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World Journal of Gastrointestinal pharmacology and Therapeutics 2016年第3期7卷 353-360页

作者： Imene Soufli Ryma Toumi Hayet Rafa Chafia Touil-Boukoffa Department of cellular and Molecular biology University of Sciences and Technology Houari Boumediene

Inflammatory bowel diseases(IBDs), including Crohn's disease and ulcerative colitis are complex disorders with undetermined etiology. Several hypotheses suggest that IBDs result from an abnormal immune response against endogenous flora and luminal antigens in genetically susceptible individuals. The dysfunction of the mucosal immune response is implicated in the pathogenesis of IBD. The balance between pro-inflammatory cytokines [tumor necrosis factor(TNF)-α, interleukin(IL)-1b, IL-8, and IL-17A], anti-inflammatory cytokines(IL-4 and IL-13), and immunoregulatory cytokines(IL-10 and transforming growth factors b) is disturbed. Moreover, evidence from animal and clinical studies demonstrate a positive correlation between an increased concentration of nitric oxide(NO) and the severity of the disease. Interestingly, proinflammatory cytokines are involved in the up-regulation of inducible oxide synthase(iN OS) expression in IBD. However, anti-inflammatory and immunoregulatory cytokines are responsible for the negative regulation of iN OS. A positive correlation between NO production and increased pro-inflammatory cytokine levels(TNF-α, IL-6, IL-17, IL-12, and interferon-γ) were reported in patients with IBD. This review focuses on the role of cytokines in intestinal inflammation and their relationship with NO in IBD.

关键词： Inflammatory bowel disease Cytokines Nitric oxide Inducible nitric oxide synthase Immuno pathogenesis

Intracellular distribution and internalization pathways of guanidinylated bioresponsive poly(amido amine)s in gene delivery

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Asian Journal of Pharmaceutical Sciences 2018年第4期13卷 360-372页

作者： Jinmina Zhang Chunxi Wang Mei Lu Haonan Xing Tianzhi Yang Cuifang Cai Xiaoyun Zhao Minjie Wei Jiankun Yu Pingtian Ding School of Pharmacy Shenyang Pharmaceutical University Department of Basic Pharmaceutical Sciences School of PharmacyHusson University Department of Microbiology and Cell biology School of life Science and BiopharmaceuticsShenyang Pharmaceutical University Department of pharmacology School of PharmacyChina Medical University Department of Ion Channel pharmacology School of PharmacyChina Medical University

Guanidinylated bioresponsive poly(amido amine)s polymers, CAR-CBA and CHL-CBA, weresynthesized by Michael-type addition reaction between guanidine hydrochloride(CAR) orchlorhexidine(CHL) and N,N-cystaminebisacrylamide(CBA). Previous studies have shownthat both polymers had high transfection efficiencies as gene delivery carriers. In this study,we investigated the nucleolus localization abilities and cellular internalization pathways ofthese two polymers in gene delivery. Each polymer condensed plasmid DNA(p DNA) andformed nanoparticle complexes, and then their transfection studies were performed inMCF-7 cells. Both complexes were found enriched in nucleolus after cellular transfection,and their transfection efficiencies were significantly improved when transfection was per-formed on MCF-7 cells arrested at M phase. The transfection efficiency of CAR-CBA-pDNAwas inhibited by chlorpromazine, and cell endosomes were disrupted after being exposedto CAR-CBA-pDNA. In regards to CHL-CBA-pDNA, its transfection efficiency was not affected by three types of endocytosis inhibitors used in the study, and CHL-CBA-pDNA showed no effect on endosomes. cellular lactate dehydrogenase release and membrane morphology were changed after cells were transfected by the two complexes. The results indicated that both CAR-CBA and CHL-CBA polymers demonstrated good nucleolus localization abilities. It was beneficial for transfection when cells were arrested at M phase. CAR-CBA-pDNA cellular internalization was involved with clathrin-mediated endocytosis pathway, and escaping from endosomal entrapment, while the cellular uptake of CHL-CBA-pDNA occurs via clathrin-and caveolae-independent mechanism.

关键词： Guanidinylated poly(amido amine)s polymers Nucleolus localization Cell cycle status Internalization pathways

Methylene blue protects mitochondrial respiration from ethanol withdrawal stress

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Advances in Bioscience and Biotechnology 2013年第7期4卷 24-34页

作者： Marianna Jung Daniel Metzger departments of pharmacology and Neuroscience University of North Texas Health Science Center Fort Worth USA

Methylene blue (MB), a tricyclic phenothiazine drug, has been reported to enhance mitochondrial functions including mitochondrial respiration. By comparison, stress associated with abrupt ethanol withdrawal (EW) impedes mitochondrial functions. We investigated whether MB protects mitochondrial respiration and cell survival from EW stress through a key mitochondrial enzyme, cytochrome c oxidase (COX). We also investigated whether the MB’s protection involves the inhibition of an excitatory neurotransmitter, glutamate. Male rats were exposed to and withdrawn from ethanol-diet (7.5%, 5 weeks). MB (0.5 mg/kg, intraperitoneal) was injected for the last 5 days of ethanol-diet and on the first day of EW. Cerebellum was then harvested to measure mitochondrial respiration and COX expression using real-time XF respirometer and immunohistochemistry, respectively. Separately, HT22 cells (a murine hippocampal cell line) were exposed to and abruptly withdrawn for 4 hours from chronic ethanol (100 mM, 3 days). MB was administered during EW with or without a COX inhibitor (NaN3) or glutamate. Mitochondrial respiration, COX content, and cell viability were then assessed using real-time XF respirometer, an immunoblot method, and Calcein assay, respectively. MB attenuated the suppressing effects of EW on mitochondrial respiration, COX content, and cell survival. This protection was reduced after NaN3 or glutamate cotreatment. These results suggest that MB treatment help maintain mitochondrial respiratory and cellular integrity through COX-upregulation and glutamateinhibition upon EW stress. MB treatment may help identify mitochondrial mechanisms underlying hyperexcitatory CNS disorders.

关键词： Cell Viability Ethanol Withdrawal Methylene Blue Mitochondrial Respiration Cytochrome C Oxidase

Molecular Mechanism Underlying Short-Term Perioperative Stress-Induced Prolongation of Postsurgical Pain

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Molecular Mechanism Underlying Short-Term Perioperative Stre...

Site-specific Proteasome Phosphorylation Controls Cell Proliferation and Tumorigenesis

2017中国中西医结合麻醉学会[CSIA]年会暨第四届全国中西医结合麻醉学术研讨会暨陕西省中西医结合学会麻醉专业委员会成立大会

作者： Yuan-Xiang Tao departments of Anesthesiology Cell Biology & Molecular MedicineNeurology &Neuroscienceand Physiology & PharmacologyNew Jersey Medical SchoolRutgersThe State University of New Jersey

We have previously reported that short-term perioperative stress prolonged postoperative ***,the molecular mechanisms underlying this prolongation are *** here shown that short-term stress caused by 6 h sleep disturbance daily for 3says significantly reduced the expression of TET1,but not TET2,TET3,DNMT1,DNMT3a and DNMT3b,in the neurons of dorsal root ganglion(DRG)and spinal cord dorsal *** reduction is triggered by glucocorticoid receptor activation and contributed to short-term stress-induced downregulation in mu opioid receptor and kappa opioid receptor in the DRG and dorsal horn and prolongation of incisional ***1may be a new potential target for prolonged postoperative pain management.

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Site-specific Proteasome Phosphorylation Controls Cell Proli...

阿西维辛或谷胱甘肽降低顺铂引起的肾脏毒性和顺铂-DNA加合物在鼠肾脏中的水平(英文)

中国生物化学与分子生物学会2016年全国学术会议

作者： Xing Guo Xiaorong Wang Zhiping Wang Sourav Banerjee Jing Yang Lan Huang Jack E.Dixon Department of pharmacology University of California-San Diego Life Sciences Institute Zhejiang University departments of Physiology and Biophysics and of Developmental and Cell biology University of California Division of Biological Sciences University of California-San Diego Department of Neurobiology Zhejiang University School of Medicine departments of cellular and Molecular Medicine and of Chemistry and Biochemistry University of California-San Diego

Despite the fundamental importance of proteasomal degradation in cells,little is known about whether and how the 26S proteasome itself is regulated in coordination with various physiological *** we show that the prote... 详细信息

关键词： Proteasome Phosphorylation DYRK2 Cell Cycle Tumorigenesis CRISPR/Cas9

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中国药理学与毒理学杂志 2004年第2期18卷 141-145页

作者：张治华 Marie H HANIGAN Miriam C POIRIER Laboratory of cellular Carcinogenesis and Tumor Promotion Department of Cell biology

目的　为了了解阿西维辛 (acivicin)和GSH预防肾脏毒性的机制 ,研究了顺铂 DNA加合物在大鼠肾脏中的水平。方法　顺铂 (6mg·kg- 1)从尾静脉注入大鼠 ,5d后处死。其他两组动物在给顺铂前2 .5h ,给予阿西维辛或者GSH。测量顺铂 DNA加... 详细信息

目的　为了了解阿西维辛 (acivicin)和GSH预防肾脏毒性的机制 ,研究了顺铂 DNA加合物在大鼠肾脏中的水平。方法　顺铂 (6mg·kg- 1)从尾静脉注入大鼠 ,5d后处死。其他两组动物在给顺铂前2 .5h ,给予阿西维辛或者GSH。测量顺铂 DNA加合物在肾脏中的浓度、血中尿素氮 (BUN)和丝氨酸肌酸的浓度。结果　在给顺铂前 2 .5h ,给 10mg·kg- 1阿西维辛完全阻断了顺铂引起的肾脏毒性。具体表现是血氮和肌酸浓度降低 ,DNA加合物减少了17.1% (P <0 .0 5 )。在给顺铂前 ,给 5 0 0mg·kg- 1GSH ,肾脏毒性和顺铂 DNA加合物水平均显著性减低 (P <0 .0 5 )。另外 ,在DNA加合物和血氮之间存在着一个弱正相关关系。结论　DNA加合物在顺铂引起的肾脏毒性中引了一些作用。但是DNA加合物和血氮之间的弱相关关系提示DNA加合物与肾脏毒性只有较弱的联系。

关键词： DNA加合物顺铂谷胱甘肽毒性阿西维辛

Circulating microparticles and micro RNAs as players in atherosclerosis

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World Journal of Hematology 2013年第2期2卷 16-19页

作者： Nicoleta Alexandru Adriana Georgescu Petru Poni Institute of Macromolecular Chemistry R-6600 Iasi Romania Department of Pathophysiology and pharmacology Institute of Cellular Biology and Pathology Nicolae Simionescu of Romanian Academy 050568 Bucharest Romania

Microparticles(MPs) are extracellular membrane vesicles released from normal, apoptotic and pathological cells following a process of detachment from cells of origin. MPs are typically defined by their size, exposure of phosphatidylserine, the expression of surface antigens, proteins and genetic material, originating from their donor cells, and as important vehicles of intercellular communication across numerous biological processes. MPs contain the major source of systemic RNA including micro RNA(mi RNA) of which aberrant expression appears to be associated with stage and progression of atherosclerosis. The involvement and influence of mi RNA during the onset and progression of atherosclerotic disease have generated a lot of inter-est in assessing the feasibility of therapeutic regulation of mi RNAs to manipulate them with a special focus on cardiovascular disease. We speculate on the future de velopments of MPs which contain mi RNA as new thera peutic targets for proliferative vascular diseases such as atherosclerosis.

关键词： Microparticles MicroRNA Atherosclerosis

脉冲升温-时间分辨中红外光谱研究蛋白质折叠动力学进展

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生物物理学报 2009年第S1期25卷 141-142页

作者：李恒柯慧敏任国平叶满萍翁羽翔王志珍 Institute of Physics Chinese Academy of Sciences National Laboratory of Biomacromolecules Institute of Biophysics Chinese Academy of Sciences Howard Hughes Medical Institute Departments of Molecular Cellular and Developmental Biology University of Michigan

蛋白质的正确折叠构型是行使其生物功能的基础,也是生命正常运转的重要因素。蛋白质如何从氨基酸序列变成具有活性功能的结构是蛋白质折叠的基本问题。

关键词：蛋白质折叠二体解聚 DsbC G49R 激光脉冲升温稳态红外光谱蛋白质盐效应

Emergent Mitotic Chromosome Motions from a Changing Intracellular pH

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Open Journal of Biophysics 2018年第1期8卷 9-21页

作者： L. John Gagliardi Daniel H. Shain departments of Physics and biology Rutgers The State University of New Jersey Camden NJ USA

The mechanism by which chromosomes establish and maintain a dynamic coupling to microtubules for force generation during the complex motions of mitosis remains elusive. Equally challenging is an explanation for the timing of poleward, antipoleward, and oscillatory chromosome movements. The molecular cell biology paradigm requires that specific molecules, or molecular geometries, for force generation are necessary for chromosome motions. We propose here that the dynamics of mitotic chromosome motions are an emergent property of a changing intracellular pH in combination with electrostatic forces. We explain this mechanism within the context of Complexity Theory, based on the electrostatic properties of tubulin, known cellular electric charge distributions, and the dynamic instability of microtubules.

关键词： Mitosis Ndc80/Hec1 Electrostatics Chromosome Motility Complexity Theory