人参皂苷对昼夜颠倒应激大鼠能量代谢干预作用的代谢组学研究

目的：利用代谢组学技术研究光照改变造成昼夜颠倒应激对大鼠能量代谢的影响,同时评价人参皂苷的干预作用。方法：大鼠24只分为正常对照组、昼夜颠倒模型组和人参皂苷干预组（100mg/kg）,适应1周后,对模型组和人参皂苷干预光照进行日/夜颠倒8天,称取实验前及开始后每天各组大鼠体重,分别称取实验前及第8天各组白天及夜晚食量。第8天结束后,取大鼠血清TMCS 衍生后,进行GC-MS分析,采用偏最小二乘判别分析法研究模型组与正常组之间的代谢物组差异,评价人参皂苷的干预作用。结果：昼夜颠倒应激对大鼠体重及食量均有促进升高作用（P<0.05）,且食量与正常组相比呈昼夜颠倒趋势;人参皂苷一定程度上抑制应激作用的升高趋势。代谢组学研究表明,昼夜颠倒应激与机体能量代谢、蛋白质吸收与降解、脂肪酸代谢、胆固醇代谢等途径改变有关,人参皂苷具有改善作用。结论：人参皂苷可改善昼夜颠倒造成的代谢物质改变,其机制可能是通过调节兴奋性和抑制性神经递质等上游代谢通路,继而改变下游的物质变化。     

传统医药的整体性与现代医药的局部性的融合——代谢组学在中药复方研究中的应用

国内外医药学家目前都认识到传统医药和现代医药的融合有利于二者自身的发展和人类征服各种复杂疾病、发现创新药物。文章在综述代谢组学主要研究步骤、方法的同时，首次提出了“微量元素组学”的概念。进一步从代谢组学在中药复方物质基础和作用机制研究、中药复方在病讧模型上的整体评价研究、中药复方安全性的研究以及中药复方与肠道菌相互作用的研究等方面，综述了代谢组学在中药复方现代化研究中的应用。这些应用结果和前景表明代谢组学是促进传统医药和现代医药达到有效融合的重要手段之一。     

车前子降糖活性部位的化学成分研究

该文研究车前子降糖活性部位的化学成分。前期研究表明车前子60%乙醇提取物对高脂饲料诱导糖尿病模型小鼠的血糖及糖耐量具有一定改善作用。该文进一步应用硅胶、ODS、Sephadex LH-20柱色谱,中压制备液相、薄层制备等色谱技术对车前子的60%乙醇提取物进行化学成分研究,共分离了8个化合物,并根据化合物的理化性质结合应用波谱技术鉴定了化合物结构,分别为车前子萜A(1)、iridolactone(2)、pedicularislacton(3)、rehmaglutin C(4)、京尼平苷酸(5)、p-hydroxylphenylglycerol(6)、4-(2-羟乙基)-1,2-苯二酚(7)、3-buten-2-one-4-[3-(β-D-glucopyranosyloxy)-4-hydroxyphenyl](8)。其中,化合物1~5为环烯醚萜类,6~8为酚酸类。其中化合物1为新的天然产物,化合物2~4,6,8为首次从车前科植物中分离得到。     

The potential of pharmacogenetics in the treatment of epilepsy.

Pharmacogenetics studies how genetic variants influence individual drug responses. Although pharmacogenetics is currently the subject of intensive research in several disease domains, it remains relatively unexplored in the field of epilepsy. Drug treatment of epilepsy is characterized by unpredictability of efficacy, adverse drug reactions and optimal doses in individual patients. Moreover, a substantial fraction of patients develop drug refractory epilepsy despite optimal treatment. Insights in the pathogenesis of epilepsy and the mechanisms of action of antiepileptic drugs (AEDs) have improved our understanding of the genetic determinants of AED response. The first reports in epilepsy pharmacogenetics are becoming available, and large-scale pharmacogenetic studies are now possible thanks to recent advances in genetics and decreasing genotyping costs. It is hoped that ultimately, findings in epilepsy pharmacogenetics will lead to a more efficacious and less harmful treatment of epilepsy, development of more effective AEDs and facilitation of clinical trials of new AEDs. However, although pharmacogenetics will undoubtedly improve our insight into the mechanisms underlying response to AEDs and perhaps into the pathogenesis of drug refractory epilepsy, clinical application of any findings is expected to be a long process, and considerable practical and theoretical hurdles need to be overcome before pharmacogenetic information will prove of any major utility in the clinical setting. This review addresses current knowledge on genetic factors contributing to AED response and discusses the potential of epilepsy pharmacogenetics in the clinical treatment of epilepsy and new AED development.     

Prospective biomarkers of Alzheimer’s disease: A systematic review and meta-analysis

ObjectiveAlzheimer’s disease (AD) involves a series of pathological changes and some biomarkers were reported to assist in monitoring and predicting disease progression before the emergence of clinical symptoms. We aimed to identify prospective biomarkers and quantify their effect on AD progression.MethodsPubMed, EMBASE and Web of Science databases were searched for prospective cohort studies published up to October 2021. Eligible studies were included, and the available data were extracted. Meta-analyses were conducted based on random-effect models. Relative risk (RR) with 95% confidence interval (CI) was adopted as the final effect size.ResultsTotally 48,769 articles were identified, of which 84 studies with 20 prospective biomarkers were included in meta-analyses. In the present study, 15 biomarkers were associated with AD progression, comprising CSF Aβ42 (RR=2.49, 95%CI=1.68–3.69), t-tau (RR=1.88, 95%CI=1.49–2.37), p-tau (RR=1.74, 95%CI=1.37–2.21), tau/Aβ42 ratio (RR=5.11, 95%CI=2.01–13.00); peripheral blood Aβ42/Aβ40 (RR=1.26, 95%CI=1.05–1.51), t-tau (RR=1.33, 95%CI=1.08–1.64), NFL (RR=1.75, 95%CI=1.07–2.87); whole, left and right hippocampal volume (HV) (whole: RR=1.65, 95%CI=1.39–1.95; left: RR=2.60, 95%CI=1.02–6.64; right: RR=1.43, 95%CI=1.23–1.66), entorhinal cortex (EC) volume (RR=1.69, 95%CI=1.24–2.30), medial temporal lobe atrophy (MTA) (RR=1.52, 95%CI=1.33–1.74), 18 F-FDG PET (RR=2.24, 95%CI=1.29–3.89), 11 C-labeled Pittsburgh Compound B PET (11 C-PIB PET) (RR=3.91, 95%CI=1.06–14.41); APOE ε4 (RR=2.16, 1.83–2.55). A total of 70 articles were included in the qualitative review, in which 61 biomarkers were additionally associated with AD progression.ConclusionCSF Aβ42, t-tau, p-tau, tau/Aβ42; peripheral blood t-tau, Aβ42/Aβ40, NFL; whole, left and right HV, EC volume, MTA, 18 F-FDG PET, 11 C-PIB PET; APOE ε4 may be promising prospective biomarkers for AD progression.