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| 1 | Contribution of oxidative stress to pulmonary arterial hypertension显示文摘Recent data implicate oxidative stress as a mediator of pulmonary hypertension (PH) and of the associated pathological changes to the pulmonary vasculature and right ventricle (RV). Increases in reactive oxygen species (ROS), altered redox state, and elevated oxidant stress have been demonstrated in the lungs and RV of several animal models of PH, including chronic hypoxia, monocrotaline toxicity, caveolin-1 knock-out mouse, and the transgenic Ren2 rat which overexpresses the mouse renin gene. Generation of ROS in these models is derived mostly from the activities of the nicotinamide adenine dinucleotide phosphate oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase. As disease progresses circulating monocytes and bone marrow-derived monocytic progenitor cells are attracted to and accumulate in the pulmonary vasculature. Once established, these inflammatory cells generate ROS and secrete mitogenic and fibrogenic cytokines that induce cell proliferation and fibrosis in the vascular wall resulting in progressive vascular remodeling. Deficiencies in antioxidant enzymes also contribute to pulmonary hypertensive states. Current therapies were developed to improve endothelial function, reduce pulmonary artery pressure, and slow the progression of vascular remodeling in the pulmonary vasculature by targeting deficiencies in either NO (PDE-type 5 inhibition) or PGI 2 (prostacyclin analogs), or excessive synthesis of ET-1 (ET receptor blockers) with the intent to improve patient clinical status and survival. New therapies may slow disease progression to some extent, but long term management has not been achieved and mortality is still high. Although little is known concerning the effects of current pulmonary arterial hypertension treatments on RV structure and function, interest in this area is increasing. Development of therapeutic strategies that simultaneously target pathology in the pulmonary vasculature and RV may be beneficial in reducing mortality associated with RV failure. | Vincent G DeMarco Adam T Whaley-Connell James R Sowers Javad Habibi Kevin C Dellsperger | 2010 | World Journal of Cardiology2010,2,10: | 21 |
| 2 | Adenine制作雄性Wistar大鼠不育症动物模型最佳时相的小样本研究显示文摘目的:探讨阿拉伯胶助溶后的Aden ine对W istar大鼠生殖毒性的时效关系。方法:将Aden ine按500mg/mL浓度配制,按与Aden ine 1∶10比例加入阿拉伯胶作为助溶剂,1mL/kg.d-1剂量灌胃,每3天处死1组,做精子质量分析、用放免法检测性激素的变化,并对时效关系进行了观察。结果:精子活动率及密度随给药时间延长呈下降趋势,在给药后第15天精子活动率呈显著性差异;睾酮(T)呈进行性下降,给药后前者第3天、后者第12天全部即出现显著性差异,FSH呈进行性上升,第9天出现显著性差异,第12天秩次最高。结论:初步推定将Aden ine按500mg/mL浓度配制,并加助溶剂后,1mL/kg.d-1剂量W istar大鼠灌胃12天为其生殖毒性反映最佳时效,也可能为该给药剂量雄性大鼠不育症模型的最佳时相。 | 贾金铭 王家辉 李森恺 | 2006 | 中医药学刊2006,24,2: | 8 |
| 3 | Discriminated sgRNAs-Based SurroGate System Greatly Enhances the Screening Efficiency of Plant Base-Edited Cells显示文摘The development of CRISPR/Cas9-mediated base editing has made genomic modification more efficient. However, selection of genetically modified cells from millions of treated cells, especially plant cells, is still challenging. In this study, an efficient surrogate reporter system based on a defective hygromycin resistance gene was established in rice to enrich base-edited cells. After step-by-step optimization, the Discriminated sgRNAs-based SurroGate system (DisSUGs) was established by artificially differentiating the editing abilities of a wild-type single guide RNA (sgRNA) targeting the surrogate reporter gene and an enhanced sgRNA targeting endogenous sites. The DisSUGs enhanced the efficiency of screening base-edited cells by 3- to 5-fold for a PmCDA1-based cytosine-to-tyrosine base editor (PCBE), and 2.5- to 6.5-fold for an adenine base editor (ABE) at endogenous targets. These targets showed editing efficiencies of <25% in the conventional systems. The DisSUGs greatly enhanced the frequency of homozygous substitutions and expanded the activity window slightly for both a PCBE and an ABE. Analyses of the total number of single-nucleotide variants from whole-genome sequencing revealed that, compared with the no-enrichment PCBE strategy, the DisSUGs did not alter the frequency of genome-wide sgRNA-independent off-target mutations, but slightly increased the frequency of target-dependent off-target mutations. Collectively, the DisSUGs developed in this study greatly enhances the efficiency of screening plant base-edited cells and will be a useful system in future applications. | Wen Xu Yongxing Yang Ya Liu Guiting Kang Feipeng Wang Lu Li Xinxin Lv Si Zhao Shuang Yuan Jinling Song Ying Wu Feng Feng Xiaoqing He Chengwei Zhang Wei Song Jiuran Zhao Jinxiao Yang | 2020 | Molecular Plant2020,13,1: | 8 |
| 4 | CRISPR/Cas9-Mediated Adenine Base Editing in Rice Genome显示文摘Precise base editing is highly desired in plant functional genomic research and crop molecular breeding. In this study, we constructed a rice-codon optimized adenine base editor(ABE)-nC as9 tool that induced targeted A·T to G·C point mutation of a key single nucleotide polymorphism site in an important agricultural gene. Combined with the modified single-guide RNA variant, our plant ABE tool can efficiently achieve adenine base editing in the rice genome. | LI Hao QIN Ruiying LIU Xiaoshuang LIAO Shengxiang XU Rongfang YANG Jianbo WEI Pengcheng | 2019 | Rice science2019,26,2: | 7 |
| 5 | Nicotinamide adenine dinucleotide phosphate oxidase activation and neuronal death after ischemic stroke显示文摘Nicotinamide adenine dinucleotide phosphate oxidase(NOX) is a multisubunit enzyme complex that utilizes nicotinamide adenine dinucleotide phosphate to produce superoxide anions and other reactive oxygen species. Under normal circumstances, reactive oxygen species mediate a number of important cellular functions, including the facilitation of adaptive immunity. In pathogenic circumstances, however,excess reactive oxygen species generated by NOX promotes apoptotic cell death. In ischemic stroke, in particular, it has been shown that both NOX activation and derangements in glucose metabolism result in increased apoptosis. Moreover, recent studies have established that glucose, as a NOX substrate, plays a vital role in the pathogenesis of reperfusion injury. Thus, NOX inhibition has the potential to mitigate the deleterious impact of hyperglycemia on stroke. In this paper, we provide an overview of this research,coupled with a discussion of its implications for the development of NOX inhibition as a strategy for the treatment of ischemic stroke. Both inhibition using apocynin, as well as the prospect of developing more specific inhibitors based on what is now understood of the biology of NOX assembly and activation, will be highlighted in the course of our discussion. | Jiamei Shen Radhika Rastogi Xiaokun Geng Yuchuan Ding | 2019 | Neural Regeneration Research2019,14,6: | 6 |
| 6 | Oxidative and nitrosative stress enzymes in relation to nitrotyrosine in Helicobacter pylori-infected humans显示文摘AIM: To compare a possible relation between Helicobacter pylori(H. pylori) and the oxygen- and nitrogen radical system in humans. METHODS: Mechanisms for H. pylori to interfere with the oxygen and nitrogen radical system is of great importance for understanding of the H. pylori persistence and pathogenesis. Biopsies were obtained from the gastric wall of 21 individuals. Ongoing infection with H. pylori was detected using direct analyze from the biopsies using campylobacter-like organism test(CLO-test) and/or by using 14C-urea breath test. The individuals were divided in a negative H. pylori and a positive H. pylori group. Expression in the gastric mucosa of induc-ible nitric oxide syntase(iNOS), nicotinamide adenine dinucleotide phosphate-oxidase(NADPH-oxidase) myeloperoxidase(MPO), and nitrotyrosine were assessed by Western blotting.RESULTS: The individuals who undervent gastroscopy were divided in a H. pylori neg. [n = 13, m/f = 7/6, age(mean) = 39] and a H. pylori pos. group [n = 8, m/f = 5/3, age(mean) = 53]. Using western blot analysis iNOS was detected as a 130 kDa band. The iNOS expression was upregulated in the antrum of H. pylori infected individuals in comparison to the controls, mean ± SD being 12.6 ± 2.4 vs 8.3 ± 3.1, P < 0.01. There was a markedly upregulated expression of MPO in the antrum of H. pylori infected individuals in comparison to the control group without infection. In several of noninfected controls it was not possible to detect any MPO expression at all, whereas the expression was high in all the infected subjects, mean ± SD being 5.1 ± 3.4 vs 2.1 ± 1.9, P < 0.05. The NADPH-oxidase expression was analysed by detecting the NADPH-oxidase subunit p47-phox expression. P47-phox was detected as a 47 kDa band using Western blot, and showed a significantly higher expression of p47-phox in the antrum of the H. pylori infected individuals compared to the controls, mean ± SD being 3.1 ± 2.2 vs 0.3 ± 0.2, P < 0.01. Regarding nitrotyrosine formation, Western blot did not show any significant increase or decrease compared to controls, 7.0 ± 0.9 vs 6.9 ± 1.1, not significant.CONCLUSION: iNOS, MPO and NADPH-oxidase was up-regulated among H. pylori infected. Regarding nitrotyrosine no difference was found. This support an H. pylori related inhibition of radical formation. | Anders Elfvin Anders Edebo Peter Hallersund Anna Casselbrant Lars Fndriks | 2014 | World Journal of Gastrointestinal Pathophysiology2014,5,3: | 5 |
| 7 | Potential role of NADPH oxidase in pathogenesis of pancreatitis显示文摘Studies have demonstrated that reactive oxygen species(ROS) are closely related to inflammatory disorders. Nicotinamide adenine dinucleotide phosphate oxidase(NOX), originally found in phagocytes, is the main source of ROS in nonphagocytic cells. Besides directly producing the detrimental highly reactive ROS to act on biomolecules(lipids, proteins, and nucleic acids), NOX can also activate multiple signal transduction pathways, which regulate cell growth, proliferation, differentiation and apoptosis by producing ROS. Recently, research on pancreatic NOX is no longer limited to inflammatory cells, but extends to the aspect of pancreatic acinar cells and pancreatic stellate cells, which are considered to be potentially associated with pancreatitis. In this review, we summarize the literature on NOX protein structure, activation, function and its role in the pathogenesis of pancreatitis. | Wei-Li Cao Xiao-Hui Xiang Kai Chen Wei Xu Shi-Hai Xia | 2014 | World Journal of Gastrointestinal Pathophysiology2014,5,3: | 5 |
| 8 | 活性氧在免疫应答中的作用显示文摘活性氧(Reactive oxygen species,ROS)是一群具有较强氧化能力的分子的总称[1]。生物体内的ROS包括超氧阴离子(O·-2)、羟自由基(·OH)、过氧化氢(H2O2)、单线态氧(O2)。活性氧在免疫系统中主要来源于细胞膜的NADPH氧化酶复合体2(Nicotinamide adenine dinucleotide phosphate oxidase,NOX2),并在淋巴细胞间的信号转导发挥巨大作用。 | 陈洁 赵明峰 | 2015 | 中国免疫学杂志2015,31,6: | 4 |
| 9 | Roles and mechanisms of the CD38/cyclic adenosine diphosphate ribose/Ca^(2+) signaling pathway显示文摘Mobilization of intracellular Ca2+ stores is involved inmany diverse cell functions, including: cell proliferation;differentiation; fertilization; muscle contraction; secre-tion of neurotransmitters, hormones and enzymes;and lymphocyte activation and proliferation. Cyclic ad-enosine diphosphate ribose(cADPR) is an endogenousCa2+ mobilizing nucleotide present in many cell typesand species, from plants to animals. cADPR is formedby ADP-ribosyl cyclases from nicotinamide adenine di-nucleotide. The main ADP-ribosyl cyclase in mammalsis CD38, a multi-functional enzyme and a type Ⅱ mem-brane protein. It has been shown that many extracel-lular stimuli can induce cADPR production that leadsto calcium release or influx, establishing cADPR as asecond messenger. cADPR has been linked to a widevariety of cellular processes, but the molecular mecha-nisms regarding cADPR signaling remain elusive. Theaim of this review is to summarize the CD38/cADPR/Ca2+ signaling pathway, focusing on the recent advanc-es involving the mechanism and physiological functionsof cADPR-mediated Ca2+ mobilization. | Wenjie Wei Richard Graeff Jianbo Yue | 2014 | World Journal of Biological Chemistry2014,5,1: | 4 |
| 10 | Two Preparation Methods-dominated Cd^(Ⅱ)-Based Coordination Polymers with Mixed Adenine Nucleobase and 5-Nitroisophathalate Ligands: Synthesis, Structure and Fluorescence显示文摘Two new CdⅡ-based coordination polymers(CPs) with mixed adenine(Hade) nucleobase and 5-nitroisophathalate(nip) ligands, {[Cd(Hade)_(0.5)(H_2O)_2(nip)]·H_2O}n 1 and {[Cd(Hade)(H_2O)_(1.25)(CH_3OH)0.75(nip)]·0.75 CH_3OH·0.5H_2 O}_n 2, were successfully obtained by varying the preparation methods and structurally characterized. Crystal data for 1: monoclinic, C2/c space group with a = 10.5546(6), b = 17.3496(6), c = 16.1198(9) ?, β = 104.2800(10)o, V = 2860.6(2) ?3, Dc = 2.058 g/cm^3, Mr = 443.13, Z = 8, F(000) = 1752, μ = 1.585 mm^(–1), the final R = 0.0394 and wR = 0.1109 for 2285 observed reflections with I > 2σ(I). For 2: triclinic, P1 space group with a = 10.2032(7), b = 10.5098(8), c = 11.0223(8) ?, a = 65.7050(10)o, β = 74.5750(10)o, g = 61.5280(10)o, V = 943.38(12) ?~3, Dc = 1.888 g/cm3, Mr = 536.24, Z = 2, F(000) = 537, μ = 1.225 mm^(–1), the final R = 0.0225 and wR = 0.0702 for 3143 observed reflections with I > 2σ(I). 1 presents a crisscrossed layer with mutually orthogonal {Cd(nip)} chains aggregated by neutral m-N(7),N(9)-Hade connector. By contrast, 2 displays a linear chain with CdⅡ ions extended by bis-bidentate chelating-nip2–connectors, which are further assembled into a broad ribbon by N-H···N hydrogen-bonding interactions. Additionally, the two solid-state samples with comparable thermal stability exhibit favorable luminescent emissions at room temperature, suggesting their potential applications as fluorescence materials. | 刘正宇 付敏 王修光 王丽丽 杨恩翠 赵小军 | 2019 | Chinese Journal of Structural Chemistry2019,38,4: | 3 |
| 11 | Evaluation of various solutions for small bowel graft preservation显示文摘EvaluationofvarioussolutionsforsmalbowelgraftpreservationLIYouSheng1,LIJieShou1,LINing1,JIANGZhiWei1,ZHAOYunZhao1,LINan?.. | Li YS Li JS Li N Jiang ZW Zhao YZ Li NY Liu FN | 1998 | World Journal of Gastroenterology1998,4,2: | 2 |
| 12 | Purines:From Diagnostic Biomarkers to Therapeutic Agents in Brain Injury显示文摘The purines constitute a family of inter-related compounds that serve a broad range of important intracellular and extracellular biological functions.In particular,adenosine triphosphate(ATP)and its metabolite and precursor,adenosine,regulate a wide variety of cellular and systems-level physiological processes extending from ATP acting as the cellular energy currency,to the adenosine arising from the depletion of cellular ATP and responding to reduce energy demand and hence to preserve ATP during times of metabolic stress.This inter-relationship provides opportunities for both the diagnosis of energy depletion during conditions such as stroke,and the replenishment of ATP after such events.In this review we address these opportunities and the broad potential of purines as diagnostics and restorative agents. | Bruno G.Frenguelli Nicholas Dale | 2020 | Neuroscience Bulletin2020,36,11: | 2 |
| 13 | Therapeutic implications of advanced age at time of spinal cord injury显示文摘A recent demographic shift towards increased age at time of spinal cord injury (SCI), as well as decreased functional recovery following SCI in older populations, create the need to investigate how age effects SCI pathology and repair (Scivoletto et al., 2003). While decreased neuroplasticity or physical strength with age may contribute to functional deficits, work from our lab and others have identified exacerbated acute inflammatory events as contributors to age-dependent secondary injury. Specifically, our recent paper identified that increased production of reactive oxygen species (ROS) from macrophage nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) with age exacerbates secondary injury after SCI (Zhang et al., 2019). | Andrew N. Stewart John C. Gensel Bei Zhang | 2019 | Neural Regeneration Research2019,14,11: | 1 |
| 14 | Roles of AKR1C3 in malignancy显示文摘The superfamily of aldo-keto reductases(AKRs)is composed of over 190 members and can be classified into 16 different families(visit www.med.upenn.edu/akr).AKR1C3(C3 subtype of aldosterone reductase family 1)refers to the first AKR in family 1,subfamily C,and is encoded by the AKR1C3 gene.AKR1C3 was first cloned and expressed from a human prostate cDNA library.This protein is a soluble monomeric NADP(H)(nicotinamideadenine dinucleotide phosphate or reduced form of nicotinamide adenine dinucleotide phosphate)dependent oxidoreductase. | Xin-Zhu Xiao Li-Ying Lin Ming-Kai Zhuang Can-Mei Zhong Feng-Lin Chen | 2021 | Chinese Medical Journal2021,,9: | 1 |
| 15 | Structure effect of nucleotides in terbium(Ⅲ)-nucleotide fluorescent reaction—-New evidence for the binding sites of terbium(Ⅲ) on nucleotides显示文摘Upon addition of Tb3+ to 16 nucleotides and homopolynucleotides, all of them showeda characteristic green emission from Tb3+, but with much different intensity, upon excitation inthe aromatic region of bases. The result suggested that nucleotides with at least one carbonylgroup in nucleotide bases are better enhancers to the fluorescence of Tb3+. The complexes of ATP,GDP and GTP with T53+ are synthesized as two types of models. Guanine tpye nucleotides withone carbonyl group in the bases are the best enhancers, while adenine type nucleotides with nocarbonyl group in the bases are poorest enhancers to the fluorescence of Tb3+. Comparing theIR spectra of ATP, GTP, GDP and their Tb3+ complexes suggested that C-6 carbonyl group inGTP and GDP may be involved in complex formation, which may be responsible for the effectiveenergy transfer. This is further supported by comparing the UV spectra of ATP, Poly(A), GTP,and Poly(G) with their Tb3+ complexes in water solution. | LI, Yuan-Zong CHANG, Wen-Bao CI, Yun-Xiang*, Department of Chemistry, Beijing University, Beijing 100871 | 1993 | Chinese Journal of Chemistry1993,11,6: | 1 |
| 16 | Towards understanding the mechanisms of proton pumps in Complex-I of the respiratory chain显示文摘INTRODUCTION Complex-I(z.e.,nicotinamide adenine dinucleotide(NADH):ubiquinone(quinone or Q)oxidoreductase)of the respiratory chain is crucial for converting energy from its redox form(/.e.,electron transfer)to the transmembrane electrochemical potential(Hirst 2013;Kaila 201&Verkhovskaya and Bloch 2013;Walker 1992).Homologs of Complex-I are ubiquitously expressed throughout all forms of life,from bacteria to human cells(Friedrich and Scheide 2000). | Xuejun C.Zhang Bin Li | 2019 | Biophysics Reports2019,5,5: | 1 |
| 17 | Shen-Qi-Wan Protects the Renal Peritubular Capillary Injury from Adenine-mediated Damage by Upregulating Aquaporin 1显示文摘Background:Shen-Qi-Wan(SQW),a commonly used prescription against chronic kidney disease(CKD)in Tradi-tional Chinese Medicine(TCM),has a nephroprotective action in adenine-induced kidney injury.However,the mechanism of SQW in renal injury remains unclear.Objective:This study was undertaken to measure the effect of SQW on peritubular capillary injury both in vivo and in vitro assays.Methods:The effect of SQW on the peritubular capillary injury was evaluated according to measuring hypothalamic-pituitary-adrenal(HPA)function,inflammatory cytokines,VEGF(vascular endothelial growth fac-tor),CD34(Cluster of differentiation 34),and AQP1(Aquaporin 1)levels in the kidney,cell migration,and lumen forming capacity.Results:SQW supplementation could ameliorate dysfunction of the HPA and renal function loss induced by adenine.SQW also significantly inhibited the inflammatory cytokines including MCP-1(monocyte chemotactic protein-1)and VCAM-1(vascular cell adhesion molecule-1)level.Alternatively,SQW administration showed an ameliorating effect from the toxicity and alleviated the injury of capillaries around renal tubules instigated by adenine through increasing AQP1 mRNA and protein level.SQW medicated the serum enhanced the migration and lumen formation ability of HMEC-1 cells,and significantly increased AQP1 protein level.Moreover,AQP1 knockdown efficiently inhibited the migration and lumen formation ability in HMEC-1 cells,and weakened the effect of SQW medicated serum.Conclusion:These results suggested that SQW attenuated peritubular capillary injury in adenine-induced CKD model rats through boosting angiogenesis in endothelial cell,and AQP1 may be a potential target of SQW for treating the renal injury. | Yuting Bao Yehui Zhang Yuanxiao Yang Xueming Chen Luning Lin Yunbo Fu Liting Ji Changyu Li | 2022 | Clinical Complementary Medicine and Pharmacology2022,2,1: | 1 |
| 18 | MDR:an integrative DNA N6-methyladenine and N4-methylcytosine modification database for Rosaceae显示文摘Eukaryotic DNA methylation has been receiving increasing attention for its crucial epigenetic regulatory function.The recently developed single-molecule real-time(SMRT)sequencing technology provides an efficient way to detect DNA N6-methyladenine(6mA)and N4-methylcytosine(4mC)modifications at a single-nucleotide resolution.The family Rosaceae contains horticultural plants with a wide range of economic importance.However,little is currently known regarding the genome-wide distribution patterns and functions of 6mA and 4mC modifications in the Rosaceae.In this study,we present an integrated DNA 6mA and 4mC modification database for the Rosaceae(MDR,http://gffzze097936153d24d72hwbx9vnqno0vq6cux.ffgz.tsg.suse.edu.cn).MDR,the first repository for displaying and storing DNA 6mA and 4mC methylomes from SMRT sequencing data sets for Rosaceae,includes meta and statistical information,methylation densities,Gene Ontology enrichment analyses,and genome search and browse for methylated sites in NCBI.MDR provides important information regarding DNA 6mA and 4mC methylation and may help users better understand epigenetic modifications in the family Rosaceae. | Zhao-Yu Liu Jian-Feng Xing Wei Chen Mei-Wei Luan Rui Xie Jing Huang Shang-Qian Xie Chuan-Le Xiao | 2019 | Horticulture Research2019,6,1: | 1 |
| 19 | Crystal Structure and Luminescence of a Cd(Ⅱ) Compound Based on the 3,3’,5,5’-Tetrafluorobiphenyl-4,4’-dicarboxylate and Adenine Ligands显示文摘A one-dimensional(1 D) coordination polymer, [Cd2(TFBPDC)2(ad)2(CH3 OH)2]n(1), based on the 3,3’,5,5’-tetrafluorobiphenyl-4,4’-dicarboxylate(TFBPDC2-) and adenine(ad) ligands, was synthesized. Compound 1 crystallizes in the triclinic system, space group P1 with a = 9.7067(3), b = 9.9501(3), c = 11.6903(4) ?, α = 93.036(3), β = 107.793(3), γ = 107.107(3)°, V = 1014.77(6) ?3, Z = 2, C40H26F8N10O10Cd2, Mr = 1183.51, Dc = 1.937 g/cm3, μ = 1.160 mm-1, F(000) = 584, the final R = 0.0284 and wR = 0.0635 for 3791 observed reflections with Ⅰ> 2s(I). In 1, a pair of adenine(ad) ligands bridge two octahedrally coordinated Cd(Ⅱ) atoms to form a dinuclear [Cd2(ad)2] unit, which is linked by TFBPDC2- to generate a 1 D double chain. The neighboring chains are connected by N-H×××O hydrogen bonds to give a two-dimensional(2 D) layer, which is further linked by the O-H×××N hydrogen bonds to give a three-dimensional(3 D) supramolecular framework. IR spectrum, thermogravimetric analysis, and powder X-ray diffraction of 1 were provided. Compound 1 shows luminescent emission. | LIN Zhao-Ting WANG Yu-Ling LIU Qing-Yan | 2020 | Chinese Journal of Structural Chemistry2020,39,11: | 1 |
| 20 | Repetitive administration of cultured human CD34+cells improve adenine-induced kidney injury in mice显示文摘BACKGROUND There is no established treatment to impede the progression or restore kidney function in human chronic kidney disease(CKD).AIM To examine the efficacy of cultured human CD34+cells with enhanced proliferating potential in kidney injury in mice.METHODS Human umbilical cord blood(UCB)-derived CD34+cells were incubated for one week in vasculogenic conditioning medium.Vasculogenic culture significantly increased the number of CD34+cells and their ability to form endothelial progenitor cell colony-forming units.Adenineinduced tubulointerstitial injury of the kidney was induced in immunodeficient non-obese diabetic/severe combined immunodeficiency mice,and cultured human UCB-CD34+cells were administered at a dose of 1×106/mouse on days 7,14,and 21 after the start of adenine diet.RESULTS Repetitive administration of cultured UCB-CD34+cells significantly improved the time-course of kidney dysfunction in the cell therapy group compared with that in the control group.Both interstitial fibrosis and tubular damage were significantly reduced in the cell therapy group compared with those in the control group(P<0.01).Microvasculature integrity was significantly preserved(P<0.01)and macrophage infiltration into kidney tissue was dramatically decreased in the cell therapy group compared with those in the control group(P<0.001).CONCLUSION Early intervention using human cultured CD34+cells significantly improved the progression of tubulointerstitial kidney injury.Repetitive administration of cultured human UCB-CD34+cells significantly improved tubulointerstitial damage in adenine-induced kidney injury in mice via vasculoprotective and anti-inflammatory effects. | Takayasu Ohtake Shoichi Itaba Amankeldi A Salybekov Yin Sheng Tsutomu Sato Mitsuru Yanai Makoto Imagawa Shigeo Fujii Hiroki Kumagai Masamitsu Harata Takayuki Asahara Shuzo Kobayashi | 2023 | World Journal of Stem Cells2023,15,4: | 0 |