经递质反应等中发挥治疗作用,并与cAMP信号通路有关.结论 柴贝止痫汤可能是通过调节神经递质反应、氧化应激、神经细胞死亡等发挥治疗癫痫的作用.仍需进一步的实验研究验证该结果.

Objective: Systematically assessing the safety and effectiveness of spraying rhubarb powder solution under gastroscope for the treatment of acute non-varicose upper gastrointestinal bleeding, and confirmation for further clinical research and application. Methods: We searched the following databases up till November 2019: PubMed, the Cochrane Library, EMBASE, CNKI, WanFang Data, VIP and SinoMed. Randomized controlled trials (RCTs) were used to compare the curative effect of spraying rhubarb powder solution with other drugs under gastroscope for the treatment of acute nonvaricose upper gastrointestinal bleeding. Results: Out of 171 articles, 14 RCTs involving 1493 patients were included. All control groups included in the RCTs were treated with norepinephrine solution. The hemostatic effect of spraying rhubarb powder solution under gastroscope was examined for 24 hat high concentration (0.1 g/mL). The hemostatic effect at higher conc. (0.1 g/mL) found far more better than low conc.(RR = 1.48;95 %CI:1.25,1.75;P<0.00001) (0.03 g/mL)as homeostatic effect at low conc.is same that of norepinephrine solution (RR = 1.02;95 %CI:0.94,1.10;P = 0.62). Moreover within 48 h, rhubarb powder solution with 0.1 g/mL or 0.15 g/mL conc. have of significantly higher hemostatic effects than norepinephrine solution (RR = 1.18;95 % CI: 1.08, 1.30;P = 0.0003). Occurrence of rebleeding event within 48 h after successful hemostasis (RR = 0.42;95 %CI:0.24,0.74;P = 0.003) reduced exceptionally. After that the hemostatic effect of rhubarb powder solution with 0.1 g/mL conc.examined within 72 h again exhibited significant improvement than norepinephrine solution (RR = 1.19;95 %CI:1.12,1.26;P < 0.00001). On par with immediate hemostasis time, rhubarb powder solution took unprecedented less time than norepinephrine solution;(MD = -5.565;95 %CI:-6.16, -4.95;P<0.00001). Additionally, the adverse reaction produced by rhubarb powder solution is much lower than norepinephrine solution (RR = 0.22;95 %CI:0.11,0.42;P < 0.00001). Conclusions: According to meta-analysis, Spraying rhubarb powder solution under gastroscope in the treatment of acute non-varicose upper gastrointestinal bleeding is superior to norepinephrine solution in improving hemostasis effect. Shortening immediate hemostasis time and reducing rebleeding,and is safe to use. Based on the results of this study, physicians can treat patients with acute non-varicose upper gastrointestinal bleeding by spraying rhubarb powder solution under gastroscope according to the patients' condition.However, the sample size included in this study is small and of substandard quality qu, and a large sample size clinical trial with strict design and normative report is needed to verify the safety and efficacy of rhubarb powder solution under gastroscope for acute non-varicose upper gastrointestinal bleeding.

目的:探究柴贝止痫汤对海人酸诱导的慢性自发性癫痫模型大鼠认知功能及海马组织p-Tau蛋白表达的影响.方法:大鼠随机分为假手术组及癫痫模型组,其中癫痫模型组侧脑室注射海人酸造模,2周后筛选造模成功大鼠,随机分为模型组及中药组,中药组给予柴贝止痫汤配方颗粒8.48g/kg灌胃,其余两组给予等量0.9％氯化钠溶液灌胃.干预4周后进行Morris水迷宫实验;干预5周后检测p-Tau及Tau蛋白表达.结果:与假手术组比较,模型组大鼠逃避潜伏期显著延长(P＜0.01,P＜0.05),第一次穿越时间显著升高(P＜0.01),穿越原平台位置次数显著减少(P＜0.01),海马组织结构不完整,神经缺失明显,p-Tau表达量显著升高(P＜0.01).与模型组比较,中药组大鼠空间学习及记忆能力显著提高(P＜0.01,P＜0.05),海马组织相对完整,神经元缺失减少,p-Tau表达量显著降低(P＜0.01).结论:柴贝止痫汤能改善海人酸诱导癫痫大鼠认知功能,减少海马神经元缺失,其作用机制可能与下调p-Tau表达相关.

目的:观察柴贝止痫汤及其入血成分α细辛醚对难治性癫痫(IE)大鼠脑内P-糖蛋白(P-gp)表达及卡马西平(CBZ)含量的影响.方法:采用侧脑室注射海人酸法建立IE大鼠模型.分为模型组、西药组、中西药组、α细辛醚+CBZ组,设假手术组,给药时间60d.以Western Blot、RT-PCR、LC-MS对比脑内海马P-gp和Mdr1b mRNA表达及脑内CBZ、10,11环氧化卡马西平(CBZE)含量.结果:模型组及西药组大鼠海马中P-gp和Mdr1b mRNA含量显著高于假手术组(P＜0.05);中西药组及α细辛醚+西药组大鼠海马中P-gp和Mdr1bmRNA含量显著低于模型组、西药组(P＜0.01,P＜0.05).中西药组和α细辛醚+西药组脑内CBZE含量显著高于西药组(P＜0.01).结论:柴贝止痫汤及α细辛醚可能降低IE大鼠海马Mdr1b mRNMP-gp表达,促进CBZ和CBZE入脑,对CBZE作用突出.

目的 研究急性脑梗死经静脉溶栓治疗的患者,其在发病14天内的证候要素分布和随时间的演变情况.方法 纳入脑梗死发病6 h内,经静脉重组组织型纤维蛋白酶原激活剂(rt-PA)溶栓的患者56例.分别在其发病的第1、3、5、7、14天采集中医证候要素信息.综合各项信息与数据,进行统计学处理分析.结果 在患者的证候要素演变中,第1天内风证占主导地位,其次血瘀证及痰湿证所占比例也较高,随着病程进展,内风证在第3天迅速降低,至第14天消失;痰湿证、血瘀证有下降趋势,但所占比例仍较高.随着时点推移,气虚证逐渐增多,在第7天成为最主要证候要素.内火证在第5天升高后又趋于初始比例,阴虚证所占比例始终较低,且随时间推移有下降趋势.结论 脑梗死超早期,患者证候要素以实证为主,其中以风证为主导,证候组合以风、痰、瘀之间的2个基本证候组合最多,其次是3个基本证候的组合.与既往研究脑梗死证候要素的演变规律结果相比较,本研究中患者在溶栓治疗后,其临床证候组合形式逐渐减少,且实证逐渐减少,气虚证更加突出.

目的 探究黄连素对阿尔兹海默症大鼠外周血辅助性T细胞(T helper cell,Th)17、调节性T细胞(regulatory T-cell,Treg)亚群比例,以及脑组织炎性细胞因子水平的影响.方法 大鼠分为假手术组、模型组、黄连素组,除假手术组外,其余各组采用腹腔注射D-半乳糖联合Aβ25-35海马注射的方法建立阿尔兹海默症大鼠模型,药物干预4周后,留取标本,流式细胞技术检测两组大鼠外周血中Th17、Treg细胞比例,实时荧光定量PCR检测两组大鼠海马组织炎性细胞因子白细胞介素(interleukin,IL)-1β、IL-6、IL-17、IL-22、肿瘤坏死因子(tumor necrosis factor,TNF)-α、转化生长因子(transforming growth factor,TGF)-βmRNA转录水平.结果 (1)与假手术组相比,模型组Th17、Treg细胞比例升高(P<0.05),与模型组相比,黄连素组大鼠外周Th17细胞比例降低(P<0.05);(2)与假手术组相比,模型组大鼠海马组织促炎性细胞因子IL-1β、IL-6、IL-17、IL-22、TNF-α转录水平均显著升高(P<0.01),抑炎性细胞因子TGF-β转录水平显著降低(P<0.01);与模型组相比,IL-1β、IL-6、IL-17、TNF-α转录水平均降低(P<0.05),TGF-β转录水平升高(P<0.05).结论 黄连素能降低阿尔兹海默症大鼠外周血Th17亚群比例,减轻脑组织内炎性反应.