Introduction: Hepatic steatosis is a hepatic pathological change closely associated with metabolic disorders, commonly observed in various metabolic diseases such as metabolic syndrome (MetS), with a high global prevalence. Dai-Zong-Fang (DZF), a traditional Chinese herbal formula, is widely used in clinical treatment for MetS, exhibiting multifaceted effects in reducing obesity and regulating blood glucose and lipids. This study aims to explore the mechanism by which DZF modulates the gut microbiota and reduces hepatic steatosis based on the gut-liver axis.Methods: This study utilized db/db mice as a disease model for drug intervention. Body weight and fasting blood glucose were monitored. Serum lipid and transaminase levels were measured. Insulin tolerance test was conducted to assess insulin sensitivity. Hematoxylin and eosin (HE) staining was employed to observe morphological changes in the liver and intestine. The degree of hepatic steatosis was evaluated through Oil Red O staining and hepatic lipid determination. Changes in gut microbiota were assessed using 16S rRNA gene sequencing. Serum lipopolysaccharide (LPS) levels were measured by ELISA. The expression levels of intestinal tight junction proteins, intestinal lipid absorption-related proteins, and key proteins in hepatic lipid metabolism were examined through Western blot and RT-qPCR.Results: After DZF intervention, there was a decrease in body weight, alleviation of glucose and lipid metabolism disorders, reduction in serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, and mitigation of insulin resistance in mice. DZF significantly modulated the diversity of the gut microbiota, with a notable increase in the abundance of the Bacteroidetes phylum. PICRUSt indicated that DZF influenced various functions in gut microbiota, including carbohydrate and amino acid metabolism. Following DZF intervention, serum LPS levels decreased, intestinal pathological damage was reduced, and the expression of intestinal tight junction protein occludin was increased, while the expression of intestinal lipid absorption-related proteins cluster of differentiation 36 (CD36) and apolipoprotein B48 (ApoB48) were decreased. In the liver, DZF intervention resulted in a reduction in hepatic steatosis and lipid droplets, accompanied by a decrease fatty acid synthase (FASN) and stearoyl-CoA desaturase 1 (SCD1) and fatty acid transport protein 2 (FATP2). Conversely, there was an increase in the expression of the fatty acid oxidation-related enzyme carnitine palmitoyltransferase-1𝛂 (CPT-1𝛂).Conclusion: DZF can regulate the structure and function of the intestinal microbiota in db/db mice. This ameliorates intestinal barrier damage and the detrimental effects of endotoxemia on hepatic metabolism. DZF not only inhibits intestinal lipid absorption but also improves hepatic lipid metabolism from various aspects, including de novo lipogenesis, fatty acid uptake, and fatty acid oxidation. This suggests that DZF may act on the liver and intestine as target organs, exerting its effects by improving the intestinal microbiota and related barrier and lipid absorption functions, ultimately ameliorating hepatic steatosis and enhancing overall glucose and lipid metabolism.

中土主运化饮食水谷,升清降浊,是人体代谢之核心.调节机体代谢的重要器官之一为脂肪组织,其生理、病理与中土运化关联紧密.能量过剩引起脂质沉积,脂肪组织过度肥大,继发脂解、胰岛素抵抗,可致糖脂代谢紊乱.糖原周转是最新发现的一种脂肪组织代谢途径,可促进白色脂肪棕色化,调节机体产热和能量消耗,从而改善代谢.中土不运,清浊失常是肥胖、糖尿病等糖脂代谢紊乱疾病的常见病机,斡旋中土枢机以调和阴阳为主要治则.中土调运则精微得以正化,消减膏浊之积.黄连在代谢性疾病的治疗中应用广泛,其气寒味苦,行"中土之制"而清中土湿热浊邪痞结,配伍组方常围绕"中土之制",从"辛开苦降""苦寒直折"及"寒热并用"等展开.

从"阳化气、阴成形"的视角重新认识肥胖症的成因,并将现代分子生物学机制与传统中医理论结合,梳理探讨"转静为动、化形为气"理念在肥胖症辨治中的应用.形气理论指导下的中医方药内涵分为补气化形使精微归于正化、益火之源以消阴翳之形、苦辛开结以畅气调形3个方面,均围绕激活脂肪产热的核心机制,发挥改善肥胖症的作用.

Introduction: The global prevalence of obesity is rising rapidly. Conversion of white adipose tissue (WAT) into beige adipose tissue with heat-consuming characteristics, i.e., WAT browning, effectively inhibits obesity. Dai-Zong-Fang (DZF), a traditional Chinese medicine formula, has long been used to treat metabolic syndrome and obesity. This study aimed to explore the pharmacological mechanism of DZF against obesity.Methods:In vivo, C57BL/6J mice were fed high-fat diets to establish the diet-induced obese (DIO) model. DZF (0.40 g/kg and 0.20 g/kg) and metformin (0.15 g/kg, positive control drug) were used as intervention drugs for six weeks, respectively. The effects of DZF on body size, blood glucose and lipid level, structure and morphology of adipocytes and browning of inguinal WAT (iWAT) in DIO mice were observed. In vitro, mature 3T3-L1 adipocytes were used as the model. Concentrations of DZF (0.8 mg/mL and 0.4 mg/mL) were selected according to the Cell Counting Kit-8 (CCK8). After 2d intervention, lipid droplet morphology was observed by BODIPY493/503 staining, and mitochondria number was observed by mito-tracker Green staining. H-89 dihydrochloride, a PKA inhibitor, was used to observe the change in browning markers′ expression. The expression levels of browning markers UCP1 and PGC-1α and key molecules of PKA pathway were detected in vivo and in vitro.Results:In vivo, compared with vehicle control group, 0.40 g/kg DZF significantly reduced obesity in DIO mice from body weight, abdomen circumference, Lee′s index, and WAT/body weight (p < 0.01 or p < 0.001). 0.40 g/kg DZF also significantly reduced fasting blood glucose (FBG), serum triglycerides (TG), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C) (p < 0.01 or p < 0.001). The iWAT′s morphology and mitochondria were browning after DZF intervention. In HE-staining, the lipid droplets became smaller, and the number of mitochondria increased. The mitochondrial structure was remodeled under the electron microscope. The expression of UCP1, PGC-1α and PKA was elevated in iWAT detected by RT-qPCR (p < 0.05 or p < 0.001). In vitro, compared with the control group, 0.8 mg/mL DZF intervention significantly increased the number of mitochondria and expression of UCP1, PGC-1α, PKA, and pCREB (p < 0.05 or p < 0.01). In contrast, UCP1 and PGC-1α expression were significantly reversed after adding PKA inhibitor H-89 dihydrochloride.Conclusion: DZF can promote UCP1 expression by activating the PKA pathway, thereby promoting browning of WAT, attenuating obesity, and reducing obesity-related glucose and lipid metabolism abnormalities, indicating that DZF has the potential to be selected as an anti-obesity drug to benefit obese patients.

高热是临床常见症状,其病因错综复杂,属危重症范畴,中医在退热方面有天然的优势.但中医多种证型均可能出现高热症状,针对不同的证型,应当仔细思辨,分而治之.本文从中医辨证入手,从阴分郁热、伏暑晚发、阳气亏虚、邪伏少阳四个角度出发分析讨论,并附有治疗妇女经前高热、儿童感冒高热、老年高热、青年亚急性甲状腺炎高热的临床验案,以示其临床思路.

总结刘喜明教授从火热论治耳鸣的经验.遵《素问·脉解》"所谓耳鸣者,阳气万物盛上而跃",提出"火热上燔耳窍"为耳鸣核心病机,以虚实为纲,将火热病机分为阳盛、气郁、邪壅、阴亏4类,并依此确立直折火热、行气解郁、祛邪散壅、益阴潜阳四大治法,注重青葱管、石菖蒲、灵磁石等通窍引经药物的使用,多脏同调,虚实并治,清火热之源,复耳窍之机,并以验案4则佐证.

目的 观察中药代综方对棕榈酸(Palmitic acid,PA)诱导胰岛素抵抗(Insulin resistance,IR)的3T3-L1脂肪细胞中细胞因子瘦素、抵抗素、肿瘤坏死因子α(Tumor necrosis factor-α,TNF-α)的影响.方法 采用传统"鸡尾酒式"诱导3T3-L1前脂肪细胞分化成熟,用0.5 mmol/L PA建立IR模型.分为空白对照组、模型组、代综方低浓度组(含代综方生药量0.5 mg/ml)、代综方高浓度组(含代综方生药量2.0 mg/ml),干预48 h.葡萄糖氧化酶法检测培养上清中的葡萄糖浓度,计算葡萄糖基础消耗量(GBasic)和胰岛素刺激下消耗量(GIns),评价胰岛素敏感性指数(ISI).ELISA检测上清中瘦素、抵抗素、TNF-α的含量,Real-Time PCR检测瘦素、抵抗素、TNF-α的mRNA表达.结果 与空白对照组比较,模型组GIns、ISI均明显降低(P<0.01);与模型组比较,代综方高、低浓度组GBasic、GIns、ISI均明显升高(P<0.05,P<0.01),且代综方高浓度组GBasic、GIns、ISI较代综方低浓度组明显升高(P<0.05,P<0.01);与模型组比较,代综方高浓度组3T3-L1脂肪细胞上清中瘦素的含量明显增加(P<0.01),且抵抗素、TNF-α的含量明显减少(P<0.05,P<0.01);与模型组比较,代综方高浓度组3T3-L1脂肪细胞瘦素mRNA表达水平明显升高(P<0.01),且代综方低浓度和高浓度组抵抗素、TNF-αmRNA表达水平均明显降低(P<0.05,P<0.01).结论 代综方能够增加PA诱导的IR脂肪细胞葡萄糖消耗,提高胰岛素敏感性,同时上调瘦素水平,降低抵抗素、TNF-α水平.

医籍文献中清浊概念广泛存在"同词异义"现象,因不同取象来源构建的清浊概念具备不同的内涵.取象于天地生成意象的清浊观念,以升降属性为核心特征,后世升清降浊治法、谷气清浊体系、宣清导浊学说等分支理论或由此发展而来.取象于水流动静意象的清浊观念,则以动静属性为核心特征,继而演变出营卫清浊、病机清浊等学说.而中药药性认知也因受取象比类的清浊理论影响,形成了以质重味厚主降者为浊和以辛香雄烈主动者为浊的两种特色鲜明的药性清浊理论.

目的:探讨中药代综方(DZF)对不同方式诱导的脂肪细胞胰岛素抵抗(IR)的改善作用.方法:鸡尾酒式联合诱导3T3-L1前脂肪细胞分化成熟,分别采用棕榈酸(PA),高浓度葡萄糖(HG),地塞米松(DEX)诱导建立IR模型.不同质量浓度DZF提取物(含生药质量浓度2.0,0.5,0.1 g·L-1)干预24 h,另设模型组,罗格列酮(RSG)组,空白组.采用葡萄糖氧化酶法(GOD-POD)法检测培养上清中的葡萄糖浓度,计算葡萄糖基础消耗量(GBasic)和胰岛素刺激下葡萄糖消耗量(GIns),评价胰岛素敏感性指数(ISI).实时荧光定量聚合酶链式反应(Real-time PCR)测葡萄糖转运蛋白4(GLUT4) mRNA表达.结果:与模型组比较,3种模型中,DZF高浓度组GBasic,G1ns,ISI均明显增加(P＜0.05,P＜0.01);另外,PA诱导的IR模型中,DZF中浓度组GBasic,G1ns显著增加(P＜0.01),RSG组的GBasic,GIns,ISI明显增加(P＜0.05,P＜0.01);HG诱导的IR模型中,DZF中浓度组的G1ns,ISI显著增加(P＜0.05),RSG组GBasic,G1ns,ISI显著增加(P＜0.01);DEX诱导的IR模型中,RSG组GIns,ISI显著增加(P＜0.01);3种模型中,不同质量浓度组间存在差异,DZF高浓度组GBasic,G1ns,ISI较DZF中、低浓度组有不同程度的增加(p＜0.05).3种模型中,DZF高浓度组,RSG组均提高了GLUT4 mRNA表达(P＜0.05).结论:代综方能够减轻HG,DEX,PA诱导的脂肪细胞IR,存在一定的量效关系,同时具有非胰岛素依赖的增加葡萄糖摄取作用;其机制可能与提高GLUT4表达有关.

升降散出自清代陈良佐《二分析义·赔赈散方》之"赔赈散",为治疗温热与瘟疫名方.刘喜明教授认为温热疫疠之邪自口鼻而入为高热的常见病因,病机核心为邪热怫郁,临床辨证以高热、不恶寒、无汗、咽痛等为主症,治法为宣透开郁,逐秽解毒,服用必佐生蜂蜜与黄酒,另外根据热郁的部位,津液耗伤情况,以及是否兼有湿邪进行加减变化,服法以散剂为主,亦可用汤剂,空腹服用效果加倍.

目的 系统评价小儿推拿治疗12岁以下儿童迁延性、慢性腹泻的疗效及安全性. 方法 检索中国知网、万方数据知识平台、维普数据库等7个电子数据库及中国、美国临床试验注册系统,查找符合纳入标准的随机对照试验,检索时间为建库至2017年9月30日.采用偏倚风险评估量表评价纳入研究的方法学质量.对异质性较小的研究采用RevMan 5.3软件进行Meta分析,并根据GRADE证据分级标准评价证据级别.结果 共纳入13项随机对照试验,906例患者,纳入研究均存在高偏倚风险.Meta分析结果显示,小儿推拿单用[RR=2.70,95％CI (1.57,4.65),P＜0.05]或联合西药[RR=1.76,95％CI (1.21,2.55),P＜0.05]对照西药均能增加临床治愈率.单个研究结果也显示,小儿推拿联合参苓白术散或食疗临床治愈率优于参苓白术散[RR =2.35,95％CI (1.51,3.65),p＜0.05]或食疗[RR=2.70,95％CI(1.09,6.74),P=0.03]单独应用.现有证据不足以对小儿推拿的安全性进行评判.结论 小儿推拿单独使用或联合西药治疗12岁以下儿童迁延性、慢性腹泻的治愈率优于单纯西药治疗.但纳入文献质量较低,确切结论尚需更高质量的试验证实.