Publications by authors named "Wenxiu Qi"

17 Publications

  • Page 1 of 1

Ginseng in vascular dysfunction: A review of therapeutic potentials and molecular mechanisms.

Phytother Res 2022 Jan 13. Epub 2022 Jan 13.

Jilin Ginseng Academy, Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Jilin Provincial Key Laboratory of Bio-Macromolecules of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, China.

Vascular dysfunction can lead to a variety of fatal diseases, including cardiovascular and cerebrovascular diseases, metabolic syndrome, and cancer. Although a large number of studies have reported the therapeutic effects of natural compounds on vascular-related diseases, ginseng is still the focus of research. Ginseng and its active substances have bioactive effects against different diseases with vascular dysfunction. In this review, we summarized the key molecular mechanisms and signaling pathways of ginseng, its different active ingredients or formula in the prevention and treatment of vascular-related diseases, including cardiac-cerebral vascular diseases, hypertension, diabetes complications, and cancer. Moreover, the bidirectional roles of ginseng in promoting or inhibiting angiogenesis have been highlighted. We systematically teased out the relationship between ginseng and vascular dysfunction, which could provide a basis for the clinical application of ginseng in the future.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/ptr.7369DOI Listing
January 2022

Evidence of TCM Theory in Treating the Same Disease with Different Methods: Treatment of Pneumonia with and as an Example.

Evid Based Complement Alternat Med 2020 28;2020:8873371. Epub 2020 Nov 28.

Changchun University of Chinese Medicine, Changchun 130117, China.

Pneumonia is a serious global health problem and the leading cause of mortality in children. Antibiotics are the main treatment for bacterial pneumonia, but there are serious drug resistance problems. Traditional Chinese medicine (TCM) has been used to treat diseases for thousands of years and has a unique theory. This article takes the treatment of pneumonia with as a representative hot medicine and as a representative cold medicine as an example. We explore and explain the theory of treating the same disease with different TCM treatments. Using transcriptomics and network pharmacology methods, GO, KEGG enrichment, and PPI network construction were carried out, demonstrating that plays a therapeutic role through the NF-B and apoptosis signaling pathways targeting PLAU, CD40LG, BLC2L1, CASP7, and CXCL8. The targets of through the IL-17 signaling pathway are MMP9, CXCL8, and MAPK14. Molecular docking technology was also used to verify the results. In short, our results provide evidence for the theory of treating the same disease with different treatments, and we also discuss future directions for traditional Chinese medicine.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1155/2020/8873371DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7737398PMC
November 2020

The effects of cytarabine combined with ginsenoside compound K synergistically induce DNA damage in acute myeloid leukemia cells.

Biomed Pharmacother 2020 Dec 12;132:110812. Epub 2020 Oct 12.

Research Center of Traditional Chinese Medicine, the Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China; Key Laboratory of Active Substances and Biological Mechanisms of Ginseng Efficacy, Ministry of Education, Changchun, Jilin, China. Electronic address:

AML is a kind of hematological malignant tumor that urgently requires different treatment options in order to increase the cure rate and survival rate. Cytarabine (ara-C) is currently the main drug used to treat AML patients and is usually combined with different chemotherapeutic agents. However, due to resistance to ara-C, a new combination is needed to reduce ara-C resistance and improve treatment outcome. As is known to all, ginseng is a traditional Chinese herb; compound K is the principal metabolic product of ginsenoside which also has anti-cancer activity in some cancer cells, while the mechanism is unclear. In our previous study, we found that compound K inhibited AML cell viability and induced apoptosis, and compound K combined with ara-C synergistically induced AML cell proliferation arrest. Thus, we sought to investigate the reason for this by focusing on the mitochondrial dysfunction and DNA damage. In this paper, our results provide a foundation for the clinical evaluation of concomitant administration of compound K and ara-C in order to reduce the resistance to ara-C and improve AML treatment.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.biopha.2020.110812DOI Listing
December 2020

Protective effect of pig brain polypeptides against corticosterone-induced oxidative stress, inflammatory response, and apoptosis in PC12 cells.

Biomed Pharmacother 2019 Jul 22;115:108890. Epub 2019 Apr 22.

Research Center of Traditional Chinese Medicine, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China. Electronic address:

Objective: Pig brain polypeptides (PBP), active polypeptides hydrolysate extracted from fresh porcine brain tissue, has been shown to have neuroprotective effects in both in vitro and in vivo studies. The present study aimed to explore the molecular mechanisms underlying the neuroprotective effects of PBP in corticosterone (CORT)-induced rat adrenal pheochromocytoma PC12 cells.

Methods: Cell viability and lactate dehydrogenase (LDH) release were measured in PC12 cells induced with 200 μM CORT in the presence or absence of various concentrations of PBP for 48 h. Intracellular reactive oxygen species (ROS) generation, the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and glutathione (GSH) content were examined to analyze the effect of PBP on CORT-induced oxidative stress. The levels of pro-inflammatory factors, the percentage of apoptotic cells, and apoptosis-related protein expression in PC12 cells were determined.

Results: PBP is mainly composed of protein subunits with molecular weights ranging from 1000 to 10,000 Da. PBP treatment increased cell viability and decreased the release of LDH in CORT-stimulated PC12 cells. Moreover, PBP reduced the level of CORT-induced oxidative stress by decreasing ROS levels and increasing SOD, GSH-Px activities and GSH content. PBP had an inhibitory effect on the CORT-induced inflammatory response through inhibition of the NF-κB signaling pathway. PBP also inhibited CORT-induced apoptosis by downregulating the mitochondrial apoptotic signaling pathway.

Conclusion: These results suggest that PBP exerts a neuroprotective effect against CORT-induced cell injury by inhibiting oxidative stress, inflammation, and apoptosis. PBP could act as a neuroprotective agent against nerve injury induced by CORT.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.biopha.2019.108890DOI Listing
July 2019

Inhibition of Wee1 sensitizes AML cells to ATR inhibitor VE-822-induced DNA damage and apoptosis.

Biochem Pharmacol 2019 06 20;164:273-282. Epub 2019 Apr 20.

Research Center of Traditional Chinese Medicine, The Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China. Electronic address:

Resistance to standard induction therapy and relapse remain the primary challenges for improving therapeutic effects in acute myeloid leukemia (AML); thus, novel therapeutic strategies are urgently required. Ataxia telangiectasia and Rad3-related protein (ATR) is a key regulator of different types of DNA damage, which is crucial for the maintenance of genomic integrity. The ATR-selective inhibitor VE-822 has proper solubility, potency, and pharmacokinetic properties. In this study, we investigated the anti-leukemic effects of VE-822 alone or combined with Wee1-selective inhibitor AZD1775 in AML cells. Our results showed that VE-822 inhibited AML cell proliferation and induced apoptosis in a dose-dependent manner. AZD1775 significantly promoted VE-822-induced inhibition of AML cell proliferation and led to a decreased number of cells in the G2/M phase. VE-822 and AZD1775 decreased the protein levels of ribonucleotide reductase M1 (RRM1) and M2 (RRM2) subunits, key enzymes in the synthesis of deoxyribonucleoside triphosphate, which increased DNA replication stress. VE-822 combined with AZD1775 synergistically induced AML cell apoptosis and led to replication stress and DNA damage in AML cell lines. Our study demonstrated that AZD1775 synergistically promotes VE-822-induced anti-leukemic activity in AML cell lines and provides support for clinical research on VE-822 in combination with AZD1775 for the treatment of AML patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.bcp.2019.04.022DOI Listing
June 2019

Synergistic anti-leukemic interactions between panobinostat and MK-1775 in acute myeloid leukemia ex vivo.

Cancer Biol Ther 2015 ;16(12):1784-93

b Department of Oncology ; Wayne State University School of Medicine ; Detroit , MI USA.

MK-1775 is the first-in-class selective Wee1 inhibitor which has been demonstrated to synergize with CHK1 inhibitors in various malignancies. In this study, we report that the pan-histone deacetylase inhibitor (HDACI) panobinostat synergizes with MK-1775 in acute myeloid leukemia (AML), a malignancy which remains a clinical challenge and requires more effective therapies. Using both AML cell line models and primary patient samples, we demonstrated that panobinostat and MK-1775 synergistically induced proliferation arrest and cell death. We also demonstrated that panobinostat had equal anti-leukemic activities against primary AML blasts derived from patients either at initial diagnosis or at relapse. Interestingly, treatment with panobinostat alone or in combination with MK-1775 resulted in decreased Wee1 protein levels as well as downregulation of the CHK1 pathway. shRNA knockdown of CHK1 significantly sensitized AML cells to MK-1775 treatment, while knockdown of Wee1 significantly enhanced both MK-1775- and panobinostat-induced cell death. Our results demonstrate that panobinostat synergizes with MK-1775 in AML cells, at least in part through downregulation of CHK1 and/or Wee1, providing compelling evidence for the clinical development of the combination treatment in AML.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1080/15384047.2015.1095406DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4847803PMC
October 2016

Bleach etches nanosilver: HOCl-responsive drug delivery system to target leukemic cells.

J Mater Chem B 2015 Jul 17;3(28):5711-5719. Epub 2015 Jun 17.

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, College of Chemistry, Jilin University, Changchun, 130012, China.

In addition to their well-known antibacterial property, silver nanoparticles (Ag NPs) have also been highlighted as anti-leukemic agents; however, the underlying mechanism responsible for inhibiting the growth of hematopoietic cancer cells is so far poorly understood. In previous reports, Ag NP-induced oxidative stress was implicated for therapeutic efficacy but the excessive production of ROS in several hematopoietic malignant cells, which can potentially induce the dissolution of Ag NPs, was not taken into consideration. In this study we proposed Ag NP dissolution, in response to increased oxidative stress in leukemic cells, as the most probable mechanism for their anticancer activity. Hypochlorous acid-mediated dissolution of therapeutically active and ultrasmall (<5 nm) Ag NPs was also exploited to develop an oxidant responsive combinatorial drug delivery system. When Ag-capped and anticancer drug loaded pores of mesoporous silica were exposed to HOCl, the ready disintegration of Ag NPs resulted in a controlled release of drug molecules. The drug release profile and growth inhibition of myeloperoxidase positive (MOLM-13) leukemic cells support the role of the oxidant in the dissolution of Ag NPs. Besides combinational chemotherapy, the current study also provides us with an opportunity to investigate the interaction of Ag NPs with biorelevant oxidants.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1039/c5tb00554jDOI Listing
July 2015

Using oxidant susceptibility of thiol stabilized nanoparticles to develop an inflammation triggered drug release system.

J Mater Chem B 2015 Feb 16;3(8):1597-1604. Epub 2015 Jan 16.

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, College of Chemistry, Jilin University, Changchun, 130012, China.

Inflammation is a complex and dynamic defensive cellular approach to safeguard against deleterious agents; however, an overexpression of such responses frequently results in the development of a number of devastating diseases, such as atherosclerosis, cancer, inflammatory bowel, Alzheimer's and Parkinson's diseases. At the site of the inflammation, excessive amount of reactive oxygen species (ROS) are produced, and therefore researchers are now earnestly trying to exploit ROS pathological signals to design oxidative triggered drug release systems. In this study, we report a straightforward strategy to develop an oxidative stress responsive drug release systems. Newly developed, ultra-small, and thiol stabilized zinc sulfide quantum dots (ZnS QDs) are used as nanocaps to regulate the release of anticancer drug (camptothecin) from mesoporous silica nanoparticles (MSNs) in response to oxidative environment. The exposure of capped nanocarrier to a higher concentration of HO fails to open the drug loaded nanochannels; however, an addition of a minute amount of divalent iron, the most abundant transition-metal in the body, readily unseals the nanochannels at considerably lower HO concentrations due to the generation of highly reactive hydroxyl radicals (˙OH). Thiol groups, which stabilize the ZnS nanolids, are actually oxidized by ˙OH and as a result unleash the loaded drug molecules from the channels of silica. In addition to the inflammation-induced drug delivery, this study also provides basic insight into the fate of thiol stabilized nanoparticles upon interaction with hydroxyl radicals.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1039/c4tb01709aDOI Listing
February 2015

Intracellular antioxidants dissolve man-made antioxidant nanoparticles: using redox vulnerability of nanoceria to develop a responsive drug delivery system.

ACS Appl Mater Interfaces 2014 22;6(21):19424-33. Epub 2014 Oct 22.

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, College of Chemistry, ‡College of Life Science, Jilin University , Changchun 130012, P. R. China.

Regeneratable antioxidant property of nanoceria has widely been explored to minimize the deleterious influences of reactive oxygen species. Limited information is, however, available regarding the biological interactions and subsequent fate of nanoceria in body fluids. This study demonstrates a surprising dissolution of stable and ultrasmall (4 nm) cerium oxide nanoparticles (CeO2 NPs) in response to biologically prevalent antioxidant molecules (glutathione, vitamin C). Such a redox sensitive behavior of CeO2 NPs is subsequently exploited to design a redox responsive drug delivery system for transporting anticancer drug (camptothecin). Upon exposing the CeO2 capped and drug loaded nanoconstruct to vitamin c or glutathione, dissolution-accompanied aggregation of CeO2 nanolids unleashes the drug molecules from porous silica to achieve a significant anticancer activity. Besides stimuli responsive drug delivery, immobilization of nanoceria onto the surface of mesoporous silica also facilitates us to gain a basic insight into the biotransformation of CeO2 in physiological mediums.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/am5055367DOI Listing
October 2015

Responsive delivery of drug cocktail via mesoporous silica nanolamps.

J Colloid Interface Sci 2014 Nov 2;434:1-8. Epub 2014 Aug 2.

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, College of Chemistry, Jilin University, Qianjin Street 2699, Changchun 130012, PR China; Queensland Micro- and Nanotechnology Centre, Griffith University, Nathan, QLD 4111, Australia. Electronic address:

After a substantial advancement in single drug nanocarrier, nanomedicine now demands an integration of nanotechnology with combination therapy to achieve synergistic therapeutic effects. In this respect, a smart and multiple drug shuttling nanotheranostic system is developed which transport diverse kinds of anticancer drugs to cancer cells in a controlled and responsive manner respectively. Synthetically, a significantly high dose of hydrophobic camptothecin (CPT) is first loaded into the porous structure of quantum dots (CdS) coupled mesoporous silica nanocomposite. Subsequently, fluorescent doxorubicin (DOX) molecules are exclusively anchored onto the surface of CdS; as a result, the fluorescence of both CdS and DOX is quenched. Upon exposing to mildly acidic conditions, the fluorescence of both species is recovered, such fluorescent "on-off" states provides an added opportunity to real time sense drug release. In-vitro cell experiment reveals an excellent anticancer efficacy of drug cocktail, merely 3 μg/ml concentration of multiple drugs loaded nanocarrier reduces the cell viability to 30%. Furthermore, confocal imaging indicates a successful release of both therapeutic entities. We visualize that our newly fabricated multifunctional double drug-carrying nanoparticles can be a valuable addition to next generation of materials that simultaneously deliver cocktail of drugs with imaging functionality.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.jcis.2014.07.024DOI Listing
November 2014

CHK1 plays a critical role in the anti-leukemic activity of the wee1 inhibitor MK-1775 in acute myeloid leukemia cells.

J Hematol Oncol 2014 Aug 1;7:53. Epub 2014 Aug 1.

National Engineering Laboratory for AIDS Vaccine, Key Laboratory for Molecular Enzymology & Engineering, the Ministry of Education, and School of Life Sciences, Jilin University, Changchun, China.

Background: Acute myeloid leukemia (AML) remains a difficult disease to treat and requires new therapies to improve treatment outcome. Wee1 inhibitors have been used to prevent activation of the G2 cell cycle checkpoint, thus enhancing the antitumor activity of DNA damaging agents. In this study, we investigated MK-1775 in AML cell lines and diagnostic blast samples to identify sensitive subtypes as well as possible mechanisms of resistance.

Methods: In vitro MK-1775 cytotoxicities of AML cell lines and diagnostic blasts were measured using MTT assays. The effects of MK-1775 on cell cycle progression and related proteins were determined by propidium iodide (PI) staining and flow cytometry analysis and Western blotting. Drug-induced apoptosis was determined using annexin V/PI staining and flow cytometry analysis.

Results: We found that newly diagnosed and relapsed patient samples were equally sensitive to MK-1775. In addition, patient samples harboring t(15;17) translocation were significantly more sensitive to MK-1775 than non-t(15;17) samples. MK-1775 induced apoptosis in both AML cell lines and diagnostic blast samples, accompanied by decreased phosphorylation of CDK1 and CDK2 on Tyr-15 and increased DNA double-strand breaks (DSBs). Time-course experiments, using AML cell lines, revealed a time-dependent increase in DNA DSBs, activation of CHK1 and subsequent apoptosis following MK-1775 treatment, which could be attenuated by a CDK1/2 inhibitor, Roscovitine. Simultaneous inhibition of CHK1 and Wee1 resulted in synergistic anti-leukemic activity in both AML cell lines and primary patient samples ex vivo.

Conclusions: Our study provides compelling evidence that CHK1 plays a critical role in the anti-leukemic activity of MK-1775 and highlights a possible mechanism of resistance to MK-1775. In addition, our study strongly supports the use of MK-1775 to treat both newly diagnosed and relapsed AML, especially cases with t(15;17) translocation, and supports the development of combination therapies with CHK1 inhibitors.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/s13045-014-0053-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4237862PMC
August 2014

Acid-induced release of curcumin from calcium containing nanotheranostic excipient.

ACS Appl Mater Interfaces 2014 Aug 21;6(16):14377-83. Epub 2014 Jul 21.

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, College of Chemistry, and ‡College of Life Science, Jilin University , Changchun 130012, China.

Poor water solubility is believed one of the most critical problems of numerous promising pharmaceutical ingredients in their successful clinical utilization. Nanomedicine holds considerable promise to address this challenge, because it extends the therapeutic window of hydrophobic drugs through nanonization approach. Recently, the integration of diagnostic agents with smart therapeutic nanocarriers is also an emerging research arena to simultaneously visualize diseased tissues, achieve site specific drug release and track the impact of therapy. In this study, we have developed a biocompatible smart theranostic nanosystem which transports a highly promising hydrophobic drug (curcumin) in response to mildly acidic environment. As calcium is a main constituent of human body, hence we exploited the reversible calcium chelate formation tendency of divalent calcium to load and unload curcumin molecules. Moreover, an emerging T1 contrast agent is also tethered onto the surface of nanocarrier to realize MRI diagnosis application. In-vitro cell experiments revealed a significantly high chemotherapeutic efficiency of curcumin nanoformulation (IC50; 1.67 μg/mL), whereas free curcumin was found ineffective at the corresponding concentration (IC50; 29.72 μg/mL). MR imaging test also validated the performance of resulting system. Our strategy can be extended for the targeted delivery of other hydrophobic pharmaceutical ingredients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/am503655zDOI Listing
August 2014

Redox-mediated dissolution of paramagnetic nanolids to achieve a smart theranostic system.

Nanoscale 2014 May;6(10):5270-8

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, College of Chemistry, Jilin University, Changchun, 130012, China.

Manganese oxide (Mn3O4) nanoparticles have recently emerged as a promising T1 contrast agent. In this study, for the first time, we demonstrated an interaction of Mn3O4 with a biological system, and found redox sensitive behavior of these paramagnetic nanoparticles in intracellular reducing environment. Inspired by these findings, we for the first time used this interaction for some therapeutic advantages and designed a versatile mesoporous silica based nanotheranostic system to realize redox-activated enhanced magnetic resonance imaging and responsive anticancer drug delivery. Contrary to previous reports, we firstly prepared high quality amine terminated hydrophilic Mn3O4 nanolids, without using multistep ligand exchange strategies. The resulting water stable and small-sized Mn3O4 nanolids were subsequently used as nanolids to cap drug loaded nanochannels of a porous carrier. Exposure to highly prevalent intracellular reducing environment resulted in the steady-state dissolution of these nanolids and attained an intelligent drug release. Furthermore, the redox receptive dissolution of paramagnetic Mn3O4 nanolids into Mn(2+) in turn increases the T1 signal to twofold, providing an added opportunity to even track the feedback of therapy. This study, in addition to simultaneously realizing drug delivery and imaging, also provides a new insight into the fate and interaction of manganese oxide nanoparticles with components of biological systems.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1039/c3nr05687bDOI Listing
May 2014

pH dictates the release of hydrophobic drug cocktail from mesoporous nanoarchitecture.

ACS Appl Mater Interfaces 2013 Nov 5;5(22):11828-35. Epub 2013 Nov 5.

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, College of Chemistry, Jilin University , Changchun 130021, China.

Combination therapy has been a norm in clinical practice to effectively treat cancer. Besides polytherapy, nowadays, smart and nanobased drug carriers are extensively being explored to deliver drugs according to pathophysiological environment of diseases. In this regard, herein we designed intelligent mesoporous architecture, incorporating both combinational therapy with smart nanotechnology, to simultaneously deliver two highly hydrophobic chemotherapeutic drugs in response to extracellular and/or intracellular acidic environ of tumor. Novelty of the system lies in the employment of acid responsive ZnO QDs to clog not only the nanochannels of mesoporous silica, encapsulating one hydrophobic drug, but also exploitation of chelate forming propensity of another hydrophobic drug (curcumin) to load a significant quantity onto the surface of ZnO nanolids. Cell viability results revealed an extraordinarily high cytotoxic efficiency of that lethal drug cocktail even at a concentration as low as 3 μg/mL nanocarrier. We envision that this sophisticated nanocarrier, which utilizes both interior pore and exterior surface of nanolids for loading different hydrophobic guest molecules and their subsequent acid responsive release, will undoubtedly, illustrates its remarkable potential in targeted chemotherapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/am4035027DOI Listing
November 2013

Magnesium hydroxide nanoplates: a pH-responsive platform for hydrophobic anticancer drug delivery.

J Mater Chem B 2013 Oct 17;1(39):5273-5278. Epub 2013 Jul 17.

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, Jilin University, Changchun, 130012, China.

The cost of conventional chemotherapeutic drugs is substantially high, and biomedical researchers are constantly hunting for cheap and effective chemotherapeutic alternatives. Recently, curcumin has emerged as a cost effective anticancer remedy, however, the low bioavailability of curcumin has been a major impediment to its successful utilization for disease management. In this work, we developed a highly biocompatible magnesium hydroxide as an intelligent nanocarrier for delivering curcumin into cancer cells. Curcumin was loaded onto magnesium hydroxide nanoplates via a complexation strategy. Furthermore, these drug conjugated nanoparticles not only achieve efficient loading of a highly hydrophobic drug, but also exhibit pH responsive release in extracellular or intracellular acid environments, validated by in vitro drug release, confocal microscopy and MTT assay. These biocompatible nanoplates can be promising candidates for the further development of smart drug delivery nanodevices.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1039/c3tb20466aDOI Listing
October 2013

Synergistic antitumor interactions between gemcitabine and clofarabine in human pancreatic cancer cell lines.

Mol Med Rep 2012 03 23;5(3):734-8. Epub 2011 Dec 23.

The State Engineering Laboratory of AIDS Vaccine, College of Life Science, Jilin University, Changchun, PR China.

Pancreatic cancer is a highly malignant disease, with a 5-year survival rate of less than 4%. Thus, new therapies for this deadly disease are urgently required. In this study, we sought to investigate whether combination treatments with gemcitabine and clofarabine result in synergistic cytotoxic effects against human pancreatic cancer cells. The type and extent of cytotoxic interactions between gemcitabine and clofarabine in three human pancreatic cancer cell lines were determined by MTT assays and standard isobologram analysis. The effects of the two agents on cell cycle distribution and apoptosis were determined by flow cytometry. Clofarabine significantly and synergistically enhanced gemcitabine cytotoxicities in all of the cell lines tested. This was accompanied by a nearly complete S phase arrest and synergistic induction of apoptosis (cooperativity index = 0.67). Combined treatment of gemcitabine and clofarabine resulted in synergistic cytotoxicities in vitro. Our results strongly suggest potential clinical benefits for using this drug combination to treat pancreatic cancer patients.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3892/mmr.2011.738DOI Listing
March 2012

pH-Triggered controlled drug release from mesoporous silica nanoparticles via intracelluar dissolution of ZnO nanolids.

J Am Chem Soc 2011 Jun 23;133(23):8778-81. Epub 2011 May 23.

State Key Laboratory of Inorganic Synthesis and Preparative Chemistry, College of Chemistry, Jilin University, Changchun 130021, China.

Acid-decomposable, luminescent ZnO quantum dots (QDs) have been employed to seal the nanopores of mesoporous silica nanoparticles (MSNs) in order to inhibit premature drug (doxorubicin) release. After internalization into HeLa cells, the ZnO QD lids are rapidly dissolved in the acidic intracellular compartments, and as a result, the loaded drug is released into the cytosol from the MSNs. The ZnO QDs behave as a dual-purpose entity that not only acts as a lid but also has a synergistic antitumor effect on cancer cells. We anticipate that these nanoparticles may prove to be a significant step toward the development of a pH-sensitive drug delivery system that minimizes drug toxicity.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/ja200328sDOI Listing
June 2011
-->