Obesity has become a critical public health challenge worldwide. Prioritizing prevention and tackling root causes—rather than merely managing symptoms—is critical to curbing this pandemic. Strategies that activate and expand brown adipose tissue and beige adipose tissue increase energy expenditure in animal models and offer therapeutic promise to treat obesity. Sanhuang Xiexin Decoction (SHX) is a well-known traditional Chinese medicine that possesses several beneficial effects, including anti-inflammatory and anti-atherosclerotic properties. This study aims to investigate whether SHX can alleviate obesity by promoting the browning process in adipose tissue. UPLC MS/MS was used to detect the constituents of SHX extraction, as well as the absorbed components of SHX in rat plasma. In vivo, C57BL/6 J mice were fed with 60

针对中药药理学沟通中西医、联系中西药、跨越医学和药学、衔接基础与临床的桥梁性课程特点,其专业知识体系中蕴含丰富的思想价值和精神内涵.在授课过程中,科学合理拓展课程广度、深度和温度,从课程涉及的专业、行业、国家、国际、文化、历史等角度深入挖掘思政元素,并结合中医药在新冠疫情防控中的积极作用,增加课程的知识性、人文性,加强医学生、药学生的医德医风教育,从中药药理学课程思政元素挖掘、实践与成效、建设的难点问题与解决方法以及未来实施的着力方向开展综述.

Ginkgo biloba Extract( GBE50) Dispersible Tablets is a new standardized prescription,which is widely used in the treatment of ischemic cardiovascular and cerebrovascular diseases. However,there are still many problems in its clinical application.Rational and safe use of GBE50 Dispersible Tablets is pivotal to the medication safety and clinical prognosis of patients. This consensus has been jointly formulated by clinical experts of traditional Chinese medicine and western medicine in cardiovascular and cerebrovascular diseases and followed the Manual for the Clinical Experts Consensus of Chinese Patent Medicine published by the China Association of Chinese Medicine. The present study identified clinical problems based on clinical investigation,searched the research papers according to PICO clinical problems,carried out evidence evaluation,classification,and recommendation by GRADE system,and reached the expert consensus with nominal group technique. The consensus combines evidence with expert experience. Sufficient evidence of clinical problems corresponds to " recommendations",while insufficient evidence to " suggestions". Safety issues of GBE50 Dispersible Tablets,such as indications,usage and dosage,and medication for special populations,are defined to improve clinical efficacy,promote rational medication,and reduce drug risks. This consensus needs to be revised based on emerging clinical issues and evidencebased updates in practical applications in the future.

"异病同治"是指不同的疾病,在其发展过程中,由于出现了相同的病机,而采用同一方法治疗的法则.恒古骨伤愈合剂由三七、红花、人参、黄芪、杜仲、鳖甲、钻地风、洋金花、陈皮组成,是现代中医临床"异病同治"的一种代表性药物.多项临床研究表明,恒古骨伤愈合剂治疗骨折、股骨头坏死、骨关节炎、腰椎间盘突出症等均取得了较好疗效.虽然现代医学认为这4种骨伤疾病的发病机制不同,但中医学认为其病因病机基本相同,均为瘀血、风湿痹阻、肝肾气血亏虚、经脉筋骨失养所致.恒古骨伤愈合剂针对这4种骨伤疾病"瘀血阻络、筋骨失养"的共同病机遣方用药,具有活血化瘀、散结生新、滋补肝肾、荣筋养骨的功效,充分体现了中医"圆机活法""异病同治""辨证用药"的理法特色.同时恒古骨伤愈合剂的现代药理机制研究及临床应用研究,也为其"一药多用"和"异病同治"提供了现代科学依据.本文从中医对4种骨伤疾病发病机理的认识、恒古骨伤愈合剂的方解及其治疗4种骨伤疾病的药理机制和临床运用4个方面,探讨并揭示了恒古骨伤愈合剂能"一药多用"和"异病同治"的科学内涵,为指导临床合理用药提供了借鉴.

Background Adipose tissue (e.g. white, brown and brite) plays a critical role in modulating energy metabolism. Activating brown adipose tissue (BAT) and inducing browning in white adipose tissue (WAT) has been proposed to be a potential molecular target for obesity treatment. Emodin is a natural anthraquinone derivative that exhibits variety of pharmacologic effects including lowering lipids and regulating glucose utilization. However, the underlying mechanism of action is still unclear. In the present study, we investigated whether emodin could alleviate obesity via promoting browning process in adipose tissue. Methods C57BL/6J mice were fed with high fat diet to induce obesity. Emodin at the doses of 40 and 80 mg/kg were orally given to obesity mice for consecutive 6 weeks. Parameters including fasting blood glucose, oral glucose tolerance, blood lipids, and the ratios of subcutaneous white adipose tissue (scWAT) or BAT mass to body weight, and morphology of adipose tissue were observed. Besides, the protein expression of uncoupling protein 1 (UCP1) and prohibitin in BAT and scWAT was determined by immunohistochemistry method. Relative mRNA expression of Cd137, transmembrane protein 26 (Tmem26) and Tbx1 in scWAT was analyzed using qRT-PCR. And the protein expression of UCP1, CD36, fatty acid transporter 4 (FATP4), peroxisome proliferator-activated receptor alpha (PPARα) and prohibitin of scWAT and BAT were analyzed using western blotting. In addition, ultra-high-performance liquid chromatography with electrospray ionization tandem mass spectrometry was utilized to detect the small lipid metabolites of scWAT and BAT. Results Emodin decreased the body weight and food intake in HFD-induced obesity mice, and it also improved the glucose tolerance and reduced the blood lipids. Emodin treatment induced beiging of WAT, and more multilocular lipid droplets were found in scWAT. Also, emodin significantly increased markers of beige adipocytes, e.g. Cd137, Tmem26 and Tbx1 mRNA in scWAT, and UCP1, CD36, FATP4, PPARα and prohibitin protein expression in scWAT and BAT. Furthermore, emodin perturbed the lipidomic profiles in scWAT and BAT of obese mice. Emodin increased total ceramides (Cers), lysophosphatidylcholines (LPCs), lyso-phosphatidylcholines oxygen (LPCs-O), and phosphatidylethanolamines oxygen (PEs-O) species concentration in scWAT. Specifically, emodin significantly up-regulated levels of Cer (34:1), LPC (18:2), LPC-(O-20:2), PC (O-40:7), PE (O-36:3), PE (O-38:6), PE (O-40:6), and sphingolipid (41:0) [SM (41:0)], and down-regulated PC (O-38:0), PE (O-40:4), PE (O-40:5) in scWAT of obesity mice. In terms of lipid matabolites of BAT, the emodin remarkably increased the total PCs levels, which was driven by significant increase of PC (30:0), PC (32:1), PC (32:2), PC (33:4) and PC (38:0) species. In addition, it also increased species of LPCs, e.g. LPC (20:0), LPC (20:1), LPC (22:0), LPC (22:1), LPC (24:0), and LPC (24:1). Especially, emodin treatment could reverse the ratio of PC/PE in HFD-induced obese mice. Conclusions These results indicated that emodin could ameliorate adiposity and improve metabolic disorders in obese mice. Also, emodin could promote browning in scWAT and activate the BAT activities. In addition, emodin treatment-induced changes to the scWAT and BAT lipidome were highly specific to certain molecular lipid species, indicating that changes in tissue lipid content reflects selective remodeling in scWAT and BAT of both glycerophospholipids and sphingolipids in response to emodin treatment.

目的 研究大黄素对老龄小鼠脂质代谢的影响及其潜在机制.方法 40只10月龄SPF级C57BL/6J小鼠随机分为老龄组、大黄素40 mg·kg-1组、大黄素80 mg·kg-1组和罗格列酮10 mg·kg-1组,另设10只8周龄C57BL/6J小鼠为非老龄组,各给药组连续灌胃给药6周.监测各组小鼠体质量,末次给药后取材,测定血清三酰甘油(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、游离脂肪酸(FFA)、瘦素(LEP)和脂联素(ADPN)含量;HE染色观察小鼠皮下脂肪组织及棕色脂肪组织形态变化;免疫组化法检测皮下白色脂肪组织和棕色脂肪组织解偶联蛋白1(UCP1)表达.结果 大黄素干预可显著降低TC、TG、FFA含量(P<0.05),升高血清ADPN含量(P<0.05).此外,大黄素干预组小鼠皮下白色脂肪细胞出现多室,细胞变小、变圆,具有棕色化趋势,同时白色脂肪组织(WAT)和棕色脂肪组织(BAT)中UCP1阳性细胞表达升高(P<0.05).结论 老龄小鼠可出现脂质代谢紊乱,白色脂肪组织比重增加,脂肪呈现白色化趋势.大黄素可改善老龄动物的脂质代谢紊乱,其作用可能与促进脂肪棕色化有关.

糖尿病心肌病(DCM)是糖尿病特异性心脏并发症,可独立于冠状动脉疾病、高血压或瓣膜性心脏病发生.目前公认的发病机制包括高血糖、蛋白非酶糖基化、氧化应激、钙离子转运异常等,其中炎症是导致左心室舒张功能障碍的独立因素.NLRP3是最常见的炎性小体,可诱导分泌IL-1β、IL-18等促炎细胞因子以及介导细胞焦亡.DCM发生时NLRP3表达上调,加剧胰岛β细胞功能受损、心肌损伤、心肌纤维化进程.已有研究证实,中药可通过抑制NLRP3炎性小体的启动和活化,以及其下游基因的表达,改善DCM心脏功能.本文就NLRP3炎性小体参与DCM发生及中药干预作用进行综述.

目的 研究益肾强身丸和防衰益寿丸对雄性小鼠生殖功能的改善作用.方法 将48只2月龄C57BL/6J小鼠随机分为对照组,益肾强身丸+防衰益寿丸低剂量组(YS 0.25 g·kg-1+FS 0.25 g·kg-1组)、高剂量组(YS 0.5 g·kg-1+FS 0.5 g·kg-1组),五子衍宗丸1 g·kg-1组(简称阳性药组).高、低剂量组每日上午灌胃对应剂量的益肾强身丸溶液,下午灌胃对应剂量的防衰益寿丸溶液;对照组及阳性药组每日上午灌胃相应的饮用水和五子衍宗丸,连续30 d.记录小鼠7、14、21、28 d跨骑次数、相关脏器指数、精子数目和活性、血清睾酮、海绵体组织NO和cGMP水平.结果 与对照组比较,低剂量组可提高小鼠性行为次数(P<0.01),低、高剂量组均可增加精子数目、提高精子活率及活力且降低精子畸形率(P<0.01,P<0.001);高剂量组可提高海绵体cGMP水平(P<0.001);低、高剂量组均对性器官指数没有影响.结论 益肾强身丸和防衰益寿丸可改善雄性小鼠的生殖功能.

中药药理实验属于生命科学研究范畴,是中药药理学的重要组成部分.在中药药理实验教学中,要强化基本实验技能训练,建立实验操作规范;减少验证性试验,开展综合性、设计性实验,培养学生运用知识的能力和创新能力.

目的 探究LDLR基因敲除(LDLR-/-)小鼠皮下腹股沟脂肪基因表达谱的变化及差异基因涉及的生物过程和信号通路.方法 采用高脂饲料喂养LDLR基因敲除小鼠的肥胖模型,利用基因芯片技术分析正常C57BL/6J小鼠与肥胖模型小鼠皮下腹股沟脂肪组织中基因表达谱的差异及差异基因涉及的信号通路.结果 与正常C57BL/6J小鼠比较,LDLR基因敲除小鼠皮下腹股沟脂肪组织中差异表达基因有602个,其中上调基因有394个,下调基因308个.GO富集和Pathways分析结果显示,这些差异基因的生物过程主要有炎症反应、免疫系统过程、及T细胞增殖的正向调控;信号通路主要有B细胞受体信号通路、自然杀伤细胞介导的细胞毒性、Toll样受体信号通路和趋化因子信号通路.结论 B细胞受体信号通路、自然杀伤细胞介导的细胞毒性、Toll样受体信号通路和趋化因子信号通路中的差异基因可能涉及肥胖发病的机制,为肥胖及相关代谢疾病药物的研发提供依据.

目前,全球大约22亿人超重,约占全球总人口的1/3,其中约7.12亿人(占全球总人口的10％)是肥胖人群[1].肥胖主要是由于机体长期处于能量储存大于能量消耗的一种状态下所造成的体内白色脂肪组织与棕色脂肪失衡.白色脂肪组织的功能主要是将机体中过剩的能量以中性脂肪的形式贮存起来,以供机体需求时利用.棕色脂肪组织的主要功能是促进机体产热.近年来,随着对肥胖和相关代谢疾病的深入研究,发现棕色脂肪组织具有提高机体能量代谢的特殊生理功能,在维持体温和调控能量平衡方面发挥着重要的作用.棕色脂肪组织中含有一种位于线粒体内膜上的载体蛋白,即解偶联蛋白-1(Uncoupling protein 1,UCP-1).UCP-1可以将H+从线粒体内膜渗漏到线粒体基质中,阻止ADP磷酸化形成ATP,将能量以热能的形式散失.

<span id="ChDivSummary" name="ChDivSummary" class="abstract-text">目的观察冷暴露对高脂饮食小鼠脂肪棕色化的影响。方法 8周龄♂C57BL/6J小鼠高脂饮食8周后,随机分为高脂冷暴露组和高脂室温组;同周龄♂C57BL/6J小鼠给予基础饲料喂养8周后,随机分为正常冷暴露组及正常室温组。各组小鼠每天在同一时间段相应温度干预2 h,连续干预8周。检测体质量、进食量、i WAT及BAT重量、血糖、血脂、LEP、ADPN、脂肪组织病理特征,以及UCP1和PHB在i WAT、BAT中原位蛋白表达。结果冷暴露可明显降低高脂饮食小鼠体质量、血糖、i WAT重量/体质量比值、血清中TC、TG、LDL-C及LEP含量,增加进食量及BAT重量/体质量比值; HE染色显示,i WAT和BAT细胞变小且出现多室,i WAT具有棕色化趋势;免疫组化染色显示,i WAT和BAT中UCP1和PHB蛋白表达明显增加。结论冷暴露能对抗高脂饮食造成的体质量增长,其作用可能与激活棕色脂肪组织及诱导脂肪棕色化,增加产热,减少白色脂肪堆积有关。</span>

Objective To investigate the effects of Maiqi-Jiangtang pill on the glycolipid level in type 2 diabetic ob/ob mice.Methods The 8-week old male ob/ob mice were randomly divided into Maiqi-Jiangtang pill high- (8 g/kg), medium- (4 g/kg), low- (2 g/kg) dose groups. All the mice orally adiministered with the drugs once a day for 10 weeks. The same week age normal C57BL/6J control mice and ob/ob model group mice were orally administered with the equal volume solvent. The body weight per week were recorded. The fasting blood-glucose (FBG) was measured by glycemic instrument. The content of TG, TC, HDL-C, LDL-C in serum, and TG and TC content in liver were determined by biochemical method. The liver index was calculated.Results Compared with ob/ob model group, there was no significant change in body weight of mice administered with Maiqi-Jiangtang pill for 10 weeks. Compared with the model group, the low-, medium- dose Maiqi-Jiangtang pill could significantly decrease the FBG (7.43 ± 1.71 mmol/L,7.84 ± 1.09 mmol/L vs.8.95 ± 0.96mmol/L), the high- dose Maiqi-Jiangtang pill could significantly reduce the TG (0.93 ± 0.16 mmol/L vs.1.18 ± 0.26 mmol/L) and LDL-C (2.10 ± 0.51 mmol/L vs.2.56 ± 0.44 mmol/L) content in serum of ob/ob mice (P<0.05), increase the HDL-C/LDL-C ratio (2.40 ± 0.39vs.1.96 ± 0.24) in serum (P<0.01), decrease the liver weight (3.52 ± 0.26 gvs. 3.98 ± 0.35 g) and the liver index (0.063 ± 0.004vs. 0.071 ± 0.006) (P<0.05). Compared with the model group, the low dose Maiqi-Jiangtang pill could also significantly decrease the TG level (0.63 ± 0.25 mmol/gvs. 1.05 ± 0.67 mmol/g) in liver and significantly increase the HDL-C/LDL-C ratio (2.30 ± 0.44vs. 1.96 ± 0.24) in serum (P<0.05).Conclusions The Maiqi-Jiangtang pill can reduce lipid in serum and liver of ob/ob mice while it can decrease the blood glucose, which need to further study its mechanism.

目的 研究麦芪降糖丸对ob/ob小鼠血糖的影响.方法 8周龄雄性ob/ob小鼠随机分成模型组,麦芪降糖丸高、中、低剂量(8 g/kg、4 g/kg、2 g/kg)组和二甲双胍(250 mg/kg)组,各给药组分别灌胃给予相应剂量的药物,每天1次,连续10周,同周龄正常对照组C57BL/6 J小鼠和模型对照组ob/ob小鼠给予等体积的溶剂.检测每组小鼠日平均进食量和体重、空腹血糖、血清胰岛素水平和胰腺病理变化.结果 麦芪降糖丸给药2周、6周、8周、10周时能明显降低ob/ob小鼠空腹血糖(P<0.05,P<0.01),给药10周对小鼠日平均进食量和体重无明显影响,能减轻ob/ob小鼠的胰腺胰岛细胞的病变程度,提高ob/ob小鼠空腹血清胰岛素水平(P<0.05).结论 麦芪降糖丸能降低ob/ob小鼠血糖,可能与减轻胰腺病理损伤,促进胰岛素分泌有关.

创新和创新思维为推动创新中国建设提供重要遵循,创造性人才的培养符合当代国情要求.药理学是医药院校重要的基础学科,在指导临床合理用药和新药研发中发挥重要作用.该课程的理论体系涉及多个学科的内容,知识点复杂,给教学带来很多挑战.同时,药理学理论体系也具备丰富的内在逻辑.创新思维的逻辑训练在提高药理学课程的学习效率和知识转化率、提升学生的学习主动性、培养创新人才方面发挥了重要作用.常用的逻辑训练方法包括演绎推理法、归纳推理法、实验法和批判性思维法等.实践结果发现,在教学过程中嵌入逻辑方法训练,有助于增加师生互动、提高学生自主学习能力及培养创新思维.

Cultivating students' autonomic learning ability is an important research area . It is very important to build a reasonable evaluation system in the process of cultivating students' autonomic learning ability. Based on the autonomic learning content and teaching methods of pharmacology of traditional Chinese medicine, this paper discusses the design and implementation strategies of pluralistic evaluation system including learning in the classroom, expands the learning out of the classroom, experimental operation and final examination, which emphasizes the combination of process evaluation and the participation of teachers and students. It is beneficial to stimulate students'self-learning motivation and improve their self-learning ability and learning effect.

Background: Diabetic cardiomyopathy (DCM) is considered to be a distinct clinical entity independent of concomitant macro- and microvascular disorders, which is initiated partly by disturbances in energy substrates. This study was to observe the dynamic modulations of berberine in DCM rats and explore the changes of lipidomic profiles of myocardial tissue. Methods: Sprague-Dawley (SD) rats were fed high-sucrose and high-fat diet (HSHFD) for totally 22 weeks and intraperitoneally (i.p.) injected with 30 mg/kg of streptozotocin (STZ) at the fifth week to induce DCM. Seventy-two hours after STZ injection, the rats were orally given with berberine at 10, 30 mg/kg and metformin at 200 mg/kg, respectively. Dynamic changes of cardiac function, heart mass ratios and blood lipids were observed at f 4, 10, 16, and 22, respectively. Furthermore, lipid metabolites in myocardial tissue at week 16 were profiled by the ultra-high-performance liquid chromatography coupled to a quadruple time of flight mass spectrometer (UPLC/Q-TOF/MS) approach. Results: Berberine could protect against cardiac diastolic and systolic dysfunctions, as well as cardiac hypertrophy, and the most effective duration is with 16-week of administration. Meanwhile, 17 potential biomarkers of phosphatidylcholines (PCs), phosphatidylethanolamines (PEs) and sphingolipids (SMs) of DCM induced by HSFD/STZ were identified. The perturbations of lipidomic profiles could be partly reversed with berberine intervention, i.e., PC (16:0/20:4), PC (18:2/0:0), PC (18:0/18:2), PC (18:0/22:5), PC (20:4/0:0), PC (20:4/18:0), PC (20:4/18:1), PC (20:4/20:2), PE (18:2/0:0), and SM (d18:0/16:0). Conclusions: These results indicated a close relationship between PCs, PEs and SMs and cardiac damage mechanisms during development of DCM. The therapeutic effects of berberine on DCM are partly caused by interferences with PCs, PEs, and SMs metabolisms.