Atopic dermatitis (AD) is a chronic relapsing disease with complex pathogenesis. Among them, inflammation is one of the primary pathogenesis of AD. AD is characterized by infiltration of lymphocytes into the skin’s dermis, and the skin homing of lymphocytes plays an essential role in the recurrence of AD. Currently, there is more and more evidence to support this view. This article reviews the relevant role of T lymphocyte skin-homing-related molecules in the recurrence of AD to provide a reference for the cure of AD.

Primary cilia (PC) are essential signaling hubs for proper epithelial formation and the maintenance of skin homeostasis. Found on most cells in the human body, including skin cells, PC facilitate signal transduction that allows ciliated cells to interact with the immune system via multiple pathways, helping to maintain immune system homeostasis. PC can be altered by various microenvironmental stimuli to develop corresponding regulatory functions. Both PC and ciliary signaling pathways have been shown to be involved in the immune processes of various skin lesions. However, the mechanisms by which PC regulate cellular functions and maintain immune homeostasis in tissues are highly complex, and our understanding of them in the skin remains limited. In this paper, we discuss key ciliary signaling pathways and ciliated cells in the skin, with a focus on their immunomodulatory functions. We have compiled evidence from various cells, tissues and disease models to help explore the potential immunomodulatory effects of PC in the skin and their molecular mechanisms.

Ethnopharmacological relevance: Mahuang-Lianqiao-Chixiaodou decoction (MLCD) is a traditional Chinese medicinal (TCM) formula recorded in the Treatise on Febrile Diseases. It is commonly used for clinical treatment of atopic dermatitis (AD). However, the potential mechanisms of MLCD intervention in AD combined with mental disorders behaviors such as anxiety and depression remain elusive and deserves further investigation.Aim of the study: The study aims to observe the effect of MLCD on anxiety-and depression-like behaviors in AD mice and explore the possible neuroinflammatory mechanism of NOD-like receptor 3 (NLRP3) inflammasome.Materials and methods: The chemical components of MLCD extracts were identified using UHPLC-MS. The AD mice were induced by 2,4-dinitrofluorobenzene and treated with MLCD or mometasone furoate (MF, as a positive control) for 7 days. The pathological changes in their skin tissue and brain hippocampus were observed by hematoxylin-eosin staining. Elevated plus-maze test (EPM), open field test (OFT), and the suspended tail (TST) were used to measure the anxiety-and depressive-like behaviors in AD mice. Expression of NLRP3 inflammasome-related proteins in brain hippocampus were measured by the quantitative real-time polymerase chain reaction (qPCR) and western blotting (WB).Results: We found that MLCD contain many active ingredients, including ephedrine, Forsythoside A, phillyrin, glycyrrhizic acid, etc. Both MLCD and MF alleviated skin lesions and promoted positive histopathological changes in the hippocampus of AD mince to varying degrees. MLCD however, could further increase their proportion of open arm entry times (Oentries%) in EPM, residence time in the central area (Ctime) and the proportion of the number of times in the central area (Centries%) in OFT significantly. MLCD also reduces their immobility time in TST considerably. Mechanistically, MLCD downregulated the relative mRNA expression and protein level of NLRP3, Caspase-1, IL-1 beta, and IL-18 in hippocampal tissue compared to the model group.Conclusions: MLCD can alleviate anxiety-like and depression-like behaviors in AD mice by intervening in the gene and protein expression of NLRP3 inflammasome-related factors, thus treating AD.

Ethnopharmacological relevance: Shuyu decoction (SYD), an effective traditional Chinese medicine (TCM), has been widely used for treating deficiency-related diseases for thousands of years. Meanwhile, exercise-induced fatigue (EF), a common physiological phenomenon observed in physical training, has been treated as a deficient condition in TCM for decades. Currently, not many studies have been conducted on the effect of SYD on EF and little is known about its underlying pharmacological mechanism.Aim of the study: This current study was designed to assess the anti-fatigue roles of SYD and explore its effect on exercise-induced immune dysfunction.Materials and methods: Eighteen rats were randomly divided into three groups: normal control (NC) group, model (M) group, and SYD group (27.8 g/kg). The M and SYD group were given treadmill training for 6 weeks. From the fourth week, the SYD group was administered SYD intragastrically for 3 consecutive weeks. After three weeks of treatment, the rats were anesthetized, and the blood and spleen tissue samples were dissected. The blood sample was devoted to the blood biochemical-related indicators, which were used to evaluate the anti-fatigue of SYD. The expression of Interleukin (IL)-6, IL-18, tumor necrosis factor-alpha (TNF-alpha), IL -17, CD3(+), and CD4(+) were detected by ELISA and the level of CD8+ of blood was measured through Flow Cytometry (FC). The histopathological changes of spleen tissue samples were determined by Hematoxylin and eosin (H&E) staining and an estimation of CD3(+), CD4(+), and CD8(+) expression of spleen tissues were calculated through FC.Results: Compared with the M group, the SYD group observed an increase in tensile force and the ratio of cortisol to testosterone (TTE/COR), whereas a reduction in the levels of lactic acid (LAC), blood urea nitrogen (BUN), creatine kinase (CK), (P < 0.01 or P < 0.05). ELISA experiments showed that SYD reduced the expressions of IL-6, IL-18, and TNF-alpha, IL-17 and increased the expression of IL-10 (P < 0.01 or P < 0.05). In the HE test, SYD treatment transformed the structure of the spleen. FC experiments further showed that SYD increased the expressions of CD3(+), CD4(+), and CD8(+) in blood and spleen tissues (P < 0.01 or P < 0.05).Conclusion: Our findings indicate that SYD can alleviate EF by improving inflammation and immunity. However, the relationship between inflammatory factors and the related immune response remains to be further investigated.

Objective: To observe the effects of Danggui Shaoyao powder (DSP) on hepatic lipid metabolism and further explore its mechanism of action by peroxisome proliferator-activated receptor (PPARγ)-liver X receptor (LXRα)-adenosine triphosphate (ATP)-binding cassette transporter A1 (ABCA1) pathway regulation. Methods: Eight C57BL/6J male mice were selected as the control group, and 24 ApoE−/− male mice were randomly divided into the atherosclerosis model (AS) group, atorvastatin calcium (AC) group, and DSP group (n = 8 each group). To establish an AS model, ApoE−/− mice were fed a high-fat diet for 16 weeks. Pathologic changes in the aortic vasculature and liver were identified using Oil Red O staining. Triglyceride (TG), cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) levels were determined in the livers using a single-reagent GPO-PAP method. Fluorescence quantitative polymerase chain reaction and western blot were used to observe and evaluate the mRNA and protein expression of the PPARγ-LXRα-ABCA1 intermediates in the liver. Results: After 16 weeks of a high-fat diet, ApoE−/− mice showed more Oil Red O staining in the aorta and liver compared to the CONT group. Compared to the AS group, the DSP and AC treatment reduced aortic plaque and hepatic lipid deposition to varying degrees. Furthermore, DSP significantly reduced the hepatic lipid area in ApoE−/− mice (P < .001) and decreased the levels of TG, TC, and LDL-C in liver (P < .001, P = .027, P < .001, respectively). DSP also significantly increased the levels of PPARγ, LXRα, ABCA1, and ABCG1 mRNA expression, as well as the PPARγ, LXRα, ABCA1, and ABCG1 protein expression in liver. Conclusion: DSP improved hepatic lipid metabolism via PPARγ-LXRα-ABCA1 pathway modulation for AS treatment.

Objective: To explore the mechanism of Huatan Sanjie Fang（HTSJ） in regulating goiter in Graves’ disease（GD） mice by detecting key factors of the Hippo signaling pathway.Methods: A mouse model of GD was established by injecting Ad-TSHR289 adenovirus into the bilateral quadriceps femoris of female mice. Successful mouse models were then randomly divided into a model group, methimazole（MMI） group, and HTSJ group, and fed with deionized water, MMI（4.5 mg/kg per day）, and HTSJ（35.10 g/kg per day）, respectively, for 10 weeks. Histopathological changes of the thyroid gland were subsequently observed by hematoxylin-eosin staining. Radioimmunoassay was used to detect serum total thyroxine（T4） and thyrotrophin-receptor antibody（TRAb） levels. The relative expression of mRNA of Mst1, YAP, and TAZ were detected by quantitative real-time polymerase chain reaction, while the protein expression of Mst1, YAP, TAZ, pMst1, and pYAP were detected by western blot.Results: After 10 weeks of drug intervention, goiter and other pathological changes in the HTSJ group significantly improved compared with the model group, and the levels of serum T4 and TRAb significantly decreased（P =.002, P ＜.001, respectively）. Decreased mRNA expression of Mst1, YAP, and TAZ, the key factors of the Hippo signaling transduction pathway, was also observed（P =.002, P =.022, P ＜.001,respectively）. In contrast, protein expression of Mst1（P =.046）, pMst1（P =.026）, and p YAP（P =.004）increased, while protein expression of YAP and TAZ decreased（P =.041, P ＜.001, respectively）.Conclusion: HTSJ can effectively improve goiter in GD mice through the Hippo signaling pathway.

Objective: To investigate the efficacy and mechanism of Mahuang Lianqiao Chixiaodou decoction (MLCD) in intervening in the “internal and external crosstalk” between skin barrier dysfunction and immune inflammation in an atopic dermatitis-like (AD-like) mouse model via the NOD-like receptor protein 3 (NLRP3) pyroptosis pathway. Methods: AD-like model mice were induced with 2,4-dinitrofluorobenzene and treated with MLCD or mometasone furoate gel (MF, positive control) for 7 days. Pathological changes in skin tissue were examined using Masson or methamphetamine blue staining. A smart skin analyzer, flow cytometry, fluorescence quantitative polymerase chain reaction, and western blotting were used to observe and evaluate skin barrier dysfunction, immune inflammatory responses, and skin cell pyroptosis in AD-like mice. Results: MLCD and MF improved skin damage and reduced pathological tissue damage and mast cell infiltration in AD-like mice to varying degrees. MLCD significantly reduced skin pigmentation and inflammatory status (P = .005 and P = .038, respectively), increased the percentage of splenic CD4+CD3+ T cells (P = .022), decreased the CD8+CD3+ T cell percentage (P = .044), decreased the CD8+CD3+/CD3+ ratio (P = .031) and increased the CD4+CD3+/CD8+CD3+ ratio (P = .027). MLCD also significantly decreased the mRNA expression levels of cell scorch-related factors NLRP3, casp-1, interleukin (IL)-1β, and IL-18 (P = .027, P < .001, P = .012, and P = .039, respectively), as well as the protein expression of NLRP3, casp-1, apoptosis-associated speck-like protein containing a CARD, and IL-1β (P = .002, P = .006, P = .004, and P = .035, respectively). Conclusion: MLCD achieved efficacy in the treatment of AD-like mice by interfering with the “internal and external crosstalk” mechanisms of skin barrier dysfunction and immune inflammation mediated by NLRP3 pyroptosis.

乌梅丸载于《伤寒杂病论》厥阴篇,历代医家多认为其有温脏安蛔之功,临床应用范围较为局限,自清代医家柯琴提出其为厥阴病之主方后乌梅丸才被医家重视,其临床应用亦得以拓展.乌梅丸证之成因,实则归于厥阴风木气运失常,阴阳不相顺接,而非仅为蛔虫内扰所致.以《黄帝内经》"开阖枢"理论分析六经之功能,并结合《伤寒杂病论》原文可证"阴枢"实为厥阴,乌梅丸为厥阴病之主方,有顺接阴阳之功,故其可治疗厥阴枢机不利,寒热错杂之证.《辅行诀五脏用药法要》与《伤寒杂病论》二者同源,均参考了《汤液经法》所载内容,《辅行诀五脏用药法要》中补泻诸方及救逆方之组成有规律可寻,均依文中所载"汤液经法图"而成,与五行理论密切相关.该文通过探索"汤液经法图"组方规律及药物五行归属,以"汤液经法图"组方规律剖析乌梅丸,可证乌梅丸主要作用于肝、脾、心三脏,依黄帝内经五脏藏神理论,此三脏与情志调节密切相关,故以乌梅丸论治厥阴枢机不利、寒热错杂所致之情志病有据可循,文末亦列举概述近年乌梅丸治疗情志病的报道.该文为临床应用乌梅丸治疗情志病提供了思路及依据,扩展了其应用范围,古方亦能为今用.

Background: The medical records of traditional Chinese medicine（TCM） contain numerous synonymous terms with different descriptions,which is not conducive to computer-aided data mining of TCM. However, there is a lack of models available to normalize synonymous TCM terms. Therefore, construction of a synonymous term conversion（STC） model for normalizing synonymous TCM terms is necessary.Methods: Based on the neural networks of bidirectional encoder representations from transformers（BERT）, four types of TCM STC models were designed: Models based on BERT and text classification, text sequence generation, named entity recognition, and text matching. The superior STC model was selected on the basis of its performance in converting synonymous terms. Moreover, three misjudgment inspection methods for the conversion results of the STC model based on inconsistency were proposed to find incorrect term conversion: Neuron random deactivation, output comparison of multiple isomorphic models, and output comparison of multiple heterogeneous models（OCMH）.Results: The classification-based STC model outperformed the other STC task models. It achieved F1 scores of 0.91, 0.91, and 0.83 for performing symptoms, patterns, and treatments STC tasks, respectively. The OCMH method showed the best performance in misjudgment inspection, with wrong detection rates of 0.80, 0.84, and 0.90 in the term conversion results for symptoms, patterns, and treatments, respectively.Conclusion: The TCM STC model based on classification achieved superior performance in converting synonymous terms for symptoms,patterns, and treatments. The misjudgment inspection method based on OCMH showed superior performance in identifying incorrect outputs.

"肝藏血,血舍魂"源于五脏藏神理论,其核心内容是肝脏储藏血液和调节血量,肝魂在肝血提供的物质基础上进行神志活动.躯体性焦虑是以躯体症状为主要表现的焦虑症.基于"肝藏血,血舍魂"理论,躯体性焦虑的病机可概括为肝不藏血、肝失疏泄与血不养魂、魂失所舍,可治以养血柔肝、调畅气机及柔肝安魂、调和阴阳,临证可灵活选用疏肝理气解郁、清泻肝火、滋阴降火、活血化瘀等治法.

目的:探讨麻黄连轺赤小豆汤对不同时期特应性皮炎(atopic dermatitis,AD)模型小鼠皮肤屏障功能的影响.方法:采用随机数字表法将120只雄性BALB/c小鼠随机分为正常组、模型组、糠酸莫米松组和麻黄连轺赤小豆汤组.除正常组外,其余组小鼠采用2,4-二硝基氟苯(2,4-dinitrofluorobenzene,DNFB)反复刺激皮肤建立AD动物模型.于实验第4、18、32、39天4个时间点分别进行药物干预,麻黄连轺赤小豆汤组灌胃给予麻黄连轺赤小豆汤(11.98 g·kg-1·d-1),每日2次;糠酸莫米松组于小鼠皮损处均匀涂抹适量0.1％糠酸莫米松凝胶,每日2次;正常组和模型组给予等量常温蒸馏水灌胃,每日2次;每个时间点连续干预7 d.于第11、25、39、46天4个时间点分别考察各组小鼠皮损评分、皮肤组织病理学、皮肤酸碱度(pondus hydrogenii,pH)及经皮水分散失(trans epidermal water loss,TEWL)情况.结果:与正常组相比,AD模型组小鼠整个观察周期各时间点皮损评分、TEWL值均明显升高(P＜0.01);第11、25、39天3个观测点pH值均明显升高(P＜0.01).与模型组相比,麻黄连轺赤小豆汤组小鼠第39、46天两个时间点TEWL值显著下降(P＜0.01);第11、25、39天3个观测点皮肤pH值均明显降低(P＜0.01).HE染色发现AD模型组小鼠四个观察点皮肤组织表现依次为:表皮增厚,以棘细胞层增厚为主→表皮增厚,棘细胞层增生变厚→表皮增厚,棘细胞层显著增厚→表皮增厚减轻,棘细胞层增生减轻等;而麻黄连轺赤小豆汤可明显改善模型小鼠皮肤病理改变.皮损评分、TEWL值、pH值的相关分析发现,皮损评分、pH值、TEWL值三者呈正相关关系,可共同加重皮肤屏障功能障碍.结论:麻黄连轺赤小豆汤可有效改善AD模型小鼠皮肤屏障功能,以亚急性期治疗效果最佳.

Objective:To explore the potential mechanism of intervention on the immune imbalance of atopic dermatitis（AD） by studying the effects of Mahuang Lianqiao Chixiaodou decoction（MLCD） on skin damage and inflammation factors in an AD-like mouse model.Methods:Ninety-six male BALB/c mice were divided into normal,model,positive control（mometasone furoate）,and traditional Chinese medicine treatment（MLCD） groups by a random number table.2,4-dinitrofluorobenzene was used to induce AD-like mice in all groups except the normal group.The treatment or intervention was administered for seven consecutive days on days 4,18,32,and 39.The mRNA relative expressions of interleukin-4（IL-4）,IL-10,interferon-γ（IFN-γ）,thymic stromal lymphopoietin（TSLP）,and the TSLP receptor（TSLPR） were measured using quantitative real-time polymerase chain reaction,and the serum immunoglobulin E,IL-4,IL-10,and IFN-γ levels were detected using enzyme-linked immunosorbent assay.Results:Compared with the normal group,the hematoxylin-eosin staining of the skin lesions of the mice in the model group was significantly thickened on days 11,25,and 39.Compared with the model group,the epidermal thickness of the positive control group was significantly alleviated on day 39（P ＜.001）,and that of the MLCD group was significantly improved on days 25 and 39（P ＜.001）.Compared with the four observation time points,MLCD had the best treatment effect on day 39 of the experiment and significantly improved the skin damage performance and relieved pathological lesions.On day 39,compared with the model group,MLCD downregulated the skin mRNA relative expressions of IL-4（P=.009）,TSLP（P=.030）,and TSLPR（P ＜.001）,and reduced the mouse serum levels of IL-4（P=.003）.For other serum indicators,no significant difference was observed between the model and MLCD groups.Conclusion:MLCD improved AD-like mice skin damage by regulating the Th1/Th2 immune imbalance.

《黄帝内经》提出"五脏藏神"理论,即心藏神、肺藏魄、肝藏魂、脾藏意、肾藏志.基于此,失眠与焦虑共病的内在病机当为"神不得藏",其中以"心神""肝魂""脾意"为辨治重点.心不藏神则神烦,治当安心神,方选天王补心丹加减;肝不藏魂则惊悸,治当归肝魂,方选一贯煎化裁;脾不藏意则郁结,治当宁脾意,方选归脾汤出入.同时,基于五脏一体观,亦应重视肺、肾二脏的藏神功能.各脏神有所藏,则失眠与焦虑得平.附验案1则以佐证.

ObjectiveTo reveal the mechanism of Mahuang Lianqiao Chixiaodou decoction and its disassembled formula for improving the skin barrier function in a mouse model of atopic dermatitis (AD).MethodsSixty specific-pathogen free male BALB/c mice were randomly divided into the control group, model group, whole formula group (WF), exterior-releasing formula group (ERF), interior-clearing formula group (ICF), and positive control group (PC). A mouse model of AD was established using the semi-antigen 2, 4-dinitrofluorobenzene induction method. The lesion scores, transepidermal water loss and pH, and skin histopathology of mice in each group were observed. The expressions of filaggrin, loricrin, and involucrin were detected by the streptavidin peroxidase immunohistochemical method and western blotting, and their mRNA expressions were detected by quantitative polymerase chain reaction.ResultsMice in the WF, ERF, ICF, and PC groups showed reduced skin lesion performance, improved histopathology, decreased skin lesion score, transepidermal water loss and pH, and upregulated expressions of proteins including filaggrin, loricrin, and involucrin, and their mRNAs. The most obvious regulatory effect was observed in the WF group, followed by the ICF, ERF, and PC groups, accordingly.ConclusionsMahuang Lianqiao Chixiaodou decoction and its disassembled formula can improve the skin barrier function in a mouse model of AD by upregulating filaggrin, loricrin, and involucrin, and their mRNA expressions, and the most optimal effect was noted in the WF group, followed by the ICF and ERF groups, which suggests that the effect of clearing heat and resolving dampness in improving the skin barrier function of AD is more obvious and is one of the key treatments for AD.

目的:探讨麻黄连翘赤小豆汤对特应性皮炎(AD)小鼠皮损修复及PAR-2、TRPA1的表达的影响.方法:选用SPF级雄性BALB/c小鼠48只,随机分为正常组、模型组、激素组、中药组.除正常组外,各组用2,4二硝基氟苯(DNFB)诱导AD模型.造模后模型组给予皮炎平外抹,中药组给予麻黄连翘赤小豆汤灌胃,其余均给予等量蒸馏水灌胃,2次/d,共7 d.于第1、15、31、37天观察小鼠一般状态及搔抓行为并统计,HE染色观察致敏区域的皮肤病理变化,qRT-PCR、免疫组化分别检测皮肤中PAR-2、TRPA1的基因与蛋白表达.结果:与正常组比较,模型组小鼠搔抓频次显著增多,致敏皮肤处有明显红斑渗出,局部潮红,皮肤增厚,伴有结痂.中药组、激素组较模型组明显改善.病理显示模型组较正常组棘层明显增厚,角化珠增多,毛囊结构明显增多,角化层明显增厚,见炎性细胞浸润,表皮不平整;激素组、中药组角化层及棘层增厚,角化珠及毛囊结构略有增多,较模型组改善明显.模型组小鼠皮肤组织中PAR-2、TRPA1的mRNA的表达较正常小鼠均显著性上调(P<0.05),经过中药、激素干预后,其表达均下调显著(P<0.01).与正常组比较,模型组皮肤组织PAR-2、TRPA1免疫反应阳性均明显增多,角质形成细胞处最为显著;中药组、模型组表达较模型组均有所降低.结论:麻黄连翘赤小豆汤改善AD皮损、减轻皮肤瘙痒,下调PAR-2、TRPA1的表达,进而调控非组胺依赖性神经信号传导有关.

目的:探索构建适用于中医学领域的分词模型.方法:采用基于SentencePiece的无监督学习分词方法,提出利用出版教材、名家著作及中医临床病历这3种不同类型的文献构建中医学分词模型;选择中医临床病历、名医医案作为测试集进行模型测试.结果:中医学分词模型在测试集中的Kappa系数为0.79(一致性程度很高),准确率为0.84,宏观精确率为0.84,宏观召回率为0.83,宏观f1得分为0.83.结论:所构建的分词模型对于中医学专业术语有着较好的切分效果,表明该方法可运用于中医学领域的分词模型的构建,可为进一步地研究中医学分词提供方法学参考.

竹叶石膏汤出自《伤寒论》第397条,主治伤寒解后,虚羸少气,气逆欲吐者.竹叶石膏汤证病机为余热仍炽、津气两伤、痰饮内停,其主证除虚羸少气、气逆欲吐外,尚有发热、心烦、便秘溲赤、潮热盗汗、舌红少苔或苔白腻、苔薄黄腻等.临床应视"虚""热""湿"之盛衰而变化方中药、量,随证加减用之.

Background The modernization of traditional Chinese medicine (TCM) demands systematic data mining using medical records. However, this process is hindered by the fact that many TCM symptoms have the same meaning but different literal expressions (i.e., TCM synonymous symptoms). This problem can be solved by using natural language processing algorithms to construct a high-quality TCM symptom normalization model for normalizing TCM synonymous symptoms to unified literal expressions. Methods Four types of TCM symptom normalization models, based on natural language processing, were constructed to find a high-quality one: (1) a text sequence generation model based on a bidirectional long short-term memory (Bi-LSTM) neural network with an encoder-decoder structure; (2) a text classification model based on a Bi-LSTM neural network and sigmoid function; (3) a text sequence generation model based on bidirectional encoder representation from transformers (BERT) with sequence-to-sequence training method of unified language model (BERT-UniLM); (4) a text classification model based on BERT and sigmoid function (BERT-Classification). The performance of the models was compared using four metrics: accuracy, recall, precision, and F1-score. Results The BERT-Classification model outperformed the models based on Bi-LSTM and BERT-UniLM with respect to the four metrics. Conclusions The BERT-Classification model has superior performance in normalizing expressions of TCM synonymous symptoms.

目的:系统评价华佗再造丸治疗缺血性脑卒中的疗效和安全性,旨在为临床治疗用药提供循证参考.方法:检索PubMed、Embase、Cochrane Library、中国知网等数据库,筛选华佗再造丸治疗缺血性脑卒中的临床随机对照试验,文献发表日期限定在从建库开始到2020年12月14日.2名研究者独立进行文献筛选及数据提取.采用Cochrane协作网提供的偏倚风险评估工具评估纳入研究的质量.根据异质性大小选择固定或随机效应模型汇总效应估计值.生成森林图以显示汇总结果,使用TSA0.9软件进行试验序贯分析.结果:共纳入16篇文献,包括1616名受试者,观察组827名,对照组789名.Meta分析结果显示,华佗再造丸组在提高治疗有效率(OR=3.36,95％CI为2.43～4.56,P<0.001)、降低NIHSS评分(MD=-2.72,95％CI为-3.72～-1.73,P<0.001)、提高日常生活能力(MD=8.89,95％CI为4.51～13.26,P<0.001)方面优于对照组;仅6项研究报告了安全性指标,有待更多研究以进一步明确临床用药安全性.TSA结果显示,华佗再造丸组治疗缺血性脑卒中有效率更优的证据确切.结论:当前研究表明华佗再造丸联合基础治疗可显著提高缺血性脑卒中患者的有效率,降低NIHSS评分,提高日常生活能力,但其安全性有待进一步确证.由于本研究纳入的研究方法质量偏低,且样本量小,需进一步进行大规模、高质量的研究验证其疗效和安全性.

目的 使用网络药理学方法筛选连翘治疗特应性皮炎的作用靶点,探索其治疗特应性皮炎的作用机制.方法 使用中药系统药理学数据库与分析平台(TCMSP),以口服利用度(OB)≥30％,类药性(DL)≥0.18为阈值,筛选得到连翘的主要化学成分,并根据相应化学成分得到其作用靶点及靶点基因.利用Uniprot数据库检索中药靶点对应的人类基因207个,从Genecard和OMIM数据库中检索特应性皮炎对应基因1505个,将疾病基因和中药基因取交集后得到103个交集基因,使用String工具对交集基因进行蛋白质互作网络(PPI)分析.采用Cytoscape软件绘制疾病靶点PPI网络,建立疾病-药物靶点关系网络,除去1个游离基因,共得到102个节点,1735条连接,进行基因本体(GO)生物过程富集和京都基因与基因组百科全书(KEGG)富集分析.结果 检索得到符合标准的连翘有效成分23个,中药靶点对应的人类基因207个,特应性皮炎疾病基因1505个,中药靶点对应基因与疾病基因的交集基因103个.对103个交集基因进行基因GO功能分析提示涉及生物过程、分子功能、细胞组成3个方面,发现特应性皮炎生物过程与脂多糖、氧化应激、类固醇激素、抗生素、机械刺激和凋亡信号通路等方面相关;分子功能与核受体活性、类固醇激素受体活性、细胞因子活性等方面相关;细胞组成与质膜、转录调节复合物、线粒体膜等方面相关.基因KEGG通路富集分析发现特应性皮炎发病机制可能与核因子κB (NF-κB)信号通路、肿瘤坏死因子(TNF)信号通路、白细胞介素-17(IL-17)信号通路、辅助性T细胞17(Th17)信号通路、辅助性T细胞1(Th1)和辅助性T细胞2(Th2)细胞分化通路、缝隙连接和紧密连接通路等通路相关.结论 连翘治疗特应性皮炎的机制可能与其有效成分能够调节炎症反应,调节缝隙连接和紧密连接通路具有相关性.