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药学学报：英文版

药学学报：英文版

《药学学报》英文刊是由中国药学会和中国医学科学院药物研究所共同主办，主编为中国医学科学院药物研究所所长蒋建东教授医学教育网编辑整|理。本刊是由《药学学报》编辑部与荷兰ElsevierB.V.出版公司合作出版的药学综合性英文期刊，是《药学学报》的系列期刊，创刊于2011年6月。其办刊宗旨是搭建世界药学前沿和高端学术交流平台，引领和促进本学科的发展。
  • 发文量：710
  • 被引量：224
  • H指数：0
  • 开始收录时间：2015(1)
  • CNKI综合因子：1.959
  • 维普期刊影响因子： 1.478
  • 万方期刊影响因子：1.26
  • 创刊时间：2011
  • 国内刊号/CN：10-1171/R
    国际刊号/ISSN：2211-3835
  • 发行周期：月刊
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    主办单位：中国药学会;中国医学科学院药物研究所
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药学学报：英文版 >2023年第7期

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  • 摘要：Having great medicinal values,Dendrobium species of"Fengdou"(DSFs)are a taxonomically complex group in Dendrobium genus including many closely related and recently diverged species.Traditionally used DNA markers have been proved to be insufficient in authenticating many species of this group.Here,we investigated 101 complete plastomes from 23 DSFs,comprising 72 newly sequenced and 29 documented,which all exhibited well-conserved genomic organization and gene order.Plastomewide comparison showed the co-occurrence of single nucleotide polymorphisms(SNPs)and insertions/deletions(indels),which can be explained by both the repeat-associated and indel-associated mutation hypotheses.Moreover,guanine-cytosine(GC)content was found to be negatively correlated with the three divergence variables(SNPs,indels and repeats),indicating that GC content may reflect the level of the local sequence divergence.Our species authentication analyses revealed that the relaxed filtering strategies of sequence alignment had no negative impact on species identification.By assessing the maximum likelihood(ML)trees inferred from different datasets,we found that the complete plastome and large single-copy(LSC)datasets both successfully identified all 23 DSFs with the maximum bootstrap values.However,owing to the high efficiency of LSC in species identification,we recommend using LSC for accurate authentication of DSFs.
  • 摘要：Dr.Hai-Bin Luo is currently a Full Professor and the Associate Dean of School of Pharmaceutical Sciences at Sun Yat-sen University(SYSU),Guangzhou,China.He received his Bachelor’s degree from Xiamen University in 1999 and Ph.D.degree from Hong Kong Baptist University in 2005.His research interests currently encompass the development of novel drug design methods and its application to discovery of selective phosphodiesterase(PDEs)inhibitors against several important diseases.
  • 摘要：Peptide inhibition of the interactions of the tumor suppressor protein P53 with its negative regulators MDM2 and MDMX activates P53 in vitro and in vivo,representing a viable therapeutic strategy for cancer treatment.Using phage display techniques,we previously identified a potent peptide activator of P53,termed PMI(TSFAEYWNLLSP),with binding affinities for both MDM2 and MDMX in the low nanomolar concentration range.Here we report an ultrahigh affinity,dual-specificity peptide antagonist of MDM2 and MDMX obtained through systematic mutational analysis and additivitybased molecular design.Functional assays of over 100 peptide analogs of PMI using surface plasmon resonance and fluorescence polarization techniques yielded a dodecameric peptide termed PMI-M3(LTFLEYWAQLMQ)that bound to MDM2 and MDMX with K_(d)values in the low picomolar concentration range as verified by isothermal titration calorimetry.Co-crystal structures of MDM2 and of MDMX in complex with PMI-M3 were solved at 1.65 and 3.0 A resolution,respectively.Similar to PMI,PMI-M3 occupied the P53-binding pocket of MDM2/MDMX,which was dominated energetically by intermolecular interactions involving Phe3,Tyr6,Trp7,and Leu 10.Notable differences in binding between PMI-M3 and PMI were observed at other positions such as Leu4 and Met11 with MDM2,and Leu1 and Met11 with MDMX,collectively contributing to a significantly enhanced binding affinity of PMI-M3 for both proteins.By adding lysine residues to both ends of PMI and PMI-M3 to improve their cellular uptake,we obtained modified peptides termed PMI-2K(KTSFAEYWNLLSPK)and M3-2K(KLTFLEYWAQLMQK).Compared with PMI-2K,M3-2K exhibited significantly improved antitumor activities in vitro and in vivo in a P53-dependent manner.This super-strong peptide inhibitor of the P53-MDM2/MDMX interactions may become,in its own right,a powerful lead compound for anticancer drug development,and can aid molecular design of other classes of P53 activators as well for anticancer therapy.
  • 摘要：Optimization efforts were devoted to discover novel PDE10 A inhibitors in order to improve solubility and pharmacokinetics properties for a long-term therapy against pulmonary arterial hypertension(PAH)starting from the previously synthesized inhibitor A.As a result,a potent and highly selective PDE10 A inhibitor,14·3 HC1(half maximal inhibitory concentration,IC50=2.8 nmol/L and>3500-fold selectivity)exhibiting desirable solubility and metabolic stability with a remarkable bioavailability of50%was identified with the aid of efficient methods of binding free energy predictions.Animal PAH studies showed that the improvement offered by 14·3 HCl[2.5 mg/kg,oral administration(p.o.)]was comparable to tadalafil(5.0 mg/kg,p.o.),verifying the feasibility of PDE10 A inhibitors for the antiPAH treatment.The crystal structure of the PDE10 A-14 complex illustrates their binding pattern,which provided a guideline for rational design of highly selective PDE10 A inhibitors.
  • 摘要：Farnesoid X receptor(FXR)is widely accepted as a promising target for various liver diseases;however,panels of ligands in drug development show limited clinical benefits,without a clear mechanism.Here,we reveal that acetylation initiates and orchestrates FXR nucleocytoplasmic shuttling and then enhances degradation by the cytosolic E3 ligase CHIP under conditions of liver injury,which represents the major culprit that limits the clinical benefits of FXR agonists against liver diseases.Upon inflammatory and apoptotic stimulation,enhanced FXR acetylation at K217,closed to the nuclear location signal,blocks its recognition by importin KPNA3,thereby preventing its nuclear import.Concomitantly,reduced phosphorylation at T442 within the nuclear export signals promotes its recognition by exportin CRM1,and thereby facilitating FXR export to the cytosol.Acetylation governs nucleocytoplasmic shuttling of FXR,resulting in enhanced cytosolic retention of FXR that is amenable to degradation by CHIP.SIRT1 activators reduce FXR acetylation and prevent its cytosolic degradation.More importantly,SIRT1 activators synergize with FXR agonists in combating acute and chronic liver injuries.In conclusion,these findings innovate a promising strategy to develop therapeutics against liver diseases by combining SIRT1 activators and FXR agonists.
  • 摘要：The chemotherapy combined with photothermal therapy has been a favorable approach for the treatment of breast cancer.In present study,nanoparticles with the characteristics of photothermal/matrix metalloproteinase-2(MMP-2)dual-responsive,tumor targeting,and size-variability were designed for enhancing the antitumor efficacy and achieving"on-demand"drug release markedly.Based on the thermal sensitivity of gelatin,we designed a size-variable gelatin nanoparticle(GNP)to encapsulate indocyanine green(ICG)and doxorubicin(DOX).Under an 808 nm laser irradiation,GNP-DOX/ICG responded photothermally and swelled in size from 71.58?4.28 to 160.80?9.51 nm,which was beneficial for particle retention in the tumor sites and release of the loaded therapeutics.Additionally,GNP-DOX/ICG showed a size reduction of the particles to 33.24?4.11 nm and further improved drug release with the degradation of overexpressed MMP-2 in tumor.In the subsequently performed in vitro experiments,it was confirmed that GNP-DOX/ICG could provide a therapeutic effect that was enhanced and synergistic.Consequently,GNP-DOX/ICG could efficiently suppress the growth of 4 T1 tumor in vivo.In conclusion,this study may provide a promising strategy in the rational design of drug delivery nanosystems based on gelatin for chemo-photothermal therapy to achieve synergistically enhanced therapeutic efficacy against breast cancer.
  • 摘要：Mutations in genes encoding key players in oncogenic signaling pathways trigger specific downstream gene expression profiles in the respective tumor cell populations.While regulation of genes related to cell growth,survival,and death has been extensively studied,much less is known on the regulation of drug-metabolizing enzymes(DMEs)by oncogenic signaling.Here,a comprehensive review of the available literature is presented summarizing the impact of the most relevant genetic alterations in human and rodent liver tumors on the expression of DMEs with a focus on phasesⅠandⅡof xenobiotic metabolism.Comparably few data are available with respect to DME regulation by p53-dependent signaling,telomerase expression or altered chromatin remodeling.By contrast,DME regulation by constitutive activation of oncogenic signaling via the RAS/RAF/mitogen-activated protein kinase(MAPK)cascade or via the canonical WNT/β-catenin signaling pathway has been analyzed in greater depth,demonstrating mostly positive-regulatory effects of WNT/β-catenin signaling and negativeregulatory effects of MAPK signaling.Mechanistic studies have revealed molecular interactions between oncogenic signaling and nuclear xeno-sensing receptors which underlie the observed alterations in DME expression in liver tumors.Observations of altered DME expression and inducibility in liver tumors with a specific gene expression profile may impact pharmacological treatment options.
  • 摘要：Leading by cytotoxicity against HepG2 cells,bioactivity-guided fractionation of the EtOAc fraction from Artemisia atrovirens led to the isolation of 18 new guaianolide dimers,artematrolides A-R and lavandiolides A,B,C,H,and J.Eight compounds(1,4,10,12,13,and 19-21) were unambiguously confirmed by the single-crystal X-ray diffraction analyses,and the others were elucidated based on IR,UV,HRESIMS,1 D and 2 D NMR experiments,and comparison of the experimental and calculated ECD data.Structurally,all of them were [4+2] Diels-Alder adducts of two monomeric guaianolides.The isolates were evaluated for their cytotoxicity against three human hepatoma cell lines,and 19 compounds demonstrated cytotoxicity against HepG2,SMMC-7721,and Huh7 cell lines.Especially,compounds 1,12,14,and 15 exhibited cytotoxicity with IC50 values of 4.4,3.8,7.6,and 6.7 μmol/L(HepG2),9.6,4.6,6.6,and 6.0 μmol/L(SMMC-7721),and 7.6,4.5,6.9,and 5.6 μmol/L(Huh7),respectively.Notably,compound 12 showed the most promising activity against three human hepatoma cell lines and dose-dependently inhibited cell migration and invasion,induced G2/M cell cycle arrest and cell apoptosis in HepG2 cells,down-regulated the expression of BCL-2 and PARP-1,and activated PARP-1 to up-regulate the expression of cleaved-PARP-1.
  • 摘要：Disrupted redox status primarily contributes to myocardial ischemia/reperfusion injury(MIRI).NRF2,the endogenous antioxidant regulator,might provide therapeutic benefits.Dihydrotanshinone-Ⅰ(DT)is an active component in Salvia miltiorrhiza with NRF2 induction potency.This study seeks to validate functional links between NRF2 and cardioprotection of DT and to investigate the molecular mechanism particularly emphasizing on NRF2 cytoplasmic/nuclear translocation.DT potently induced NRF2 nuclear accumulation,ameliorating post-reperfusion injuries via redox alterations.Abrogated cardioprotection in NRF2-deficient mice and cardiomyocytes strongly supports NRF2-dependent cardioprotection of DT.Mechanistically,DT phosphorylated NRF2 at Ser40,rendering its nuclear-import by dissociating from KEAP1 and inhibiting degradation.Importantly,we identified PKC-δ-(Thr505)phosphorylation as primary upstream event triggering NRF2-(Ser40)phosphorylation.Knockdown of PKC-δdramatically retained NRF2 in cytoplasm,convincing its pivotal role in mediating NRF2 nuclear-import.NRF2 activity was further enhanced by activated PKB/GSK-3βsignaling via nuclear-export signal blockage independent of PKC-δactivation.By demonstrating independent modulation of PKC-δand PKB/GSK-3β/Fyn signaling,we highlight the ability of DT to exploit both nuclear import and export regulation of NRF2 in treating reperfusion injury harboring redox homeostasis alterations.Coactivation of PKC and PKB phenocopied cardioprotection of DT in vitro and in vivo,further supporting the potential applicability of this rationale.
  • 摘要：The goal of this investigation was to develop and demonstrate a polymer/paclitaxel selfassembly(PTX-SA) formulation. Polymer/PTX-SAs were screened based on smaller size of formulation using dynamic light scattering analysis. Additionally, fluorescence microscopy and flow cytometry studies exhibited that polyvinylpyrrolidone(PVP)-based PTX-SAs(PVP/PTX-SAs) had superior cellular internalization capability in MCF7 and MDA-MB-231 breast cancer cells. The optimized PVP/PTXSAs exhibited less toxicity to human red blood cells indicating a suitable formulation for reducing systemic toxicity. The formation of PVP and PTX self-assemblies was confirmed using fluorescence quenching and transmission electron microscopy which indicated that the PVP/PTX-SAs were spherical in shape with an average size range of 53.81 nm as detected by transmission electron microscopy(TEM).FTIR spectral analysis demonstrates incorporation of polymer and paclitaxel functional groups in PVP/PTX-SAs. Both proliferation(MTS) and clonogenic(colony formation) assays were used to validate superior anticancer activity of PVP/PTX-SAs in breast cancer cells over paclitaxel. Such superior anticancer activity was also demonstrated by downregulation of the expression of pro-survival protein(Bcl-x L), upregulation of apoptosis-associated proteins(Bid, Bax, cleaved caspase 7, and cleaved PARP)and β-tubulin stabilization. These results support the hypothesis that PVP/PTX-SAs improved paclitaxel delivery to cancer cells.
  • 摘要：10-DeacetylbaccatinⅢ(10-DAB)C10 acetylation is an indispensable procedure for Taxol semi-synthesis,which often requires harsh conditions.10-DeacetylbaccatinⅢ-10-β-O-acetyltransferase(DBAT)catalyzes the acetylation but acetyl-CoA supply remains a key limiting factor.Here we refactored the innate biosynthetic pathway of acetyl-CoA in Escherichia coli and obtained a chassis with acetyl-CoA productivity over three times higher than that of the host cell.Then,we constructed a microbial cell factory by introducing DBAT gene into this chassis for efficiently converting 10-DAB into baccatinⅢ.We found that baccatinⅢcould be efficiently deacetylated into 10-DAB by DBAT with CoASH and K+under alkaline condition.Thus,we fed acetic acid to the engineered strain both for serving as a substrate of acetyl-CoA biosynthesis and for alleviating the deacetylation of baccatinⅢ.The fermentation conditions were optimized and the baccatinⅢtiters reached 2,3 and 4.6 g/L,respectively,in a 3-L bioreactor culture when 2,3 and 6 g/L of 10-DAB were supplied.Our study provides an environmentfriendly approach for the large scale 10-DAB acetylation without addition of acetyl-CoA in the industrial Taxol semi-synthesis.The finding of DBAT deacetylase activity may broaden its application in the structural modification of pharmaceutically important lead compounds.
  • 摘要：The immune checkpoints,cytotoxic T-lymphocyte-associated antigen 4(CTLA-4) and programmed cell death protein-1/ligand-1(PD-1/PD-L1) are vital contributors to immune resulation and tolerance.Recently immune checkpoint inhibitors(ICIs) have revolutionized cancer therapy;however,they come with the cost of immune related adverse events involving multiple organs such as the liver.Due to its constant expo sure to foreign antigens,the liver has evolved a high capacity for immune tolerance,therefore,blockade of the immune checkpoints can result in aberrant immune activation affecting the liver in up to 20% of patients depending on the agent(s) used and underlying factors.This type of hepatotoxicity is termed immune mediated liver injury from checkpoint inhibitors(ILICI) and is more common when CTLA4 and PD-1/PDL1 are used in combination.The underlying mechanisms of this unique type of hepatotoxicity are not fully understood;however,the contribution of CD8^(+) cytotoxic T lymphocytes,various CD4^(+) T cells populations,cytokines,and the secondary activation of the innate immune system leading to liver injury have all been suggested.This review summarizes our current understanding of the underlying mechanisms of liver injury in immunotherapy using animal models of ILICI and available patient data from clinical studies.
  • 摘要：Blood-brain barrier(BBB)breakdown and the associated microvascular hyperpermeability are hallmark features of several neurological disorders,including traumatic brain injury(TBI).However,there is no viable therapeutic strategy to rescue BBB function.Tissue inhibitor of metalloproteinase-1(TIMP1)has been considered to be beneficial for vascular integrity,but the molecular mechanisms underlying the functions of TIMP1 remain elusive.Here,we report that TIMP1 executes a protective role on neuroprotective function via ameliorating BBB disruption in mice with experimental TBI.In human brain microvessel endothelial cells(HBMECs)exposed to hypoxia and inflammation injury,the recombinant TIMP1(rTIMP1)treatment maintained integrity of junctional proteins and trans-endothelial tightness.Mechanistically,TIMP1 interacts with CD63/integrinβ1 complex and activates downstream FAK signaling,leading to attenuation of RhoA activation and F-actin depolymerization for endothelial cells structure stabilization.Notably,these effects depend on CD63/integrinβ1 complex,instead of the MMP-inhibitory function.Together,our results identified a novel MMP-independent function of TIMP1 in regulating endothelial barrier integrity.Therapeutic interventions targeting TIMP1 and its downstream signaling may be beneficial to protect BBB function following brain injury and neurological disorders.
  • 14.Front
    摘要：Certain post-translational modifications are required for proteins quality control and intracellular transportation. Here, Yuan et al. found that S-palmitoylation played an important role in the intracellular transport of CLDN3, a tight junction protein involved in ovarian cancer progression. Mechanistically, ZDHHC12-mediated S-palmitoylation is prerequisite for CLDN3 transporting to the cell membrane.
  • 摘要：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.
  • 摘要：Acta Pharmaceutica Sinica B is an English language bimonthly peer-reviewed journal published online in Science Direct which invites research articles,reviews and communications in all areas of the pharmaceutical sciences.It is one of a series of Acta Pharmaceutica Sinica journals founded in 1953 and sponsored by the Institute of Materia Medica,Chinese Academy of Medical Sciences and the Chinese Pharmaceutical Association.It is produced and hosted by Elsevier B.V.
  • 摘要：Ferroptosis is a type of cell death accompanied by iron-dependent lipid peroxidation,thus stimulating ferroptosis may be a potential strategy for treating gastric cancer,therapeutic agents against which are urgently required.Jiyuan oridonin A(JDA) is a natural compound isolated from Jiyuan Rabdosia rubescens with anti-tumor activity,unclear anti-tumor mechanisms and limited water solubility hamper its clinical application.Here,we showed a2,a new JDA derivative,inhibited the growth of gastric cancer cells.Subsequently,we discovered for the first time that a2 induced ferroptosis.Importantly,compound a2 decreased GPX4 expression and overexpressing GPX4 antagonized the anti-proliferative activity of a2.Furthermore,we demonstrated that a2 caused ferrous iron accumulation through the autophagy pathway,prevention of which rescued a2 induced ferrous iron elevation and cell growth inhibition.Moreover,a2 exhibited more potent anti-cancer activity than 5-fluorouracil in gastric canc er cell line-derived xenograft mice models.Patient-derived tumor xenograft models from different patients displayed varied sensitivity to a2,and GPX4 downregulation indicated the sensitivity of tumors to a2.Finally,a2 exhibited well pharmacokinetic characteristic s.Overall,our data suggest that inducing ferroptosis is the major mechanism mediating anti-tumor activity of a2,and a2 will hopefully serve as a promising compound for gastric cancer treatment.
  • 摘要：Protein arginine methyltransferases(PRMTs)have been implicated in the progression of many diseases.Understanding substrate recognition and specificity of individual PRMT would facilitate the discovery of selective inhibitors towards future drug discovery.Herein,we reported the design and synthesis of bisubstrate analogues for PRMTs that incorporate a S-adenosylmethionine(SAM)analogue moiety and a tripeptide through an alkyl substituted guanidino group.Compound AH237 is a potent and selective inhibitor for PRMT4 and PRMT5 with a half-maximal inhibition concentration(IC_(50)) of 2.8 and0.42 nmol/L,respectively.Computational studies provided a plausible explanation for the high potency and selectivity of AH237 for PRMT4/5 over other 40 methyltransferases.This proof-of-principle study outlines an applicable strategy to develop potent and selective bisubstrate inhibitors for PRMTs,providing valuable probes for future structural studies.
  • 摘要：We demonstrate a novel inorganic-organic crystalline nanoconstruct, where gold atoms were imbedded in the crystal lattices as defects of camptothecin nanocrystals, suggesting its potential use as simultaneous agents for cancer therapy and bioimaging. The incorporation of gold, a potential computed tomography(CT) contrast agent, in the nanocrystals of camptothecin was detected by transmission electron microscope(TEM) and further quantified by energy dispersive X-ray spectrometry(EDS) and inductively coupled plasma-optical emission spectrometers(ICP-OES). Due to gold's high attenuation coefficient, only a relatively small amount needs to be present in order to create a good noise-to-contrast ratio in CT imaging. The imbedded gold atoms and clusters are expected to share the same biological fate as the camptothecin nanocrystals, reaching and accumulating in tumor site due to the enhanced permeation and retention(EPR) effect.
  • 摘要：Growth hormone deficiency(GHD)has become a serious healthcare burden,and presents a huge impact on the physical and mental health of patients.Here,we developed an actively separated microneedle patch(PAA/NaHCO_(3)^(-)Silk MN)based on silk protein for sustained release of recombinant human growth hormone(rhGH).Silk protein,as a friendly carrier material for proteins,could be constructed in mild full-water conditions and ensure the activity of rhGH.After manually pressing PAA/NaHCO_(3)^(-)Silk MN patch to skin for 1 min,active separation is achieved by absorbing the interstitial fluid(ISF)to trigger HCO_(3)^(-)in the active backing layer to produce carbon dioxide gas(CO_(2)).In rats,the MN patch could maintain the sustained release of rhGH for more than 7 days,and produce similar effects as daily subcutaneous(S.C.)injections of rhGH in promoting height and weight with well tolerated.Moreover,the PAA/NaHCO_(3)^(-)Silk MN patch with the potential of painless self-administration,does not require cold chain transportation and storage possess great economic benefits.Overall,the PAA/NaHCO_(3)^(-)Silk MN patch can significantly improve patient compliance and increase the availability of drugs,meet current unmet clinical needs,improve clinical treatment effects of GHD patients.
  • 摘要：Nature has endowed gaseous molecules such as O_(2),CO_(2),CO,NO,H2 S,and N2 with critical and diverse roles in sustaining life,from supplying energy needed to power life and building blocks for life ’s physical structure to mediating and coordinating cellular functions.In this article,we give a brief introduction of the complex functions of the various gaseous molecules in life and then focus on carbon monoxide as a specific example of an endogenously produced signaling molecule to highlight the importance of this class of molecules.The past twenty years have seen much progress in understanding CO’s mechanism(s) of action and pharmacological effects as well as in developing delivery methods for easy administration.One remarkable trait of CO is its pleiotropic effects that have few parallels,except perhaps its sister gaseous signaling molecules such as nitric oxide and hydrogen sulfide.This review will delve into the sophistication of CO-mediated signaling as well as its validated pharmacological functions and possible therapeutic applications.
  • 摘要：Natural products have provided numerous lead compounds for drug discovery.However,the traditional analytical methods cannot detect most of these active components,especially at their usual low concentrations,from complex natural products.Herein,we reviewed the recent technological advances(2015-2019)related to the separation and screening bioactive components from natural resources,especially the emerging screening methods based on the bioaffinity techniques,including biological chromatography,affinity electrophoresis,affinity mass spectroscopy,and the latest magnetic and optical methods.These screening methods are uniquely advanced compared to other traditional methods,and they can fish out the active components from complex natural products because of the affinity between target and components,without tedious separation works.Therefore,these new tools can reduce the time and cost of the drug discovery process and accelerate the development of more effective and better-targeted therapeutic agents.
  • 摘要：Ischemic preconditioning(IPC)is a potential intervention known to protect the heart against ischemia/reperfusion injury,but its role in the no-reflow phenomenon that follows reperfusion is unclear.Dihydrotanshinone I(DT)is a natural compound and this study illustrates its role in cardiac ischemic injury from the aspect of IPC.Pretreatment with DT induced modest ROS production and protected cardiomyocytes against oxygen and glucose deprivation(OGD),but the protection was prevented by a ROS scavenger.In addition,DT administration protected the heart against isoprenaline challenge.Mechanistically,PKM2 reacted to transient ROS via oxidization at Cys423/Cys424,leading to glutathionylation and nuclear translocation in dimer form.In the nucleus,PKM2 served as a co-factor to promote HIF-1a-dependent gene induction,contributing to adaptive responses.In mice subjected to permanent coronary ligation,cardiac-specific knockdown of Pkm2 blocked DT-mediated preconditioning protection,which was rescued by overexpression of wild-type Pkm2,rather than Cys423/424-mutated Pkm2.In conclusion,PKM2 is sensitive to oxidation,and subsequent glutathionylation promotes its nuclear translocation.Although IPC has been viewed as a protective means against reperfusion injury,our study reveals its potential role in protection of the heart from no-reflow ischemia.
  • 摘要：Pesticide residue analysis plays an important role in the quality control of Chinese materia medica.This paper reports the development and validation of an analytical method for the quantitative determination of the residues of 39 pesticides in 12 different matrices of Chinese materia medica.Sample preparation utilized the QuEChERS method with acetonitrile:1% aqueous acetic acid(9:1,v/v)as extraction solvent followed by sample clean-up by dispersive solid phase extraction using primary secondary amine sorbent and graphitized carbon black.Extracts were then analysed by gas chromatography coupled with electron impact mass spectrometry in the selected ion monitoring mode.Limit of detection(LOD)and limit of quantitation(LOQ)values were in the ranges 0.5-50 ng/g and 1-100 ng/g,respectively.The recoveries of the 39 pesticides were in the range 75-112% with precision(as relative standard deviation,RSD)<15%.The results show that the modified QuEChERS method allows rapid and sensitive analysis of multiple pesticide residues in Chinese materia medica.
  • 摘要：Molecular imaging has become a hot research area since the early of this century.It utilizes the molecular interaction between the imaging probes and the particular targets to image the change of the area of interest.Molecular imaging opens up the possibility of early diagnosis as well as monitoring treatment response and outcomes that tailors individualized therapies.Researches have been focused on the development of imaging probes for various
  • 摘要：Front Cancer immunotherapy has recently attracted much attention, which mainly features the administration of antibodies that block the so-called immune checkpoint pathways. Herein, this paper examined the effect of SHP099, an SHP2 allosteric inhibitor, on tumor growth in mouse xenograft models.
  • 摘要：Acidosis,regardless of hypoxia involvement,is recognized as a chronic and harsh tumor microenvironment(TME)that educates malignant cells to thrive and metastasize.Although overwhelming evidence supports an acidic environment as a driver or ubiquitous hallmark of cancer progression,the unrevealed core mechanisms underlying the direct effect of acidification on tumorigenesis have hindered the discovery of novel therapeutic targets and clinical therapy.Here,chemical-induced and transgenic mouse models for colon,liver and lung cancer were established,respectively.miR-7 and TGF-β2 expressions were examined in clinical tissues(n=184).RNA-seq,miRNA-seq,proteomics,biosynthesis analyses and functional studies were performed to validate the mechanisms involved in the acidic TME-induced lung cancer metastasis.Our data show that lung cancer is sensitive to the increased acidification of TME,and acidic TME-induced lung cancer metastasis via inhibition of miR-7-5 p.TGF-β2 is a direct target of miR-7-5 p.The reduced expression of miR-7-5 p subsequently increases the expression of TGF-β2 which enhances the metastatic potential of the lung cancer.Indeed,overexpression of miR-7-5 p reduces the acidic p H-enhanced lung cancer metastasis.Furthermore,the human lung tumor samples also show a reduced miR-7-5 p expression but an elevated level of activated TGF-β2;the expressions of both miR-7-5 p and TGF-β2 are correlated with patients’survival.We are the first to identify the role of the miR-7/TGF-β2 axis in acidic p H-enhanced lung cancer metastasis.Our study not only delineates how acidification directly affects tumorigenesis,but also suggests miR-7 is a novel reliable biomarker for acidic TME and a novel therapeutic target for non-small cell lung cancer(NSCLC)treatment.Our study opens an avenue to explore the p H-sensitive subcellular components as novel therapeutic targets for cancer treatment.
  • 摘要：The research process for new drug is complicated,time-consum-ing,and costly.Thousands of chemical compounds must be made and tested in an effort to find one that can achieve a desirable result.It may take approximately ten years to study and test a new drug before it can be approved for the general public.However,in today's pharmaceutical industry drug delivery has become keys in drug product development.New innovative pharmaceutical technologies allow for increased performance of new and existing pharmaceutical compounds.
  • 摘要：Lysosome is a ubiquitous acidic organelle fundamental for the turnover of unwanted cellular molecules,particles,and organelles.Currently,the pivotal role of lysosome in regulating cell death is drawing great attention.Over the past decades,we largely focused on how lysosome influences apoptosis and autophagic cell death.However,extensive studies showed that lysosome is also prerequisite for the execution of regulated necrosis(RN).Different types of RN have been uncovered,among which,necroptosis,ferroptosis,and pyroptosis are under the most intensive investigation.It becomes a hot topic nowadays to target RN as a therapeutic intervention,since it is important in many patho/physiological settings and contributing to numerous diseases.It is promising to target lysosome to control the occurrence of RN thus altering the outcomes of diseases.Therefore,we aim to give an introduction about the common factors influencing lysosomal stability and then summarize the current knowledge on the role of lysosome in the execution of RN,especially in that of necroptosis,ferroptosis,and pyroptosis.
  • 摘要：Fresh from being archived by Pub Med Central(PMC),the world’s largest and most-used biomedical literature database,Acta Pharmaceutica Sinica B is now indexed by Thomson Reuters Web of Science:Emerging Sources Citation

    药学学报：英文版的期刊信息

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    • 地区：CHINA MAINLAND
    • 语言：中文
    • 热门主题：ACTA SINICA AUTHORS DRUG INFORMATION NANOPARTICLES TARGETING PHARMACEUTICAL CANCER METABOLISM
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      1

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