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arsenic trioxide induces regulatory functions of plasmacytoid dendritic cells through interferon-α inhibition

Acta Pharmaceutica Sinica B 2020年第6期10卷 1061-1072页

作者： Yishan Ye Laure Ricard Lama Siblany Nicolas Stocker Frédéric De Vassoigne Eolia Brissot Baptiste Lamarthée Arsène Mekinian Mohamad Mohty Béatrice Gaugler Florent Malard Sorbonne Université INSERMCentre de Recherche Saint-Antoine(CRSA)Paris F-75012France Bone Marrow Transplantation Center the First Affiliated HospitalSchool of MedicineZhejiang UniversityHangzhou 310003China AP-HP Hôpital Saint-AntoineService d’Hématologie Clinique et Thérapie CellulaireParis F-75012France AP-HP Hôpital Saint-AntoineService de Médecine Interne et de l'Inflammation-(DHU i2B)Paris F-75012France

arsenic trioxide(As2O3)is recently found to have therapeutic potential in systemic sclerosis(SSc),a life-threatening multi-system fibrosing autoimmune disease with type I interferon(IFN-I)*** activated plasmacytoid dendritic cells(pDCs)are responsible for IFN-I secretion and are closely related with fibrosis establishment in *** this study,we showed that high concentrations of As2O3 induced apoptosis of pDCs via mitochondrial pathway with increased BAX/BCL-2 ratio,while independent of reactive oxygen species ***,at clinical relevant concentrations,As2O3 preferentially inhibited IFN-αsecretion as compared to other cytokines such as TNF-α,probably due to potent down-regulation of the total protein and mRNA expression,as well as phosphorylation of the interferon regulatory factor7(IRF7).In addition,As2O3 induced a suppressive phenotype,and in combination with cytokine inhibition,it down-regulated pDCs’capacity to induce CD4+T cell proliferation,Thl/Th22 polarization,and B cell differentiation towards ***,chronically activated pDCs from SSc patients were not resistant to the selective IFN-αinhibition,and regulatory phenotype induced by ***,our data suggest that As2O3 could target pDCs and exert its treatment efficacy in SSc,and more autoimmune disorders with IFN-I signature.

关键词： arsenic trioxide Plasmacytoid dendritic cell Immunotherapy Systemic sclerosis IFN-I

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arsenic trioxide alleviates airway hyperresponsiveness and eosinophilia in a murine model of asthma

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Cellular & Molecular Immunology 2010年第5期7卷 375-380页

作者： Kuan-Hua Chu Chen-Chen Lee Shao-Chi Hsin Bao-Chang Cai Jin-Hong Wang Bor-Luen Chiang Graduate Institute of Immunology National Taiwan UniversityTaipeiTaiwan School of Medicine China Medical UniversityTaichungTaiwan Nanjing University of Traditional Chinese Medicine NanjingChina Department of Pediatrics National Taiwan University HospitalTaipeiTaiwan

Asthma is one of the most common chronic airway inflammatory *** clinical hallmarks of asthma include elevated serum levels of immunoglobulin E(IgE),eosinophilic inflammation and airway hyper-responsiveness(AHR).arsenic trioxide(As2O3)is considered a carcinogen;however,it has also been used to treat diseases,such as syphilis,in traditional Chinese and Western ***,As2O3 is used as one of the standard therapies for acute promyelocytic leukemia(APL).Previous studies have indicated that As2O3 can induce apoptosis in ***,the effect of As2O3 on asthma has not been *** used ovalbumin(OVA)-immunized mice as a model for asthma and treated mice with As2O3 at doses of 2.5 and 5 mg/*** mice were then monitored for OVA-specific IgE production,airway inflammatory cell infiltration and *** found that administration of As2O3 in OVA-immunized mice abrogated airway eosinophil recruitment by downregulating eotaxin expression but did not alter serum IgE or IL-5 levels in bronchoalveolar lavage fluid(BALF).Furthermore,the development of AHR and cellular infiltration into the airway were reduced by treating mice with *** vitro data suggested that low concentrations of As2O3 could induce only a small degree of apoptosis in primary pulmonary cells but could significantly inhibit the secretion of eotaxin by these *** results indicate that the administration of As2O3 to OVA-immunized mice can suppress lung allergic inflammatory ***2O3 might therefore have therapeutic potential in treating allergic airway inflammatory diseases.

关键词： arsenic trioxide asthma eosinophils

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arsenic trioxide Combining Leflunomide Activates Nrf2-ARE-HO-1 Signaling Pathway and Protects Heart Xenografts

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Chinese Journal of Integrative Medicine 2021年第10期27卷 760-766页

作者： WANG Teng-da XU Song-lin YU Zheng-yi Nl Shao-bin ZHANG Cheng JIAO Zhi-xing Department of Urology The First Affiliated Hospital of Harbin Medical UniversityHarbin(150000)China

Objective:To investigate the molecular mechanisms underlying the effects of arsenic trioxide(As_(2)0_(3))in combination with leflunomide on the hamster-to-rat heart ***:Transplantation of LVG hamster hearts to Lewis rats was performed by anastomosis of vessels in the neck using end-to-end anastomosis with a non-suture cuff *** groups of recipient rats(n=6 in each)were treated with normal saline(control),As_(2)0_(3)[5 mg/(kg*day)intraperitoneally],leflunomide[5 mg/(kg*d)orally],or leflunomide[5 mg/(kg.d)+As_(2)0_(3)5 mg/(kg.d)]in *** hearts and/or rat spleens were harvested and analyzed 4 days after *** reverse-transcription polymerase chain reaction and Western blot analysis were performed to detect the expression of the nuclear factor erythroid-derived factor 2-related factor(Nrf2)and its target gene heme oxygenase-1(HO-1),Treg cell marker fork-head Box P3(FOXP3),apoptosis-associated proteins Bcl-2,Bax,and cleaved *** staining was used to detect the levels of inflammatory natural killer cell and macrophage infiltration,intercellular cell adhesion molecule-1(ICAM-1)and complement ***:Expression of Nrf2-ARE-HO-1 signaling pathway was upregulated in heart xenografts in rats treated with As_(2)0_(3) plus leflunomide compared with control rats or rats treated with either drug alone(P<0.01),and this was accompanied by an increased Treg cells in the recipient rat spleen(P<0.01).In contrast,the expressions of Bax,cleaved caspase-3,ICAM-1,and complement C3,and infiltration of inflammatory cells in the xenografts were inhibited by As_(2)0_(3) plus leflunomide treatment(P<0.01).Conclusion:Combination treatment with As_(2)0_(3) and leflunomide protected hamster heart-xenografts in recipient rats.

关键词： arsenic trioxide leflunomide Nrf2-ARE-HO-1 signaling pathway inflammation infiltration xenotransplantation

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arsenic trioxide elicits prophylactic and therapeutic immune responses against solid tumors by inducing necroptosis and ferroptosis

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Cellular & Molecular Immunology 2023年第1期20卷 51-64页

作者： Jinfeng Chen Ziqi Jin Shuqing Zhang Xiao Zhang Peipei Li Heng Yang Yuting Ma Institute of Systems Medicine Chinese Academy of Medical Sciences&Peking Union Medical CollegeBeijing10005China Suzhou Institute of Systems Medicine SuzhouJiangsu215123China National Key Laboratory of Medical Immunology Shanghai200433China Collaborative Innovation Center for Cancer Personalized Medicine Nanjing Medical UniversityNanjing211166China

Boosting tumor immunosurveillance with vaccines has been proven to be a feasible and cost-effective strategy to fight cancer. Although major breakthroughs have been achieved in preventative tumor vaccines targeting oncogenic viruses, limited advances have been made in curative vaccines for virus-irrelevant malignancies. Accumulating evidence suggests that preconditioning tumor cells with certain cytotoxic drugs can generate whole-cell tumor vaccines with strong prophylactic activities. However, the immunogenicity of these vaccines is not sufficient to restrain the outgrowth of existing tumors. In this study, we identified arsenic trioxide (ATO) as a wide-spectrum cytotoxic and highly immunogenic drug through multiparameter screening. ATO preconditioning could generate whole-cell tumor vaccines with potent antineoplastic effects in both prophylactic and therapeutic settings. The tumor-preventive or tumor-suppressive benefits of these vaccines relied on CD8^(+) T cells and type I and II interferon signaling and could be linked to the release of immunostimulatory danger molecules. Unexpectedly, following ATO-induced oxidative stress, multiple cell death pathways were activated, including autophagy, apoptosis, necroptosis, and ferroptosis. CRISPR‒Cas9-mediated knockout of cell death executors revealed that the absence of Rip3, Mlkl, or Acsl4 largely abolished the efficacy of ATO-based prophylactic and therapeutic cancer vaccines. This therapeutic failure could be rescued by coadministration of danger molecule analogs. In addition, PD-1 blockade synergistically improved the therapeutic efficacy of ATO-based cancer vaccines by augmenting local IFN-γ production.

关键词： Tumor vaccine arsenic trioxide Necroptosis Ferroptosis Immunosurveillance

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arsenic trioxide induced rhabdomyolysis, a rare but severe side effect, in an APL patient： a case report

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Frontiers of Medicine 2017年第2期11卷 284-286页

作者： Haiyan He Ran An Jian Hou Weijun Fu Myeloma and Lymphoma Center Department of Hematology Changzheng Hospital Shanghai 200003 China

arsenic trioxide （ATO）, a component of the traditional Chinese medicine arsenic sublimate, promotes apoptosis and induces leukemic cell differentiation. Combined with all-trans-retinotic acid （ATRA）, ATO has become the first-line induction therapy in treating acute promyelocytic leukemia （APL）. The most common side effects of ATO include hepatotoxicity, gastrointestinal symptoms, water-sodium retention, and nervous system damage. In this report, we present a rare side effect, rhabdomyolysis, in a 68-year-old female APL patient who was treated with ATO. After taking 10 mg ATO daily for 6 days, she presented shortness of breath, myodynia, elevated creatine kinase, and acute renal insufficiency. This report describes the first case of ATO-induced rhabdomyolysis.

关键词： arsenic trioxide APL rhabdomyolysis

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arsenic trioxide induces apoptosis of human gastrointestinal cancer cells

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World Journal of Gastroenterology 2014年第18期20卷 5505-5510页

作者： Zhi-Bin Ma Hong-Yu Xu Miao Jiang You-Lin Yang Lian-Xin Liu Ying-Hua Li Department of Gastroenterology First Affiliated Hospital of Harbin Medical University Department of Hematology First Affiliated Hospital of Harbin Medical University

AIM: To investigate the changes in apoptosis in gastrointestinal cancer cells from patients with gastrointestinal cancers treated with arsenic trioxide (As2O3); and to study the possible molecular mechanisms of such c... 详细信息

关键词： Gastrointestinal cancer arsenic trioxide Apoptosis p53 Bcl-2

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arsenic trioxide encapsulated liposomes prepared via copper acetate gradient loading method and its antitumor efficiency

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Asian Journal of Pharmaceutical Sciences 2020年第3期15卷 365-373页

作者： Shaoning Wang Chunxiu Liu Cunyang Wang Jia Ma Hui Xu Jianbo Guo Yihui Deng School of Pharmaceutical Engineering Shenyang Pharmaceutical UniversityBenxi 117004China School of Pharmacy Shenyang Pharmaceutical UniversityChina Shanxi Institute for Food and Drug Control Xi’an 710065China

In this study, arsenic trioxide(ATO) was encapsulated in liposomes via copper acetate(Cu(OAc)2) gradients and high entrapment efficiency of over 80% was obtained. The average particle size and the zeta-potential of the liposomes were detected to be 115.1 ± 29.1 nm and-21.97 ± 0.6 m V, respectively. The TEM images showed rod-like precipitates in the inner aqueous phase, which was supposed be due to the formation of insoluble ATO–Cu *** in vitro drug release of ATO–Cu liposomes exhibited a sustained release over 72 h, and the release rates decreased with the increase of the p H of release media. Pharmacokinetic and tissue distribution studies of ATO liposomes showed significantly reduced plasma clearance rate, increased AUC0–12h and T1/2, and improved tumor distribution of As compared to iv administration of ATO solution. The anti-tumor effect of ATO loaded liposomes to S180 tumor-bearing mice was significantly improved with a tumor inhibition rate of 61.2%,meanwhile the toxicity of encapsulated ATO was greatly decreased. In conclusion, ATO can be effectively encapsulated into liposomes by remote loading method via Cu(OAc)2 gradients;the co-administration of ATO and Cu(Ⅱ) via liposomal formulation may find wide applications in the treatment of various tumors.

关键词： arsenic trioxide Liposomes Copper acetate gradient Pharmacokinetics Tissue distribution Antitumor activity

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arsenic trioxide Inhibits Proliferation in K562 Cells by Changing Cell Cycle and Survivin Expression

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2004年第4期24卷 342-344,353页

作者：伍晓菲陈智超刘仲萍周浩游泳黎纬明邹萍 Department of Hematology Union Hospital Tongji Medical College Huazhong University of Science and Technology

To study the mechanisms involved in the inhibition of chronic myeloid leukemic cells (K562) proliferation induced by arsenic trioxide (As 2O 3) and to explore the potential role of Survivin, an inhibitor of apoptosis protein, in the regulation of As 2O 3 induced cell apoptosis, K562 cells were cultured with As 2O 3 of different concentrations. Cells were collected for proliferation analysis by MTT assay. Cell cycle distribution and cell apoptosis were analyzed by flow cytometry. Expression of Survivin protein and mRNA were detected by flow cytometry and RT-PCR, respectively. Our results showed that As 2O 3 (2-10 μmol/L) inhibited K562 cells growth effectively, but it did not induce cells apoptosis significantly. The percentage of K562 cells at G 2/M phase increased in proportion to As 2O 3 concentrations, and the expression of Survivin mRNA and content of Survivin protein was up-regulated accordingly. It is concluded that As 2O 3 inhibited K562 cells growth by inducing cell cycle arrest mainly at G 2/M phase. Over-expression of Survivin gene and protein might be one of the possible mechanisms contributing to K562 cells' resistance to As 2O 3-induced apoptosis.

关键词： arsenic trioxide K562 G 2/M cell cycle arrest Survivin

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Impact of arsenic trioxide on LS-174T Cell Growth in vitro and the Activity of Telomerase

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Chemical Research in Chinese Universities 2006年第2期22卷 209-212页

作者： WANG Xi-shan WANG Gui-yu XU Hai-tao DONG De-li FU Song-bin ZHANG Qi-fan YANG Bao-feng Department of Abdominal Surgery the Affiated Tumor Hospital Department of Pharmacology Department of Genetics Harbin Medical University Harbin 150001 P. R. China

The therapeutic action of arsenic trioxide（ As203 ） on solid tumors has aroused widespread interest among scholars. To study the impact of As2O3 on human colorectal carcinoma cells（ LS-174T cell） and the activity of telomerase, the methods of PCR-ELISA, flow cytometry （FCM） and MTT assay in vitro were utilized. The results show that （1） with an increase in the concentration of As2O3, the ratio of living the cells to dead cells decreases significantly, and the IC50 value is 5.23 μg/mL; （2） the cells of the experimental groups can endure a series of morphological changes similar to the features of apoptosis ; （3） the apoptotic curves of FCM pictures appear after 24 h, and the cells show the apoptosis in a time-dependent manner; （4） As2O3 can inhibit the activity of telomerase of the cell extraction obviously in a concentration-dependent and time-dependent manner after 24 h. It can be concluded from the experiment results in vitro that As2O3 can induce the apoptosis of LS-174T cells and inhibit the telomerase activity. Therefore, it has been proposed, for the first time, that these two factors （the apoptosis of LS-174T cells and the inhibition to the telomerase activity） are important causes of the LS-174T cell death caused by As2O3.

关键词： arsenic trioxide Telomerase Colorectal carcinoma Apoptosis

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arsenic trioxide DOWNREGULATES TELOMERASE ACTIVITY IN HL-60 CELLS

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Chinese Journal of Cancer Research 2002年第3期14卷 187-191页

作者： HE Dong-mei 何冬梅 ZHANG Huan 张洹 Institute of Hematology Jinan University Medical College Guangzhou 510632 Institute of Hematology Jinan University Medical College Guangzhou 510632

Objective: To evaluate whether arsenic trioxide (AS2O3) could downregulate human telomerase reverse transcriptase (hTERT) gene expression and telomerase activity during induction of apoptosis of HL-60 cells. Methods: Apoptosis was detected by morphological observation and flow cytomertric cell cycle analysis. The expression of hTERT at mRNA and protein levels was analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) and immunofluorescence using fluoresce isothiocyanate (FITC) label, respectively. Telomerase activity was determined by polymerase chain reaction enzyme-linked immunoassay (PCR-ELISA). Results: Treatment of 2 μmol/L at As2O3 could induce apoptosis of HL-60 cells. hTERT was decreased at both mRNA and protein levels during apoptosis of HL-60 cells. Telomerase activity of HL-60 cells was significantly inhibited. Conclusion: It is suggested that telomerase activity of HL-60 cells might be specifically inhibited by AS2O3 through the downregulation of hTERT gene expression.

关键词： arsenic trioxide hTERT gene HL-60 cells Telomerase Apoptosis

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