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| 1 | Reactivation of γ-globin expression through Cas9 or base editor to treat β-hemoglobinopathies显示文摘Dear Editor,Mutations in the β-globin gene,the essential component of adult hemoglobin(HbA;a2p2),results in either a production of aberrant sickle hemoglobin(HbS)leading to sickle cell disease(SCD)or an insufficient β-globin synthesis leading to β-thalassemia.These two major forms of β-hemoglobinopathies cause impaired erythropoiesis and life-threatening anemia.Clinical evidence has suggested that reaaivation of fetal γ-globin(HBG)gene expression which is normally silenced after birth by certain genetic mutations can ameliorate the clinical course of β-hemoglobinopathies. | Liren Wang Linxi Li Yanlin Ma Handan Hu Qi Li Yang Yang Wenbang Liu Shuming Yin Wei Li Bin Fu Ryo Kurita Yukio Nakamura Mingyao Liu Yongrong Lai Dali Li | 2020 | Cell Research2020，30，3： | 14 |
| 2 | Increasing targeting scope of adenosine base editors in mouse and rat embryos through fusion of TadA deaminase with Cas9 variants显示文摘 | Lei Yang Xiaohui Zhang Liren Wang Shuming Yin Biyun Zhu Ling Xie Qiuhui Duan Huiqiong Hu Rui Zheng Yu Wei Liangyue Peng Honghui Han Jiqin Zhang Wenjuan Qiu Hongquan Geng Stefan Siwko Xueli Zhang Mingyao Liu Dali Li | 2018 | Protein & Cell2018，9，9： | 13 |
| 3 | CRISPR/Cas9 system: a powerful technology for in vivo and ex vivo gene therapy显示文摘CRISPR/Cas9 is a versatile genome-editing tool which is widely used for modifying the genome of both prokaryotic and eukaryotic organisms for basic research and applications. An increasing number of reports have demonstrated that CRISPR/Cas9-mediated genome editing is a powerful technology for gene therapy. Here, we review the recent advances in CRISPR/Cas9-mediated gene therapy in animal models via different strategies and discuss the challenges as well as future prospects. | Xiaohui Zhang Liren Wang Mingyao Liu Dali Li | 2017 | Science China(Life Sciences)2017，60，5： | 12 |
| 4 | Organ preservation: from the past to the future显示文摘机关移植是为有结束阶段疾病的病人的最有效的治疗。保藏答案和技术在移植以后与病态和幸存有关直接为施主机关质量是关键的,它是。当前,静态的冷存储(SCS ) 是为机关保藏的标准方法。然而,当延长冷存储增加贡献长期的复杂并发症的早接枝机能障碍的风险,有 SCS 的保藏时间被限制。而且,对边缘的施主机关的使用的成长要求为机关评价和修理要求方法。机器灌注在机关保藏上整修了并且统治当前的研究。它被承认到它的动态性质和象生理一样环境。更复杂的机器灌注技术和更好的 perfusates 的发展可以导致机关修理 / 修理。这评论描述机关保藏的历史,总结迄今为止被做了的进步,并且讨论为机关保藏的未来方向。 | Lei JING Leeann YAO Michael ZHAO Li-ping PENG Mingyao LIU | 2018 | Acta Pharmacologica Sinica2018，39，5： | 11 |
| 5 | PGE2 activates EP4 in subchondral bone osteoclasts to regulate osteoarthritis显示文摘Prostaglandin E2(PGE2), a major cyclooxygenase-2(COX-2) product, is highly secreted by the osteoblast lineage in the subchondral bone tissue of osteoarthritis(OA) patients. However, NSAIDs, including COX-2 inhibitors, have severe side effects during OA treatment. Therefore, the identification of novel drug targets of PGE2 signaling in OA progression is urgently needed. Osteoclasts play a critical role in subchondral bone homeostasis and OA-related pain. However, the mechanisms by which PGE2 regulates osteoclast function and subsequently subchondral bone homeostasis are largely unknown. Here, we show that PGE2 acts via EP4 receptors on osteoclasts during the progression of OA and OA-related pain. Our data show that while PGE2 mediates migration and osteoclastogenesis via its EP2 and EP4 receptors, tissue-specific knockout of only the EP4 receptor in osteoclasts(EP4 Lys M) reduced disease progression and osteophyte formation in a murine model of OA. Furthermore, OA-related pain was alleviated in the EP4 Lys M mice, with reduced Netrin-1 secretion and CGRP-positive sensory innervation of the subchondral bone. The expression of plateletderived growth factor-BB(PDGF-BB) was also lower in the EP4 Lys Mmice, which resulted in reduced type H blood vessel formation in subchondral bone. Importantly, we identified a novel potent EP4 antagonist, HL-43, which showed in vitro and in vivo effects consistent with those observed in the EP4 Lys Mmice. Finally, we showed that the Gαs/PI3 K/AKT/MAPK signaling pathway is downstream of EP4 activation via PGE2 in osteoclasts. Together, our data demonstrate that PGE2/EP4 signaling in osteoclasts mediates angiogenesis and sensory neuron innervation in subchondral bone, promoting OA progression and pain, and that inhibition of EP4 with HL-43 has therapeutic potential in OA. | Wenhao Jiang Yunyun Jin Shiwei Zhang Yi Ding Konglin Huo Junjie Yang Lei Zhao Baoning Nian Tao PZhong Weiqiang Lu Hankun Zhang Xu Cao Karan Mehul Shah Ning Wang Mingyao Liu Jian Luo | 2022 | Bone Research2022，10，2： | 7 |
| 6 | FBW7 regulates endothelial functions by targeting KLF2 for ubiquitination and degradation显示文摘F 盒子和 WD 重复包含域 7 (FBW7 ) , E3 ubiquitin ligase SCF FBW7 (SKP1, cullin-1 和 FBW7 的建筑群) ,在各种各样的生理、病理学的过程起重要作用。尽管 FBW7 为脉管的开发被要求,它在内皮细胞层的函数尚待被调查。在这研究,我们证明 FBW7 是 endothelial 功能的一个重要管理者,包括 angiogenesis,白血球粘附和 endothelial 障碍正直。用 RNA 干扰,我们发现 FBW7 的弄空显著地在 vitro 并且在 vivo 损害 angiogenesis。我们识别了锌手指抄写因素 Krü象 ppel 一样因素 2 (KLF2 ) 作为在 endothelial 房间的 FBW7 的一个生理的目标。FBW7 击倒表示在 endothelial 房间导致了内长的 KLF2 蛋白质的累积。调停 FBW7 的 KLF2 破坏被显示在二保存 phosphodegrons 经由肝糖 synthase kinase-3 (GSK3 ) 取决于 KLF2 的 phosphorylation。变异这些 phosphodegron 主题废除了 KLF2 的调停 FBW7 的降级和 ubiquitination。调停 siRNA 显示出的 FBW7 击倒 KLF2 是在 endothelial 的规定的 FBW7 的一个必要目标,这工作。而且,调停 FBW7 的 KLF2 降级被显示为在 teratomas 并且在 zebrafish 开发的 angiogenesis 批评。一起拿,我们的学习在 endothelial 房间移植, angiogenesis,发炎和障碍完整的进程为 FBW7 建议一个角色,并且在 vivo 提供新奇卓见进 KLF2 稳定性的规定。 | Rui Wang Yah Wang Ning Liu Chunguang Ren Cong Jiang Kai Zhang Su Yu Yunfei Chen Hui Tang Qi Deng Cong Fu Yingcong Wang Rong Li Mingyao Liu Weijun Pan Ping Wang | 2013 | Cell Research2013，23，6： | 7 |
| 7 | Ailanthone:a new potential drug for castration-resistant prostate cancer显示文摘Prostate cancer (PCa) is the most common male cancer [1, 2]. PCa initially depends on androgen receptor (AR) signaling for growth and survival. Androgen deprivation therapy causes a temporary reduction in PCa tumor burden, but the tumor eventually develops into castrationresistant prostate cancer (CRPC) with the ability to grow again in the absence of androgens [3]. Mechanisms of CRPC progression include AR amplification and overexpression [4], AR gene rearrangement promoting synthesis of constitutively-active truncated AR splice variants (ARVs) [4], and induction of intracrine androgen metabolic enzymes [3]. Current anti-androgen therapies including MDV3100 (Enzalutamide) and abiraterone have focused on the androgen-dependent activation of AR through its ligand-binding domain (LBD), but do not provide a continuing clinical benefit for patients with CRPC and presumably fail due to multiple mechanisms including the expression of AR-Vs lacking the LBD [5]. These AR-Vs signal in the absence of ligand and are therefore resistant to LBD-targeting AR antagonists or agents that repress androgen biosynthesis [6]. | Shihong Peng Zhengfang Yi Mingyao Liu | 2017 | Chinese Journal of Cancer2017，36，5： | 6 |
| 8 | Claudin 1 mediates tumor necrosis factor alpha-induced cell migration in human gastric cancer cells显示文摘AIM:To investigate the role of claudin 1 in the regulation of genes involved in cell migration and tumor necrosis factor alpha(TNF-α)-induced gene expression in human gastric adenocarcinoma cells.METHODS:Knockdown experiments were conducted with claudin 1 small interfering RNA(si RNA),and theeffects on the cell cycle,apoptosis,migration and invasion were analyzed in human gastric adenocarcinoma MKN28 cells.The gene expression profiles of cells were analyzed by microarray and bioinformatics.RESULTS:The knockdown of claudin 1 significantly inhibited cell proliferation,migration and invasion,and increased apoptosis.Microarray analysis identified 245genes whose expression levels were altered by the knockdown of claudin 1.Pathway analysis showed that the top-ranked molecular and cellular function was the cellular movement related pathway,which involved MMP7,TNF-SF10,TGFBR1,and CCL2.Furthermore,TNFand nuclear frctor-κB were the top-ranked upstream regulators related to claudin 1.TNF-αtreatment increased claudin 1 expression and cell migration in MKN28 cells.Microarray analysis indicated that the depletion of claudin1 inhibited 80%of the TNF-α-induced m RNA expression changes.Further,TNF-αdid not enhance cell migration in the claudin 1 si RNA transfected cells.CONCLUSION:These results suggest that claudin 1 is an important messenger that regulates TNF-α-induced gene expression and migration in gastric cancer cells.A deeper understanding of these cellular processes may be helpful in establishing new therapeutic strategies for gastric cancer. | Atsushi Shiozaki Hiroki Shimizu Daisuke Ichikawa Hirotaka Konishi Shuhei Komatsu Takeshi Kubota Hitoshi Fujiwara Kazuma Okamoto Daisuke Iitaka Shingo Nakashima Yoshito Nako Mingyao Liu Eigo Otsuji | 2014 | World Journal of Gastroenterology2014，20，47： | 6 |
| 9 | The role of GPCRs in bone diseases and dysfunctions显示文摘The superfamily of G protein-coupled receptors (GPCRs) contains immense structural and functional diversity and mediates a myriad of biological processes upon activation by various extracellular signals.Critical roles of GPCRs have been established in bone development,remodeling,and disease.Multiple human GPCR mutations impair bone development or metabolism,resulting in osteopathologies.Here we summarize the disease phenotypes and dysfunctions caused by GPCR gene mutations in humans as well as by deletion in animals.To date,92 receptors (5 glutamate family,67 rhodopsin family,5 adhesion,4 frizzled/taste2 family,5 secretin family,and 6 other 7TM receptors) have been associated with bone diseases and dysfunctions (36 in humans and 72 in animals).By analyzing data from these 92 GPCRs,we found that mutation or deletion of different individual GPCRs could induce similar bone diseases or dysfunctions,and the same individual GPCR mutation or deletion could induce different bone diseases or dysfunctions in different populations or animal models.Data from human diseases or dysfunctions identified 19 genes whose mutation was associated with human BMD:9 genes each for human height and osteoporosis;4 genes each for human osteoarthritis (OA) and fracture risk;and 2 genes each for adolescent idiopathic scoliosis (AIS),periodontitis,osteosarcoma growth,and tooth development.Reports from gene knockout animals found 40 GPCRs whose deficiency reduced bone mass,while deficiency of 22 GPCRs increased bone mass and BMD;deficiency of 8 GPCRs reduced body length,while 5 mice had reduced femur size upon GPCR deletion.Furthermore,deficiency in 6 GPCRs induced osteoporosis;4 induced osteoarthritis;3 delayed fracture healing;3 reduced arthritis severity;and reduced bone strength,increased bone strength,and increased cortical thickness were each observed in 2 GPCR-deficiency models.The ever-expanding number of GPCR mutation-associated diseases warrants accelerated molecular analysis,population studies,and investigation of phenotype correlation with SNPs to elucidate GPCR function in human diseases. | Jian Luo Peng Sun Stefan Siwko Mingyao Liu Jianru Xiao | 2019 | Bone Research2019，7，2： | 5 |
| 10 | Nano-hydroxyapatite accelerates vascular calcification via lysosome impairment and autophagy dysfunction in smooth muscle cells显示文摘Vascular calcification(VC)is a common characteristic of aging,diabetes,chronic renal failure,and atherosclerosis.The basic component of VC is hydroxyapatite(HAp).Nano-sized HAp(nHAp)has been identified to play an essential role in the development of pathological calcification of vasculature.However,whether nHAp can induce calcification in vivo and the mechanism of nHAp in the progression of VC remains unclear.We discovered that nHAp existed both in vascular smooth muscle cells(VSMCs)and their extracellular matrix(ECM)in the calcified arteries from patients.Synthetic nHAp had similar morphological and chemical properties as natural nHAp recovered from calcified artery.nHAp stimulated osteogenic differentiation and accelerated mineralization of VSMCs in vitro.Synthetic nHAp could also directly induce VC in vivo.Mechanistically,nHAp was internalized into lysosome,which impaired lysosome vacuolar H+-ATPase for its acidification,therefore blocked autophagic flux in VSMCs.Lysosomal re-acidification by cyclic-3′,5′-adenosine monophosphate(cAMP)significantly enhanced autophagic degradation and attenuated nHAp-induced calcification.The accumulated autophagosomes and autolysosomes were converted into calcium-containing exosomes which were secreted into ECM and accelerated vascular calcium deposit.Inhibition of exosome release in VSMCs decreased calcium deposition.Altogether,our results demonstrated a repressive effect of nHAp on lysosomal acidification,which inhibited autophagic degradation and promoted a conversion of the accumulated autophagic vacuoles into exosomes that were loaded with undissolved nHAp,Ca^(2+),Pi and ALP.These exosomes bud off the plasma membrane,deposit within ECM,and form calcium nodules.Vascular calcification was thus accelerated by nHAP through blockage of autophagic flux in VSMCs. | Qi Liu Yi Luo Yun Zhao Pingping Xiang Jinyun Zhu Wangwei Jing Wenjing Jin Mingyao Chen Ruikang Tang Hong Yu | 2022 | Bioactive Materials2022，7，2： | 5 |
| 11 | Generation of obese rat model by transcription activator-like effector nucleases targeting the leptin receptor gene显示文摘The laboratory rat is a valuable mammalian model organism for basic research and drug discovery. Here we demonstrate an efficient methodology by applying transcription activator-like effector nucleases(TALENs) technology to generate Leptin receptor(Lepr) knockout rats on the Sprague Dawley(SD) genetic background. Through direct injection of in vitro transcribed m RNA of TALEN pairs into SD rat zygotes, somatic mutations were induced in two of three resulting pups. One of the founders carrying bi-allelic mutation exhibited early onset of obesity and infertility. The other founder carried a chimeric mutation which was efficiently transmitted to the progenies. Through phenotyping of the resulting three lines of rats bearing distinct mutations in the Lepr locus, we found that the strains with a frame-shifted or premature stop codon mutation led to obesity and metabolic disorders. However, no obvious defect was observed in a strain with an in-frame 57 bp deletion in the extracellular domain of Lepr. This suggests the deleted amino acids do not significantly affect Lepr structure and function. This is the first report of generating the Lepr mutant obese rat model in SD strain through a reverse genetic approach. This suggests that TALEN is an efficient and powerful gene editing technology for the generation of disease models. | Yuting Chen Wenqing Lu Na Gao Yi Long Yanjiao Shao Meizhen Liu Huaqing Chen Shixin Ye Xueyun Ma Mingyao Liu Dali Li | 2017 | Science China(Life Sciences)2017，60，2： | 4 |
| 12 | XB130, a Novel Adaptor Protein, Promotes Thyroid Tumor Growth显示文摘 | Atsushi Shiozaki Monika Lodyga Xiao-Hui Bai Jeya Nadesalingam Takeshi Oyaizu Daniel Winer Sylvia L. Asa Shaf Keshavjee Mingyao Liu | 2011 | The American Journal of Pathology2011，，1： | 2 |
| 13 | Efficacy of seasonal pandemic influenza hemagglutinin DNA vaccines delivered by electroporation against aseasonal H1N1 virus challenge in mice显示文摘Prophylactic DNA vaccines against the influenza virus are promising alternatives to conventional vaccines.In this study,we generated two candidate gene-based influenza vaccines encoding either the seasonal or pandemic hemagglutinin antigen(HA) from the strains A/New Caledonia/20/99(H1N1)(pV1A5) and A/California/04/2009(H1N1)(pVEH1) ,respectively.After verifying antigen expression,the immunogenicity of the vaccines delivered intramuscularly with electroporation was tested in a mouse model.Sera of immunized animals were tested in hemagglutination inhibition assays and by ELISA for the presence of HA-specific antibodies.HA-specific T-cells were also measured in IFN-γELISpot assays.The protective efficacy of the candidate influenza vaccines was evaluated by measuring mortality rates and body weight after a challenge with 100 LD50 of mouse-adapted A/New Caledonia/20/99(H1N1) .Mice immunized with either one of the two vaccines showed significantly higher T cell and humoral immune responses(P<0.05) than the pVAX1 control group.Additionally,the pV1A5 vaccine effectively protected the mice against a lethal homologous mouse-adapted virus challenge with a survival rate of 100%compared with a 40%survival rate in the pVEH1 vaccinated group(P<0.05) .Our study indicates that the seasonal influenza DNA vaccine completely protects against the homologous A/New Caledonia/20/99 virus(H1N1) ,while the pandemic influenza DNA vaccine only partially protects against this virus. | TAN Lei LU HuiJun ZHANG Dan WANG KaiYan TIAN MingYao LIU CunXia LIU YanYu HU Bo JIN NingYi | 2011 | Science China(Life Sciences)2011，54，4： | 2 |
| 14 | Photoelectrochemical regeneration of all vanadium redox species for construction of a solar rechargeable flow cell显示文摘Energy storage is pivotal for the continuous utilization of solar energy suffering from the intermittency issue. Herein, we demonstrate a solar rechargeable flow cell(SRFC) based on photoelectrochemical regeneration of vanadium redox species for in-situ solar energy harvest and storage. In this device, TiO_2 and MWCNT/acetylene black(MWCNT/AB) composite are served as the photoanode and the counter electrode,respectively, with all vanadium redox couples, VO_2^+/VO^(2+)and VO^(2+)/V^(3+), as solar energy storage media.Benefitting from solar energy, the cell can be photocharged under a bias as low as 0.1 V, which is much lower than the discharge voltage of ~0.5 V. Photocharged under the optimized condition, the cell delivers a discharge energy of 23.0 mWh/L with 67.4% input electric energy savings. This prototype work may inspire the rational design for cost-effective solar energy storage devices. | Shichao Liao Jingying Shi Chunmei Ding Mingyao Liu Fengqiang Xiong Nan Wang Jian Chen Can Li | 2018 | Journal of Energy Chemistry2018，27，1： | 2 |
| 15 | A novel synthetic small molecule YF-452 inhibits tumor growth through antiangiogenesis by suppressing VEGF receptor 2 signaling显示文摘Tumor angiogenesis is characterized by abnormal vessel morphology, endowing tumor with highly hypoxia and unresponsive toward treatment. To date, mounting angiogenic factors have been discovered as therapeutic targets in antiangiogenic drug development. Among them, vascular endothelial growth factor receptor 2 (VEGFR2) inhibitors exerts potent antiangiogenic activity in tumor therapy. Therefore, it may provide a valid strategy for cancer treatment through targeting the tumor angiogenesis via VEGFR2 pathway. In this study, we established a high-profile compounds library and certificated a novel compound named N-(N-pyrrolidylacetyl)-9-(4-bromobenzyl)-1,3,4,9-tetrahydro-β-carboline (YF-452), which remarkably inhibited the migration, invasion and tube-like structure formation of human umbilical vein endothelial cells (HUVECs) with little toxicity invitro. Rat thoracic aorta ring assay indicated that YF-452 significantly blocked the formation of microvascular exvivo. In addition, YF-452 inhibited angiogenesis in chick chorioallantoic membrane (CAM) and mouse corneal micropocket assays. Moreover, YF-452 remarkably suppressed tumor growth in xenografts mice model. Furthermore, investigation of molecular mechanism revealed that YF-452 inhibited VEGF-induced phosphorylation of VEGFR2 kinase and the downstream protein kinases including extracellular signal regulated kinase (ERK), focal adhesion kinase (FAK) and Src. These results indicate that YF-452 inhibits angiogenesis and may be a potential antiangiogenic drug candidate for cancer therapy. | Yongrui Liu Yuan He Feifei Yang Xiaonan Cong Jinhua Wang Shihong Peng Dan Gao Weifang Wang Liping Lan Xuexiang Ying Mingyao Liu Yihua Chen Zhengfang Yi | 2017 | Science China(Life Sciences)2017，60，2： | 2 |
| 16 | Dietary isoleucine improved flesh quality,muscle antioxidant capacity,and muscle growth associated with AKT/TOR/S6K1 and AKT/FOXO3a signaling in hybrid bagrid catfish(Pelteobagrus vachelli♀×Leiocassis longirostris♂)显示文摘Background:Muscle is the complex and heterogeneous tissue,which comprises the primary edible part of the trunk of fish and mammals.Previous studies have shown that dietary isoleucine(Ile)exerts beneficial effects on growth in aquatic animals.However,there were limited studies regarding the benefits of Ile on fish muscle and their effects on flesh quality and muscle growth.Thus,this study was conducted to explore whether dietary Ile had affected flesh quality and muscle growth in hybrid bagrid catfish(Pelteobagrus vachelli♀×Leiocassis longirostris♂).Methods:A total of 630 hybrid fish,with an initial average body weight of 33.11±0.09 g,were randomly allotted into seven experimental groups with three replicates each,and respectively fed seven diets with 5.0,7.5,10.0,12.5,15.0,17.5,and 20.0 g Ile/kg diets for 8 weeks.Results:In the present study,we demonstrated that Ile significantly:(1)increased muscle protein and lipid contents and the frequency distribution of myofibers with≤20μm and≥50μm of diameter;(2)improved pH value,shear force,cathepsin B and L activities,hydroxyproline content,resilience,cohesiveness,and decreased cooking loss,lactate content,hardness,springiness,gumminess,and chewiness;(3)decreased reactive oxygen species(ROS),malondialdehyde(MDA),and protein carbonyl(PC)contents,GCLC and Keap1 mRNA levels,and up-regulated CuZnSOD,CAT,GPX1a,GST,and Nrf2 mRNA levels;(4)up-regulated the insulin-like growth factor 1,2(IGF-1,IGF-2),insulin-like growth factor 1 receptor(IGF-1R),proliferating cell nuclear antigen(PCNA),Myf5,Myod,Myog,Mrf4,and MyHC mRNA levels,and decreased MSTN mRNAlevel;(5)increased muscle protein deposition by activating AKT-TOR-S6K1 and AKT-FOXO3a signaling pathways.Conclusion:These results revealed that dietary Ile improved flesh quality,which might be due to increasing nutritional content,physicochemical,texture parameters,and antioxidant ability;promoting muscle growth by affecting myocytes hyperplasia and hypertrophy,and muscle protein deposition associated with protein synthesis and degradation signaling pathways.Finally,the quadratic regression analysis of chewiness,ROS,and protein contents against dietary Ile levels suggested that the optimal dietary Ile levels for hybrid bagrid catfish was estimated to be 14.19,12.36,and 12.78 g/kg diet,corresponding to 36.59,31.87,and 32.96 g/kg dietary protein,respectively. | Qin Jiang Mingyao Yan Ye Zhao Xiaoqiu Zhou Long Yin Lin Feng Yang Liu Weidan Jiang Pei Wu Yan Wang Defang Chen Shiyong Yang Xiaoli Huang Jun Jiang | 2021 | Journal of Animal Science and Biotechnology2021，12，4： | 2 |
| 17 | In vitro and in vivo evaluation of cucurbitacin E on rat hepatic CYP2C11 expression and activity using LC-MS/MS显示文摘This study explored the effects of cucurbitacin E(Cu E), a bioactive compound from Cucurbitaceae, on the metabolism/ pharmacokinetic of tolbutamide, a model CYP2C9/11 probe substrate, and hepatic CYP2C11 expression in rats. Liquid chromatography-(tandem) mass spectrometry(LC-MS/MS) assay was used to detect tolbutamide as well as 4-hydroxytolbutamide, and then successfully applied to the pharmacokinetic study of tolbutamide in rats. The effect of Cu E on CYP2C11 expression was determined by western blot. Cu E(1.25–100 μmol L-1) competitively inhibited tolbutamide 4-hydroxylation(CYP2C11) activity only in concentration-dependent manner with a Ki value of 55.5 μmol L-1 in vitro. In whole animal studies, no significant difference in metabolism/pharmacokinetic of tolbutamide was found for the single pretreatment groups. In contrast, multiple pretreatments of Cu E(200 μg kg-1 d-1, 3 d, i.p.) significantly decreased tolbutamide clearance(CL) by 25% and prolonged plasma half-time(T1/2) by 37%. Moreover, Cu E treatment(50–200 μg kg-1 d-1, i.p.) for 3 d did not affect CYP2C11 expression. These findings demonstrated that CuE competitively inhibited the metabolism of CYP2C11 substrates but had no effect on rat CYP2C11 expression. This study may provide a useful reference for the reasonable and safe use of herbal or natural products containing Cu E to avoid unnecessary drug-drug interactions. | Jian Lu Tonggui Ding Xuan Qin Mingyao Liu Xin Wang | 2017 | Science China(Life Sciences)2017，60，2： | 2 |
| 18 | Small molecule 1′-acetoxychavicol acetate suppresses breast tumor metastasis by regulating the SHP-1/STAT3/MMPs signaling pathway显示文摘 | Jieqiong Wang Li Zhang Guoliang Chen Jing Zhang Zhenxi Li Weiqiang Lu Mingyao Liu Xiufeng Pang | 2014 | Breast Cancer Research and Treatment2014，，2： | 2 |
| 19 | Novel hemostatic agents based on gelatin-microbial transglutaminase mix显示文摘Hemostasis is a major challenge in surgical procedures and traumas. Conventional hemostatic methods have limited efficacy and may cause additional tissue damage. In this study, we designed a novel hemostatic agent based on the in situ gel formation of gelatin cross-linked by a novel microbial transglutaminase(mTGase), in which the amino acid sequences differed from commercial mTGases. The new hemostatic agent showed the same biochemical crosslinking chemistry as the final stages of the blood coagulation cascade while using gelatin as a 'structural' protein(rather than fibrin) and a calcium-independent mTGase as the crosslinking catalyst(rather than factor XIIIa). In rat liver hemostasis models, the hemostatic agent not only showed a similar hemostatic effect as that of SURGIFLO~(positive control), but also stronger adhesion strength and elasticity than SURGIFLO~.Therefore, this biomimetic gelatin-mTGase mix hemostatic is a novel and effective surgical sealant. | Fang Lv Xiaonan Cong Wenshu Tang Yiming Han Yu Tang Yongrui Liu Liqiang Su Mingyao Liu Mingfei Jin Zhengfang Yi | 2017 | Science China(Life Sciences)2017，60，4： | 2 |
| 20 | Grain boundary optimization induced substantial squareness enhancement and high performance in iron-rich Sm-Co-Fe-Cu-Zr magnets显示文摘Increasing iron content has been witnessed an essential method to improve the remanence of 2:17-type Sm-Co-Fe-Cu-Zr magnets,however,the inferior squareness factor accompanied with the increased iron content turns into a neck sticking problem.In this work,the grain boundary optimization induced substantial squareness enhancement from 63.4%to 91.4%,and consequently an excellent maximum energy product of 32.63 MGOe have been achieved in iron-rich Sm-Co-Fe-Cu-Zr magnets via tuning solution process.It is clearly revealed that the grain boundary(GB)phases as well as the micro-twins’density in grain interiors can be controlled and interprets the enhancement mechanism of squareness. | Jun Cao Tianli Zhang Jinghua Liu Hao Xu Mingyao Hu Wei Xia Ao Wang Hui Wang Chengbao Jiang | 2021 | Journal of Materials Science & Technology2021，，26： | 2 |
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