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| 1 | Duhuo Jisheng Decoction inhibits SDF-1-induced inflammation and matrix degradation in human degenerative nucleus pulposus cells in vitro through the CXCR4/NF-KB pathway显示文摘 | Zong-chao LIU Zhen-long WANG Chen-yi HUANG Zhi-jiang FU Yong LIU Zhang-chao WEI Shi-gui LIU Chuan MA Jie-liang SHEN Dayue Darrel DUAN | 2018 | Acta Pharmacologica Sinica2018，39，6： | 29 |
| 2 | The CIC-3 chloride channels in cardiovascular disease显示文摘 | Dayue Darrel DUAN | 2011 | Acta Pharmacologica Sinica2011，32，6： | 26 |
| 3 | Fangjiomics: revealing adaptive omics pharmacological mechanisms of the myriad combination therapies to achieve personalized medicine显示文摘 | Dayue Darrel DUAN Zhong WANG Bo-li ZHANG Yong-yan WANG | 2015 | Acta Pharmacologica Sinica2015，36，6： | 11 |
| 4 | 药物表型组学:药理毒理学和个体化医学的新模式(英文)显示文摘近年来,药物基因组学(pharmacogenomics)研究收集了大量有关遗传多态性对药物反应(疗效和毒性反应)的普遍影响的信息,并突出显示了基因组指导下的个体化药物治疗的必要性。然而,由于疾病和药物治疗临床效果和毒性反应的内在复杂性,并且往往涉及数十个或数百个基因和环境因素的动态变化的影响,将药物基因组学的知识转化为个体化医学的临床实践面临着重大的挑战和障碍。为了克服这些障碍,些包括药物蛋白质组学(pharmacoproteomics)和药物代谢组学(pharmacometabolomics)等在内的新学科应运而生。同时,这些'组学'研究也揭示了在越来越详细的基因组/蛋白质组学/代谢组学的变异性与目前定义的各种临床疾病和药物治疗表型的复杂性之间存在着种非平行关系。因而要种新的研究模式来重新定义这种表型与基因组/蛋白质组/代谢组之间的非平行关系。此文将介绍个跨领域的新学科,它能为从只注重于单纯的表型-基因型关系的研究模式转化到系统性的表型组-基因组关系的研究方法提供整套新的技术平台,从而在系统生物学水平重新定义具有整合性的药物治疗靶点群,改进药物研究的模式,使其更适合于临床个体化医学与药物治疗。这个新学科就是'药物表型组学(pharmacophenomics)'。表型组(phenome)是在特定环境影响下有机体基因组/蛋白质组/代谢组表达的整体表型特征的总和。表型组学(phenomics)则是对表型组与基因组/转录组(transcritome)/蛋白质组/代谢组/相互作用组(interactome)和环境因素变化之间的复杂关系的定量研究。药物表型组学将系统性地确定对应于定义明确的疾病表型组的综合性药物靶标群。因此,药物表型组学将与药物基因组学、药物蛋白质组学组学和药物代谢组学等学科互补,为药物作用和毒性的研究提供个革命性的新模式。 | Dayue Darrel DUAN 韩业山 李立 赵建中 王忠 | 2014 | 中国药理学与毒理学杂志2014，28，1： | 10 |
| 5 | Tumor exosomes: a double-edged sword in cancer therapy显示文摘肿瘤房间比正常房间生产并且藏匿更多的 nucleic 酸,蛋白质和类脂化合物。这些分子在包含膜的 exosomes 在血或在房间附近被搬运。导出肿瘤或联系肿瘤的 exosomes (通常在直径的 30-100 nm ) 包含与为涉及癌症的致病,发展,前进,和转移的细胞间的通讯表明送信人一起父母房间类似于那些的丰富的生物内容。当这些 exosomes 能从各种各样的身体液体被检测并且孤立,他们为癌症的诊断和预后成为了吸引人的新 biomarkers。而且,肿瘤 exosomes 也为癌症的治疗由于他们的潜在的同样新奇的治疗学的策略吸引了增加的注意。在一方面,包含膜的泡正在答应药和指向特定的癌症房间的另外的治疗学的材料的搬运人的类脂化合物 bilayer。在另一方面,肿瘤 exosomes 是为象 chemoresistance 一样安排对癌症房间的生长和转移批评的事件的微型环境的调整的重要调停人。这里,我们在最近的年里在我们联系肿瘤或导出肿瘤的 exosomes 的理解总结进展,并且更重要地在癌症的癌症开发,前进,侵略,和转移并且,讨论他们的角色,他们在为各种各样的癌症以及重要警告的精确治疗的策略的潜力。 | Wei SUN Ju-dong LUO Hua JIANG Dayue Darrel DUAN | 2018 | Acta Pharmacologica Sinica2018，39，4： | 9 |
| 6 | Characterization of a critical role for CFTR chloride channels in cardioprotection against ischemia/ reperfusion injury显示文摘目的: 进一步描绘膀胱的纤维变性 transmembrane 传导力管理者(CFTR ) 的功能的角色在早、迟了(第二扇窗户) ischemic preconditioning (欧洲电脑生产厂商)- 并且 postconditioning (停靠港) 调停了对 ischemia/reperfusion (I/R ) 的 cardioprotection 损害。 | Sunny Yang XIANG Linda L YE Li-lu Marie DUAN Li-hui LIU Zhi-dong GE John A AUCHAMPACH Garrett J GROSS Dayue Darrel DUAN | 2011 | Acta Pharmacologica Sinica2011，32，6： | 9 |
| 7 | Chrysophanol protects against doxorubicin-induced cardiotoxicity by suppressing cellular PARylation显示文摘The clinical application of doxorubicin(DOX) in cancer chemotherapy is limited by its lifethreatening cardiotoxic effects. Chrysophanol(CHR), an anthraquinone compound isolated from the rhizome of Rheum palmatum L., is considered to play a broad role in a variety of biological processes.However, the effects of CHR’s cardioprotection in DOX-induced cardiomyopathy is poorly understood. In this study, we found that the cardiac apoptosis, mitochondrial injury and cellular PARylation levels were significantly increased in H9 C2 cells treated by Dox, while these effects were suppressed by CHR. Similar results were observed when PARP1 activity was suppressed by its inhibitors 3-aminobenzamide(3 AB)and ABT888. Ectopic expression of PARP1 effectively blocked this CHR’s cardioprotection against DOX-induced cardiomyocyte injury in H9 C2 cells. Furthermore, pre-administration with both CHR and 3 AB relieved DOX-induced cardiac apoptosis, mitochondrial impairment and heart dysfunction in Sprague–Dawley rat model. These results revealed that CHR protects against DOX-induced cardiotoxicity by suppressing cellular PARylation and provided critical evidence that PARylation may be a novel target for DOX-induced cardiomyopathy. | Jing Lu Jingyan Li Yuehuai Hu Zhen Guo Duanping Sun Panxia Wang Kaiteng Guo Dayue Darrel Duan Si Gao Jianmin Jiang Junjian Wang Peiqing Liu | 2019 | Acta Pharmaceutica Sinica B2019，9，4： | 8 |
| 8 | Chloride channels in stroke显示文摘脉管包括脉管的光滑的肌肉房间(VSMC ) 的增长,移植,和 apoptosis,服的小动脉改变在大脑是在动脉和血流动或出血的突然的打断的代表性的区域和直径的变化的主要原因,即,中风。积累的证据强烈为氯化物支持一个重要角色(在脉管的改变和击的 Cl −) 隧道。至少三 Cl − 隧道基因在 VSMC 被表示:1 ) TMEM16A (或 Ano1 ) ,它可以编码激活钙的 Cl − 隧道(CACC ) ;2 ) CLC-3 Cl − 隧道和 Cl −/H+ antiporter,它是仔细与调整卷的 Cl − 隧道(VRCC ) 有关;并且 3 ) 膀胱的纤维变性 transmembrane 传导力管理者(CFTR ) 它编码激活 PKA 、激活 PKC 的 Cl − 隧道。由细胞内部的 Ca 2+ 的导致收缩筋的增加的 CACC 的激活引起 VSMC 的膜去极,血管缩小,和抑制增长。由房间体积增加或膜段的 VRCC 的激活支持反应的氧种类的生产,导致增长并且禁止 VSMC 的 apoptosis。CFTR 的激活禁止氧化应力并且可以阻止高血压的发展。另外, Cl − 电流由 gamma-aminobutyric 酸(伽马氨基丁酸) 调停了受体也被含有在 ischemic 神经原死亡的一个角色。这评论在中风的发展集中于 Cl − 隧道的功能的角色并且在未来方向上提供一个观点让研究和潜力为中风的预防和治疗作为新目标开发 Cl − 隧道。 | Ya-ping ZHANG Hao ZHANG Dayue Darrel DUAN | 2013 | Acta Pharmacologica Sinica2013，34，1： | 8 |
| 9 | New omic and network paradigms for deep understanding of therapeutic mechanisms for Fangji of traditional Chinese medicine显示文摘 | Dayue Darrel DUAN Zhong WANG Yong-yan WANG | 2018 | Acta Pharmacologica Sinica2018，39，6： | 4 |
| 10 | Drinking water temperature affects cognitive function and progression of Alzheimer’s disease in a mouse model显示文摘Lifestyle factors may affect mental health and play a critical role in the development of neurodegenerative diseases including Alzheimer’s disease(AD).However,whether the temperatures of daily beverages have any impact on cognitive function and AD development has never been studied.In this study,we investigated the effects of daily drinking water temperatures on cognitive function and AD development and progression in mice and the underlying mechanisms.Cognitive function of mice was assessed using passive avoidance test,open field test,and Morris water maze.Wild-type Kunming mice receiving intragastric water(IW,10 mL/kg,2 times/day)at 0℃ for consecutive 15 days displayed significant cognitive defects accompanied by significant decrease in gain of body weight,gastric emptying rate,pepsin activity,and an increase in the energy charge in the cortex when compared with mice receiving the same amount of IW at 25℃(a temperature mimicking most common drinking habits in human),suggesting the altered neuroenergetics may cause cognitive decline.Similarly,in the transgenic APPwse/PS1De9 familial AD mice and their age-and gender-matched wild-type C57BL/6 mice,receiving IW at 0℃,but not at 25℃,for 35 days caused a significant time-dependent decrease in body weight and cognitive function,accompanied by a decreased expression of PI3K,Akt,the glutamate/GABA ratio,as well as neuropathy with significant amyloid lesion in the cortex and hippocampus.All of these changes were significantly aggravated in the APPwse/PS1De9 mice than in the control C57BL/6 mice.These data demonstrate that daily beverage at 0℃ may alter brain insulin-mediated neuroenergetics,glutamate/GABA ratio,cause cognitive decline and neuropathy,and promote AD progression. | Jiang-ping Wei Wen Wen Yuan Dai Li-xia Qin Yue-qiang Wen Dayue Darrel Duan Shi-jun Xu | 2021 | Acta Pharmacologica Sinica2021，42，1： | 2 |
| 11 | Extracellular vesicles as novel biomarkers and pharmaceutic targets of diseases显示文摘 | Yanfang CHEN Yaoliang TANG Guo-Chang FAN Dayue Darrel DUAN | 2018 | Acta Pharmacologica Sinica2018，39，4： | 1 |
| 12 | Astragaloside IV derivative HHQ16 ameliorates infarctioninduced hypertrophy and heart failure through degradation of lncRNA4012/9456显示文摘Reversing ventricular remodeling represents a promising treatment for the post-myocardial infarction(MI)heart failure(HF).Here,we report a novel small molecule HHQ16,an optimized derivative of astragaloside IV,which effectively reversed infarction-induced myocardial remodeling and improved cardiac function by directly acting on the cardiomyocyte to reverse hypertrophy.The effect of HHQ16 was associated with a strong inhibition of a newly discovered Egr2-affliated transcript Inc9456 in the heart.While minimally expressed in normal mouse heart,Inc9456 was dramatically upregulated in the heart subjected to left anterior descending coronary artery ligation(LADL)and in cardiomyocytes subjected to hypertrophic stimulation.The critical role of Inc9456 in cardiomyocyte hypertrophy was confirmed by specific overexpression and knockout in vitro.A physical interaction between Inc9456 and G3BP2 increased NF-kB nuclear translocation,triggering hypertrophy-related cascades.HHQ16 physically bound to Inc9456 with a high-affinity and induced its degradation.Cardiomyocyte-specific Inc9456 overexpression induced,but knockout prevented LADL-induced,cardiac hypertrophy and dysfunction.HHQ16 reversed the effect of Inc9456 overexpression while lost its protective role when Inc9456 was deleted,further confirming Inc9456 as the bona fide target of HHQ16.We further identified the human ortholog of Inc9456,also an Egr2-affliated transcript,Inc4012.Similarly,Inc4012 was significantly upregulated in hypertrophied failing hearts of patients with dilated cardiomyopathy.HHQ16 also specifically bound to Inc4012 and caused its degradation and antagonized its hypertrophic effects.Targeted degradation of pathological increased Inc4012/lnc9456 by small molecules might serve as a novel promising strategy to regress infarction-induced cardiac hypertrophy and HF. | Jingjing Wan Zhen Zhang hennan Wu Saisai Tianbei Zang Ge Jin Qingyan Sun Pin Wang Xin Luan Yili Yang Xuelin Zhan Lingyu Linda Ye Dayue Darrel Duan Xia Liu Weidong Zhang | 2023 | Signal Transduction and Targeted Therapy2023，8，11： | 0 |
| 13 | A molecular switch of "Yin and Yang": S-glutathionylation of eNOS turns off NO synthesis and turns on superoxide generation显示文摘 | Dayue Darrel DUAN Chiu-yin KWAN | 2011 | Acta Pharmacologica Sinica2011，32，4： | 0 |
| 14 | Channelopathies and drug discovery in the postgenomic era显示文摘 | Dayue Darrel DUAN Tong-hui MA | 2011 | Acta Pharmacologica Sinica2011，32，6： | 0 |
| 15 | Chloride channels in vascular function and disease显示文摘Vascular smooth muscle cells(VSMCs) are the major component of vascular wall which are often stretched and compressed by pounding intravascular pressure.These mechanical signals are usually transformed to electrical signals by the opening or closing of ion channels in VSNCs and endothelial cells.Intravascular pressure causes a graded membrane potential depolarization of the VSMCs and leads to vasoconstriction(i.e.,myogenic response),independent of the vascular endothelium. Although the important role of cation channels including L-type Ca2+ channels,K+ channels,and TRP channels in the regulation of vascular tone has been well established the functional roles played by Cl- channels in the regulation of the membrane potential and vascular tone remain essentially obscure. Recent emerging evidence implicates very important roles of Cl- channels in vascular function ranging from the control of membrane potential equilibrium, vascular contraction and relaxation to the regulation of intracellular pH,cell volume homeostasis,cell proliferation,migration,and apoptosis. | Dayue Darrel Duan Lingyu Linda Ye | 2011 | 岭南心血管病杂志2011，17，S1： | 0 |
| 16 | Phenome-wide association study and precision medicine of cardiovascular diseases in the post-COVID-19 era显示文摘SARS-CoV-2 infection causes injuries of not only the lungs but also the heart and endothelial cells in vasculature of multiple organs,and induces systemic inflammation and immune over-reactions,which makes COVID-19 a disease phenome that simultaneously affects multiple systems.Cardiovascular diseases(CVD)are intrinsic risk and causative factors for severe COVID-19 comorbidities and death.The wide-spread infection and reinfection of SARS-CoV-2 variants and the long-COVID may become a new common threat to human health and propose unprecedented impact on the risk factors,pathophysiology,and pharmacology of many diseases including CVD for a long time.COVID-19 has highlighted the urgent demand for precision medicine which needs new knowledge network to innovate disease taxonomy for more precise diagnosis,therapy,and prevention of disease.A deeper understanding of CVD in the setting of COVID-19 phenome requires a paradigm shift from the current phenotypic study that focuses on the virus or individual symptoms to phenomics of COVID-19 that addresses the inter-connectedness of clinical phenotypes,i.e.,clinical phenome.Here,we summarize the CVD manifestations in the full clinical spectrum of COVID-19,and the phenome-wide association study of CVD interrelated to COVID-19.We discuss the underlying biology for CVD in the COVID-19 phenome and the concept of precision medicine with new phenomic taxonomy that addresses the overall pathophysiological responses of the body to the SARS-CoV-2 infection.We also briefly discuss the unique taxonomy of disease as Zheng-hou patterns in traditional Chinese medicine,and their potential implications in precision medicine of CVD in the post-COVID-19 era. | Qian Cao Xin Du Xiao-yan Jiang Yuan Tian Chen-hao Gao Zi-yu Liu Ting Xu Xing-xing Tao Ming Lei Xiao-qiang Wang Lingyu Linda Ye Dayue Darrel Duan | 2023 | Acta Pharmacologica Sinica2023，44，12： | 0 |
| 17 | S1B-1 CLC-3 Chloride Channels in the Nervous System:Missed Targets in Cerebrovascular and Brain Diseases?显示文摘CLC-3 chloride(Cl-)channel,a member of an extended family of voltagegated CLC chloride channels and transporters,are ubiquitously expressed throughout the nervous system,including in the cerebrovascular smooth muscle cells(CVSMC)and neurons in the brain.CLC-3 chloride channels play critical roles in the regulation of vascular tone and cell volume regulation,migration,proliferation,and apoptosis.Remodeling of CLC-3 Cl-channels in CVSMC contributes significantly to the development of vascular pathology and remodeling and may be novel mechanisms for hypertension and stroke.Targeting Cl-channels may be a novel therapeutic strategy for the treatment of hypertension and stroke.CLC-3 Cl-channels are also involved in neuronal apoptosis and are important regulators of cell volume and hippocampal neuronal apoptosis.Expression of CLC-3 in the presynaptic vesicles determines quantal size of inhibitory transmission in the hippocampus through impact on GABAergic synaptic transmission.A distinct presynaptic CLC-3 dependent regulatory mechanism may represent a novel target for the regulation of synaptic vesicle acidification and filling.It extends the role of Cl-in inhibitory transmission from that of a postsynaptic permeant species to a presynaptic regulatory element.The CLC-3 Cl-channels are important targets for glioma and cancer therapy.CLC-3 channels(Cl.vol)/transporters may play important roles in the regulation of many cellular functions and integrate their physiological and pathological roles with multi-chloride channels,including TMEM16A(Cl.ca),CFTR at the phenomic level in the cerebrovascular and nervous system.Deep understandings of CLC-3 Cl-channels expression and function in the nervous system may provide novel molecular insights into the cerebrovascular disease and brain disease including brain cancers. | Dayue Darrel Duan Lingyu Linda Ye YANG Si-Jin | 2018 | 神经药理学报2018，8，4： | 0 |
| 18 | 大肠癌脾虚湿热证和湿热蕴结证临床表型组的代谢组学机制显示文摘目的阐明大肠癌脾虚湿热证表型组和湿热蕴结证表型组的代谢组学机制。方法2021年3月—2021年10月于西南医科大学附属中医医院招募大肠癌脾虚湿热证患者68例、湿热蕴结证患者58例,同时纳入于此进行体检的健康平和质人员62名。建立脾虚湿热证表型组、湿热蕴结证表型组和健康平和质表型组队列,以超高液相色谱和质谱联用技术对各队列血清代谢物进行分离鉴定,并进行主成分分析(PCA)、正交偏最小二乘判别分析法(OLPS-DA)分析及生物信息学分析。结果与健康平和质表型组相比,脾虚湿热证表型组有胍基乙酸下调,亚氨甲基谷氨酸、咪唑乙酸、脱氧尿苷、胞苷、假尿苷、鸟氨酸、N-乙酰鸟氨酸、5-羟吲哚乙酸、胆色素原、琥珀酸半醛、甜醇表达上调等12种差异代谢,涉及能量代谢异常为主的7条代谢途径;湿热蕴结证表型组有脱氧尿苷、胞苷、胆色素原、花生酸、前列腺素B2、异柠檬酸、古洛糖酸表达上调,胍基乙酸、尿苷、羟脯氨酸、吡咯-2-羧酸、腺苷、5,6-DHET、8,9-DiHETrE、9,10-DHOME、亚油酸、羟基丙酮酸表达下调等17种差异代谢,涉及脂类代谢和三羧酸循环异常为主的9条代谢途径;脾虚湿热证表型组与湿热蕴结证表型组存在4个相同特征性代谢物(胍基乙酸、脱氧尿苷、胞苷、胆色素原)差异。结论这些结果揭示了形成大肠癌脾虚湿热证和湿热蕴结证两个常见临床表型组的代谢组学机制,并为中医辨证和诊治提供临床表型组的循证依据和特异性代谢组学客观依据。 | 田园 杨忠明 杜鑫 黄进 YELingyu Linda DUAN Dayue Darrel | 2023 | 北京中医药大学学报2023，46，12： | 0 |
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