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Acta Pharmaceutica Sinica B 2015年第4期5卷 330-336页

作者： Yue Sheng Bo Sun Xin Xie Na Li Deli Dong The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular Research Ministry of Education Department of PharmacologyHarbin Medical University

Our previous work found that DMH1(4-[6-(4-isopropoxyphenyl)pyrazolo [1,5-a]pyrimidin-3-yl]quinoline) was a novel autophagy inhibitor. Here, we aimed to investigate the effects of DMH1 on chemotherapeutic drug-induced autophagy as well as the efficacy of chemotherapeutic drugs in different cancer cells. We found that DMH1 inhibited tamoxifen- and cispcis-diaminedichloroplatinum(II)(CDDP)-induced autophagy responses in MCF-7 and HeLa cells, and potentiated the anti-tumor activity of tamoxifen and CDDP for both cells. DMH1 inhibited 5-fluorouracil(5-FU)-induced autophagy responses in MCF-7 and HeLa cells, but did not affect the anti-tumor activity of 5-FU for these two cell lines. DMH1 itself did not induce cell death in MCF-7 and HeLa cells, but inhibited the proliferation of these cells. In conclusion, DMH1 inhibits chemotherapeutic drug-induced autophagy response and the enhancement of efficacy of chemotherapeutic drugs by DMH1 is dependent on the cell sensitivity to drugs.

关键词： Autophagy Tamoxifen 5-Fluorouracil Cancer cells

Anthelmintics nitazoxanide protects against experimental hyperlipidemia and hepatic steatosis in hamsters and mice

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Acta Pharmaceutica Sinica B 2022年第3期12卷 1322-1338页

作者： Fengfeng Li Man Jiang Minghui Ma Xuyang Chen Yidan Zhang Yixin Zhang Yuanyuan Yu Yunfeng Cui Jiahui Chen Hui Zhao Zhijie Sun Deli Dong Department of Pharmacology(the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150086China Translational Medicine Research and Cooperation Center of Northern China Heilongjiang Academy of Medical SciencesHarbin Medical UniversityHarbin 150086China Department of Pharmacology China Pharmaceutical UniversityNanjing 211198China

Lipid metabolism disorders contribute to hyperlipidemia and hepatic steatosis.It is ideal to develop drugs simultaneous improving both hyperlipidemia and hepatic steatosis.Nitazoxanide is an FDA-approved oral antiprotozoal drug with excellent pharmacokinetic and safety profile.We found that nitazoxanide and its metabolite tizoxanide induced mild mitochondrial uncoupling and subsequently activated AMPK in Hep G2 cells.Gavage administration of nitazoxanide inhibited high-fat diet(HFD)-induced increases of liver weight,blood and liver lipids,and ameliorated HFD-induced renal lipid accumulation in hamsters.Nitazoxanide significantly improved HFD-induced histopathologic changes of hamster livers.In the hamsters with pre-existing hyperlipidemia and hepatic steatosis,nitazoxanide also showed therapeutic effect.Gavage administration of nitazoxanide improved HFD-induced hepatic steatosis in C57BL/6J mice and western diet(WD)-induced hepatic steatosis in Apoe-/-mice.The present study suggests that repurposing nitazoxanide as a drug for hyperlipidemia and hepatic steatosis treatment is promising.

关键词： Nitazoxanide Tizoxanide Hyperlipidemia Hepatic steatosis AMPK Autophagy SQSTM1/P62 Mitochondrial uncoupling

Mitochondrial uncoupler triclosan induces vasorelaxation of rat arteries

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Acta Pharmaceutica Sinica B 2017年第6期7卷 623-629页

作者： Xiyue Zhang Xinzi Zhang Yanqiu Zhang Mingyu Liu Jing Jin Jie Yan Xin Shen Nan Hu Deli Dong Department of Pharmacology(the State-Province Key Laboratories of Biomedicine–Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150086China Translational Medicine Research and Cooperation Center of Northern China Heilongjiang Academy of Medical SciencesHarbin Medical UniversityHarbin 150086China

Our previous studies found that mitochondrial uncouplers induced vasodilation. Triclosan, the broad spectrum antibacterial agent, is the active ingredient in soaps and toothpastes. It was reported that triclosan induced mitochondrial uncoupling, so we aim to investigate the effects of triclosan on vascular function of rat mesenteric arteries and aorta. The isometric tension of rat mesenteric artery and thoracic aorta was recorded by multi-wire myograph system. The cytosolic [Ca^(2+)]_i, mitochondrial reactive oxygen species(mitoROS), and mitochondrial membrane potential of smooth muscle cells(A10 cells) were measured using laser scanning confocal microscopy. Triclosan treatment relaxed phenylephrine(PE)-and high K^(+)(KPSS)-induced constriction, and pre-treatment with triclosan inhibited PE-and KPSS-induced constriction of rat mesenteric arteries. In rat thoracic aorta, triclosan also relaxed PE-and KPSS-induced constriction. Triclosan induces vasorelaxation without involving KATPchannel activation in smooth muscle cells of arteries.Triclosan treatment increased cytosolic [Ca^(2+)]_i, mitochondrial ROS production and depolarized mitochondrial membrane potential in A10 cells. In conclusion, triclosan induces mitochondrial uncoupling in vascular smooth muscle cells and relaxes the constricted rat mesenteric arteries and aorta of rats. The present results suggest that triclosan would indicate vasodilation effect if absorbed excessively in vivo.

关键词： Triclosan Mitochondrial uncoupling Artery Smooth muscle cells Vasorelaxation

Mitochondrial uncoupler BAM15 inhibits artery constriction and potently activates AMPK in vascular smooth muscle cells

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Acta Pharmaceutica Sinica B 2018年第6期8卷 909-918页

作者： Yu Tai Lanjun Li Xuan Peng Junxue Zhu Xihai Mao Nan Qin Minghui Ma Rong Huo Yunlong Bai Deli Dong Department of Pharmacology (the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular Research Ministry of Education) College of Pharmacy Harbin Medical University Translational Medicine Research and Cooperation Center of Northern China Heilongjiang Academy of Medical Sciences Harbin Medical University

Our previous studies found that mitochondrial uncouplers CCCP and niclosamide inhibited artery constriction and the mechanism involved AMPK activation in vascular smooth muscle cells. BAM15 is a novel type of mitochondrial uncoupler. The aim of the present study is to identify the vasoactivity of BAM15 and characterize the BAM15-induced AMPK activation in vascular smooth muscle cells(A10 cells). BAM15 relaxed phenylephrine(PE)-induced constricted rat mesenteric arteries with intact and denuded endothelium. Pretreatment with BAM15 inhibited PEinduced constriction of rat mesenteric arteries with intact and denuded endothelium. BAM15, CCCP,and niclosamide had the comparable IC50 value of vasorelaxation in PE-induced constriction of rat mesenteric arteries. BAM15 was less cytotoxic in A10 cells compared with CCCP and niclosamide.BAM15 depolarized mitochondrial membrane potential, induced mitochondrial fission, increased mitochondrial ROS production, and increased mitochondrial oxygen consumption rate in A10 cells.BAM15 potently activated AMPK in A10 cells and the efficacy of BAM15 was stronger than that of CCCP, niclosamide, and AMPK positive activators metformin and AICAR. In conclusion, BAM15 activates AMPK in vascular smooth muscle cells with higher potency than that of CCCP, niclosamide and the known AMPK activators metformin and AICAR. The present work indicates that BAM15 is a potent AMPK activator.

关键词： BAM15 Mitochondrial uncoupling AMPK Smooth muscle cells AICAR Metformin

Adaptive pinning synchronization on nonlinearly coupled complex networks with an asymmetrical matrix

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Adaptive pinning synchronization on nonlinearly coupled comp...

第32届中国控制与决策会议

作者： deli Xuan dong Ding Ze Tang School of Internet of Things Engineering Jiangnan University Engineering Research Center of Internet of Things Technology Applications (Ministry of Education) Jiangnan University

In this paper,the global synchronization problem for a kind of complex dynamical networks with nonlinearly coupled functions and an asymmetrical coupling matrix is investigated by using pinning control.By designing the adaptive updating laws for the pinning feedback controller,some proper feedback control gains will be acquired.According to the Lyapunov stability theorem and the projection method,sufficient conditions are obtained that ensure the realisation of the global synchronization for the complex dynamical network with different initial values.Finally,the theoretical results are illustrated by a numerical experiment.

关键词： Complex networks Adaptive pinning control Nonlinearly coupled function Global synchronization Asymmetrical couplings

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我国乡村治理变迁与现代化转型路径研究

地方治理研究 2021年第3期 49-59,80页

作者：董德利新动能研究院山东济南250014

从我国乡村治理的历史变迁、未来趋势及内在约束看,乡村治理的现代化转型就是以农业、农村、农民为逻辑起点,以农民、基层政权、国家为关键治理主体,以效率、平等、稳定为基本治理目标,将法治、自治、德治相结合,不断优化治理结构、增... 详细信息

从我国乡村治理的历史变迁、未来趋势及内在约束看,乡村治理的现代化转型就是以农业、农村、农民为逻辑起点,以农民、基层政权、国家为关键治理主体,以效率、平等、稳定为基本治理目标,将法治、自治、德治相结合,不断优化治理结构、增强治理成效的过程。要实现乡村治理现代化转型,就要适应新形势新挑战,坚持问题导向,加强制度创新,特别是要在城乡一体化和协同治理原则下,破解阻碍我国乡村经济社会可持续发展的难题。

关键词：乡村治理村民自治社会治理复合治理政府职责公共服务社会协同现代化转型

Arterial relaxation is coupled to inhibition of mitochondrial fission in arterial smooth muscle cells:comparison of vasorelaxant effects of verapamil and phentolamine

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Acta Pharmaceutica Sinica B 2017年第3期7卷 319-325页

作者： Jing Jin Xin Shen Yu Tai Shanliang Li Mingyu Liu Changlin Zhen Xiuchen Xuan Xiyue Zhang Nan Hu Xinzi Zhang Deli Dong Department of Pharmacology(the State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular ResearchMinistry of Education)College of PharmacyHarbin Medical UniversityHarbin 150086China Translational Medicine Research and Cooperation Center of Northern China Heilongjiang Academy of Medical SciencesHarbin Medical UniversityHarbin 150086China

Mitochondria are morphologically dynamic organelles which undergo fission and fusion processes. Our previous study found that arterial constriction was always accompanied by increased mitochondrial fission in smooth muscle cells, whereas inhibition of mitochondrial fission in smooth muscle cells was associated with arterial relaxation. Here, we used the typical vasorelaxants, verapamil and phentolamine, to further confirm the coupling between arterial constriction and mitochondrial fission in rat aorta. Results showed that phentolamine but not verapamil induced vasorelaxation in phenylephrine(PE)-induced rat thoracic aorta constriction. Verapamil, but not phentolamine, induced vasorelaxation in high K^+(KPSS)-induced rat thoracic aorta constriction. Pre-treatment with phentolamine prevented PEbut not KPSS-induced aorta constriction and pre-treatment with verapamil prevented both PE-and KPSSinduced aorta constriction. Transmission electron microscopy(TEM) results showed that verapamil but not phentolamine inhibited KPSS-induced excessive mitochondrial fission in aortic smooth muscle cells,and verapamil prevented both PE-and KPSS-induced excessive mitochondrial fission in aortic smoothmuscle cells. Verapamil inhibited KPSS-induced excessive mitochondrial fission in cultured vascular smooth muscle cells(A10). These results further demonstrate that arterial relaxation is coupled to inhibition of mitochondrial fission in arterial smooth muscle cells.

关键词： Artery Mitochondrial fission Phentolamine Vasorelaxation Verapamil

Atrial remodeling in atrial fibrillation and association between microRNA network and atrial fibrillation

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Science China(Life Sciences) 2011年第12期54卷 1097-1102页

作者： ZHANG Ying dong deli YANG BaoFeng Department of Pharmacology State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular Research Ministry of Education Harbin 150086 China

Atrial fibrillation(AF) remains one of the leading causes of morbidity and mortality in the world which are related to palpitations,fainting,congestive heart failure or stroke.The mechanism for atrial fibrillation has been identified as electrical remodeling,structure remodeling and intracellular calcium handling remodeling.microRNAs(miRNAs) have recently emerged as one of the important factors in regulating gene expression.So far,thousands of miRNA genes have been found in diverse animals with the function of regulating cell death,cell proliferation,haematopoiesis and even participate in the processing of cardiovascular disease.In this review,we summarize the mechanism of AF and the association of microRNAs network with AF.We provide a potential perspective of miRNAs as the therapeutic target for AF.

关键词： microRNA 房颤心房网络协会 miRNA 重构 RNA基因

Semi-interpenetrating polymer networks toward sulfonated poly(ether ether ketone) membranes for high concentration direct methanol fuel cell

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Chinese Chemical Letters 2019年第2期30卷 299-304页

作者： Xupo Liu Yunfeng Zhang Shaofeng Deng Cuicui Li Jiaming dong Jiaying Wang Zehui Yang deli Wang Hansong Cheng Sustainable Energy Laboratory Faculty of Materials Science and Chemistry China University of Geosciences (Wuhan) Key Laboratory of Material Chemistry for Energy Conversion and Storage (Huazhong University of Science and Technology) Ministry of Education Hubei Key Laboratory of Material Chemistry and Service Failure School of Chemistry and Chemical Engineering Huazhong University of Science and Technology

Low methanol permeability of proton exchange membranes (PEMs) is greatly important for direct methanol fuel cells (DMFCs). Here, sulfonated poly (ether ether ketone) (SPEEK) based semiinterpenetrating polymer networks (semi-IPNs) are successfully prepared by interpenetrating SPEEK into the in-situ synthesized crosslinking networks. The polymeric networks are formed by the covalent bonds between bromobenzyl groups of bro mo methylated poly (phenylene oxide) and amine groups of diamine linkers as well as the ionic bonds between amine species and sulfonated groups. Two linkers without and with sulfonated groups are applied to fabricate the semi-IPNs. The core properties of the membranes, like phase separation, water uptake, proton conductivity and methanol permeability, are systematically studied and compared. The DMFCs assembled by using the semi-IPN membranes display better performance than Nafion 117 in high concentration methanol solutions. The present work provides a facile way to prepare PEMs with enhanced DMFC performance.

关键词： Direct methanol fuel cell Proton exchange membrane Semi-interpenetrating polymer networks Sulfonated poly(ether ether ketone) Bromomethylated poly(phenylene oxide)

5-HT_(3) receptor antagonists protect against pressure overload-induced cardiac hypertrophy in murine

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Acta Pharmaceutica Sinica B 2012年第1期2卷 16-22页

作者： Rong Huo Chang Chen Yan Chen Zhe Li Yunlong Hou Deli Dong The State-Province Key Laboratories of Biomedicine-Pharmaceutics of China Key Laboratory of Cardiovascular Research of the Ministry of EducationDepartment of PharmacologyHarbin Medical UniversityHarbin 150086China

Activation of cardiac sympathetic afferent reflex results in the increase of sympathetic activity.Serotonin(5-HT)activates cardiac sympathetic afferent through stimulating 5-HT_(3) receptors,the aim of present study is to test whether 5-HT_(3) receptor antagonists protect against cardiac hypertrophy.Cardiac hypertrophy induced by TAC for 4 weeks in mice was significantly inhibited by administration of 5-HT_(3) receptor antagonists,ondansetron(2.5 mg/kg,ip.)or tropisetron(2.5 mg/kg,ip.).Histological analysis revealed that the increased cardiac fibrosis in hypertrophic heart was relieved by ondansetron or tropisetron treatment.Ondansetron or tropisetron reduced the elevated plasma level of noradrenalin in mice with cardiac hypertrophy.Ondansetron and tropisetron had no effect on cardiomyocte hypertrophy induced by phenylephrine treatment in vitro.Finally,we took tropisetron as the representative drug and examined the effects of tropisetron on the desensitization of cardiac b-adrenergic receptor in rat treated with abdominal aortic banding(AB).Results showed that tropisetron restored the desensitization of cardiac b-adrenergic receptor in AB-treated rats.In conclusion,5-HT_(3) receptor antagonists protected against cardiac hypertrophy and restored the desensitization of cardiac adrenergic responsiveness,the mechanism in which may be through reducing the sympathetic activity.

关键词： Cardiac hypertrophy 5-HT_(3)receptor 5-HT_(3)receptor antagonists