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ruxolitinib improves the inflammatory microenvironment,restores glutamate homeostasis,and promotes functional recovery after spinal cord injury

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Neural Regeneration Research 2024年第11期19卷 2499-2512页

作者： Jiang Cao Xiao Yu Jingcheng Liu Jiaju Fu Binyu Wang Chaoqin Wu Sheng Zhang Hongtao Chen Zi Wang Yinyang Xu Tao Sui Jie Chang Xiaojian Cao Department of Orthopedics The First Affiliated Hospital of Nanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Trauma Surgery Subei People’s Hospital of JiangsuClinical Medical College of Yangzhou UniversityYangzhouJiangsu ProvinceChina Department of Orthopedics Zhongda HospitalSoutheast UniversityNanjingJiangsu ProvinceChina Department of Orthopedic Surgery Nanjing Drum Tower HospitalThe Affiliated Hospital of Medical School of Nanjing UniversityNanjingJiangsu ProvinceChina

The inflammatory microenvironment and neurotoxicity can hinder neuronal regeneration and functional recovery after spinal cord injury.ruxolitinib,a JAK-STAT inhibitor,exhibits effectiveness in autoimmune diseases,arthritis,and managing inflammatory cytokine storms.Although studies have shown the neuroprotective potential of ruxolitinib in neurological trauma,the exact mechanism by which it enhances functional recovery after spinal cord injury,particularly its effect on astrocytes,remains unclear.To address this gap,we established a mouse model of T10 spinal cord contusion and found that ruxolitinib effectively improved hindlimb motor function and reduced the area of spinal cord injury.Transcriptome sequencing analysis showed that ruxolitinib alleviated inflammation and immune response after spinal cord injury,restored EAAT2 expression,reduced glutamate levels,and alleviated excitatory toxicity.Furthermore,ruxolitinib inhibited the phosphorylation of JAK2 and STAT3 in the injured spinal cord and decreased the phosphorylation level of nuclear factor kappa-B and the expression of inflammatory factors interleukin-1β,interleukin-6,and tumor necrosis factor-α.Additionally,in glutamate-induced excitotoxicity astrocytes,ruxolitinib restored EAAT2 expression and increased glutamate uptake by inhibiting the activation of STAT3,thereby reducing glutamate-induced neurotoxicity,calcium influx,oxidative stress,and cell apoptosis,and increasing the complexity of dendritic branching.Collectively,these results indicate that ruxolitinib restores glutamate homeostasis by rescuing the expression of EAAT2 in astrocytes,reduces neurotoxicity,and effectively alleviates inflammatory and immune responses after spinal cord injury,thereby promoting functional recovery after spinal cord injury.

关键词： astrocytes EAAT2 excitotoxicity glutamate homeostasis JAK-STAT pathway locomotor function neurotoxicity ruxolitinib spinal cord injury transcriptome analysis

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Does ruxolitinib, in Comparison to Best Available Therapy (BAT), Improve Pruritis Symptoms in Patients with Polycythemia Vera?

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Journal of Biosciences and Medicines 2024年第3期12卷 35-43页

作者： Zachary Samuel Thorogood Philadelphia College of Osteopathic Medicine Philadelphia USA

Polycythemia vera manifests as a myeloproliferative neoplasm associated with diverse symptoms, including aquagenic pruritis. This systematic review addresses the pressing need to enhance the understanding of the disease’s symptomatology and optimize treatment strategies for improved patient outcomes. The rarity and low prevalence of polycythemia vera underscore the importance of this investigation, as existing standard of care involves a multifaceted approach and significant healthcare costs. Despite advancement in therapeutic options, persistent symptoms and resistance to first-line treatments pose challenges. ruxolitinib has emerged as a promising intervention, demonstrating clinically significant improvement for patients. This systematic review appraises three randomized controlled trials, shedding light on the efficacy of ruxolitinib and its potential to ameliorate pruritis symptoms in symptomatic patients.

关键词： Polycythemia Vera ruxolitinib Pruritis

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ruxolitinib attenuates secondary injury after traumatic spinal cord injury

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Neural Regeneration Research 2022年第9期17卷 2029-2035页

作者： Zhan-Yang Qian Ren-Yi Kong Sheng Zhang Bin-Yu Wang Jie Chang Jiang Cao Chao-Qin Wu Zi-Yan Huang Ao Duan Hai-Jun Li Lei Yang Xiao-Jian Cao Spine Center Zhongda Hospital of Southeast UniversityNanjingJiangsu ProvinceChina Medical School Southeast UniversityNanjingJiangsu ProvinceChina Department of Orthopedics First Affiliated Hospital of Nanjing Medical UniversityNanjingJiangsu ProvinceChina Department of Orthopedics Hospital Affiliated 5 to Nantong University(Taizhou People’s Hospital)TaizhouJiangsu ProvinceChina Taizhou Clinical Medical School of Nanjing Medical University Taizhou People’s HospitalTaizhouJiangsu ProvinceChina

Excessive inflammation post-traumatic spinal cord injury(SCI)induces microglial activation,which leads to prolonged neurological dysfunction.However,the mechanism underlying microglial activation-induced neuroinflammation remains poorly understood.ruxolitinib(RUX),a selective inhibitor of JAK1/2,was recently reported to inhibit inflammatory storms caused by SARS-CoV-2 in the lung.However,its role in disrupting inflammation post-SCI has not been confirmed.In this study,microglia were treated with RUX for 24 hours and then activated with interferon-γfor 6 hours.The results showed that interferon-γ-induced phosphorylation of JAK and STAT in microglia was inhibited,and the mRNA expression levels of pro-inflammatory cytokines tumor necrosis factor-α,interleukin-1β,interleukin-6,and cell proliferation marker Ki67 were reduced.In further in vivo experiments,a mouse model of spinal cord injury was treated intragastrically with RUX for 3 successive days,and the findings suggest that RUX can inhibit microglial proliferation by inhibiting the interferon-γ/JAK/STAT pathway.Moreover,microglia treated with RUX centripetally migrated toward injured foci,remaining limited and compacted within the glial scar,which resulted in axon preservation and less demyelination.Moreover,the protein expression levels of tumor necrosis factor-α,interleukin-1β,and interleukin-6 were reduced.The neuromotor function of SCI mice also recovered.These findings suggest that RUX can inhibit neuroinflammation through inhibiting the interferon-γ/JAK/STAT pathway,thereby reducing secondary injury after SCI and producing neuroprotective effects.

关键词： functional recovery glial scar inflammation interferon-γ JAK/STAT signaling microglia ruxolitinib spinal cord injury

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Risk of hepatitis B reactivation in patients with myeloproliferative neoplasms treated with ruxolitinib

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World Journal of Hepatology 2023年第11期15卷 1188-1195页

作者： Adeniyi Abraham Adesola Matei-Alexandru Cozma Yong-Feng Chen Bahadar Singh Srichawla Mihnea-Alexandru Găman Department of Medicine and Surgery Faculty of Clinical SciencesCollege of MedicineUniversity of IbadanIbadanNigeria Faculty of Medicine "Carol Davila"University of Medicine and PharmacyBucharest 050474Romania Department of Gastroenterology Colentina Clinical HospitalBucharest 020125Romania Department of Basic Medical Sciences Medical College of Taizhou UniversityTaizhou 318000Zhejiang ProvinceChina Department of Neurology University of Massachusetts Chan Medical SchoolWorcesterMA 01655United States Department of Hematology Center of Hematology and Bone Marrow TransplantationFundeni Clinical InstituteBucharest 022328Romania Cellular and Molecular Pathology Department Stefan S.Nicolau Institute of VirologyRomanian AcademyBucharest 030304Romania

Classical Philadelphia-negative myeloproliferative neoplasms(MPNs),i.e.,polycythemia vera,essential thrombocythemia,and primary/secondary myelofibrosis,are clonal disorders of the hematopoietic stem cell in which an uncontrolled proliferation of terminally differentiated myeloid cells occurs.MPNs are characterized by mutations in driver genes,the JAK2V617F point mutation being the most commonly detected genetic alteration in these hematological malignancies.Thus,JAK inhibition has emerged as a potential therapeutic strategy in MPNs,with ruxolitinib being the first JAK inhibitor developed,approved,and prescribed in the management of these blood cancers.However,the use of ruxolitinib has been associated with a potential risk of infection,including opportunistic infections and reactivation of hepatitis B.Here,we briefly describe the association between ruxolitinib treatment in MPNs and hepatitis B reactivation.

关键词： ruxolitinib Myeloproliferative neoplasms Hepatitis B Polycythemia vera Myelofibrosis JAK inhibitor

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ruxolitinib add-on in corticosteroid-refractory graft-vs-host disease after allogeneic stem cell transplantation:Results from a retrospective study on 38 Chinese patients

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World Journal of Clinical Cases 2020年第6期8卷 1065-1073页

作者： Si-Hua Dang Qin Liu Rong Xie Na Shen Shu Zhou Wei Shi Wen Liu Ping Zou Yong You Zhao-Dong Zhong Department of Hematology Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030Hubei ProvinceChina Department of Oncology Luohe Central HospitalLuohe 462300Henan ProvinceChina Department of Gynecology and Obstetrics Union HospitalTongji Medical CollegeHuazhong University of Science and TechnologyWuhan 430030Hubei ProvinceChina

BACKGROUND Graft-vs-host disease (GVHD) is a major cause of mortality after allogeneic hematopoietic stem cell transplantation.Some patients have steroid-refractory(SR) GVHD.AIM To evaluate the effect and safety of ruxolitinib add-on in the treatment of patients with SR acute (a) and chronic (c) GVHD.METHODS We retrospectively analyzed 38 patients administered ruxolitinib add-on to standard immunosuppressive therapy for SR-aGVHD or SR-cGVHD following allogeneic hematopoietic stem cell transplantation.ruxolitinib was administered5-10 mg/d depending on disease severity,patient status,and the use of antifungal drugs.Overall response rate,time to best response,malignancy relapse rate,infection rate,and treatment-related adverse events were assessed.RESULTS The analysis included 10 patients with SR-aGVHD (gradeⅢ/Ⅳ,n=9) and 28patients with SR-cGVHD (moderate/severe,n=24).For the SR-aGVHD and SRcGVHD groups,respectively:Median number of previous GVHD therapies was 2(range:1-3) and 2 (1-4);median follow-up was 2.5 (1.5-4) and 5 (1.5-10) mo;median time to best response was 1 (0.5-2.5) and 3 (1-9.5) mo;and overall response rate was 100%(complete response:80%) and 82.1%(complete response:10.7%) with a response observed in all GVHD-affected organs.The malignancy relapse rates for the SR-aGVHD and SR-cGVHD groups were 10.0%and 10.7%,respectively.Reactivation rates for cytomegalovirus,Epstein-Barr virus,and varicella-zoster virus,respectively,were 30.0%,10.0%,and 0%for the SR-aGVHD group and 0%,14.3%,and 7.1%for the SR-cGVHD group.CONCLUSION ruxolitinib add-on was effective and safe as salvage therapy for SR-GVHD.

关键词： Graft-vs-host disease Graft-vs-leukemia effect Allogeneic hematopoietic stem cell transplantation ruxolitinib Treatment Antifungal drugs

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Treatment with a JAK1/2 inhibitor ameliorates murine autoimmune cholangitis induced by IFN overexpression

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Cellular & Molecular Immunology 2022年第10期19卷 1130-1140页

作者： Tihong Shao Patrick S.C.Leung Weici Zhang Koichi Tsuneyama William M.Ridgway Howard A.Young Zongwen Shuai Aftab A.Ansari M.Eric Gershwi Department of Rheumatology and Immunology The First Affiliated Hospital of Anhui Medical UniversityHefeiChina Division of Rheumatology Allergyand Clinical ImmunologySchool of MedicineUniversity of CaliforniaDavisCAUSA Department of Pathology and Laboratory Medicine Institute of Biomedical SciencesTokushima University Graduate SchoolTokushimaJapan Center for Cancer Research National Cancer Institute-FrederickFrederickMDUSA

The interferon(IFN)signaling pathways are major immunological checkpoints with clinical significance in the pathogenesis of autoimmunity.We have generated a unique murine model named ARE-Del,with chronic overexpression of IFNγ,by altering IFNγmetabolism.Importantly,these mice develop an immunologic and clinical profile similar to patients with primary biliary cholangitis,including high titers of autoantibodies and portal inflammation.We hypothesized that the downregulation of IFN signaling pathways with a JAK1/2 inhibitor would inhibit the development and progression of cholangitis.To study this hypothesis,ARE-Del^(+/−)mice were treated with the JAK1/2 inhibitor ruxolitinib and serially studied.JAK inhibition resulted in a significant reduction in portal inflammation and bile duct damage,associated with a significant reduction in splenic and hepatic CD4^(+)T cells and CD8^(+)T cells.Functionally,ruxolitinib inhibited the secretion of the proinflammatory cytokines IFNγand TNF from splenic CD4^(+)T cells.Additionally,ruxolitinib treatment also decreased the frequencies of germinal center B(GC B)cells and T follicular helper(Tfh)cells and led to lower serological AMA levels.Of note,liver and peritoneal macrophages were sharply decreased and polarized from M1 to M2 with a higher level of IRF4 expression after ruxolitinib treatment.Mechanistically,ruxolitinib inhibited the secretion of IL-6,TNF and MCP1 and the expression of STAT1 but promoted the expression of STAT6 in macrophages in vitro,indicating that M1 macrophage polarization to M2 occurred through activation of the STAT6-IRF4 pathway.Our data highlight the significance,both immunologically and clinically,of the JAK/STAT signaling pathway in autoimmune cholangitis.

关键词： Primary biliary cholangitis Autoimmunity Interferons Janus Kinase Inhibitors ruxolitinib

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Turner syndrome with primary myelofibrosis,cirrhosis and ovarian cystic mass:A case report

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World Journal of Clinical Cases 2022年第9期10卷 2931-2937页

作者： Lin-Wei Xu Yong-Zhong Su Hong-Fang Tao Department of Hematology The First Affiliated Hospital of Shantou University Medical CollegeShantou 515041Guangdong ProvinceChina

BACKGROUND Turner syndrome(TS)with leukemia is a complicated clinical condition.The clinical course and outcome of these patients are poor,so the treatment and prognosis of TS with hematological malignancies deserve our attention.CASE SUMMARY Here,we report a case of a 20-year-old woman diagnosed with TS,primary myelofibrosis(PMF),cirrhosis,and an ovarian cystic mass.This is the first report on the coexistence of TS and PMF with the MPL and SH2B3 mutations.The patient was diagnosed with cirrhosis of unknown cause,splenomegaly and severe gastroesophageal varices.Additionally,an ovarian cystic mass caused the patient to appear pregnant.The patient was treated with the JAK2 inhibitor-ruxolitinib according to peripheral blood cells,although myelofibrosis was improved,the splenomegaly did not reduce.Moreover,hematemesis and melena occasionally occurred.CONCLUSION ruxolitinib may clearly reduce splenomegaly.Though myelofibrosis was improved,cirrhosis and splenomegaly in this case continued to worsen.Effective treatment should be discussed.

关键词： Turner syndrome Primary myelofibrosis Cirrhosis Ovarian cystic mass ruxolitinib Case report

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Micheliolide exerts effects in myeloproliferative neoplasms through inhibiting STAT3/5 phosphorylation via covalent binding to STAT3/5 proteins

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Blood Science 2023年第4期5卷 258-268页

作者： Huijun Huang Jinqin Liu Lin Yang Yiru Yan Meng Chen Bing Li Zefeng Xu Tiejun Qin Shiqiang Qu Liang Wang Gang Huang Yue Chen Zhijian Xiao State Key Laboratory of Experimental Hematology National Clinical Research Center for Blood DiseasesHaihe Laboratory of Cell EcosystemInstitute of Hematology&Blood Diseases HospitalChinese Academy of Medical Sciences&Peking Union Medical CollegeTianjin 300020China MDS and MPN Centre Institute of Hematology and Blood Diseases HospitalChinese Academy of Medical Sciences&Peking Union Medical CollegeTianjinChina State Key Laboratory of Medicinal Chemical Biology College of ChemistryNankai University94 Weijin RoadTianjinChina Department of Cell System&Anatomy the University of Texas Health Science Center at San AntonioSan AntonioTX 78229USA Mays Cancer Center Joe R.&Teresa Lozano Long School of Medicinethe University of Texas Health Science Center at San AntonioSan AntonioTX 78229USA Hematologic Pathology Center Institute of Hematology and Blood Diseases HospitalChinese Academy of Medical Sciences&Peking Union Medical CollegeTianjinChina.

ruxolitinib is a cornerstone of management for some subsets of myeloproliferative neoplasms(MPNs);however,a considerable number of patients respond suboptimally.Here,we evaluated the efficacy of micheliolide(MCL),a natural guaianolide sesquiterpene lactone,alone or in combination with ruxolitinib in samples from patients with MPNs,JAK2V617F-mutated MPN cell lines,and a Jak2V617F knock-in mouse model.MCL effectively suppressed colony formation of hematopoietic progenitors in samples from patients with MPNs and inhibited cell growth and survival of MPN cell lines in vitro.Co-treatment with MCL and ruxolitinib resulted in greater inhibitory effects compared with treatment with ruxolitinib alone.Moreover,dimethylaminomicheliolide(DMAMCL),an orally available derivative of MCL,significantly increased the efficacy of ruxolitinib in reducing splenomegaly and cytokine production in Jak2V617F knock-in mice without evident effects on normal hematopoiesis.Importantly,MCL could target the Jak2V617F clone and reduce mutant allele burden in vivo.Mechanistically,MCL can form a stable covalent bond with cysteine residues of STAT3/5 to suppress their phosphorylation,thus inhibiting JAK/STAT signaling.Overall,these findings suggest that MCL is a promising drug in combination with ruxolitinib in the setting of suboptimal response to ruxolitinib.

关键词： Micheliolide Myeloproliferative neoplasms ruxolitinib STAT3/5 Suboptimal response

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ruxolitinib对JAK2V617F阳性骨髓增殖性肿瘤细胞基质金属蛋白酶调控的研究

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中华血液学杂志 2017年第2期38卷 140-145页

作者：刘贵敏张丽军付建珠梁文同成志勇白萍卞永生万建设承德医学院 067001 保定市第一医院血液内科

目的探讨JAK2抑制剂ruxolitinib对JAK2V617F突变阳性的骨髓增殖性肿瘤（MPN）细胞内基质金属蛋白酶（MMP）调控的影响。方法①收集2012年1月到2015年12月保定市第-医院收治的40例未经治疗的JAK2V617F阳性MPN患者，以15名健康志愿者为对... 详细信息

目的探讨JAK2抑制剂ruxolitinib对JAK2V617F突变阳性的骨髓增殖性肿瘤（MPN）细胞内基质金属蛋白酶（MMP）调控的影响。方法①收集2012年1月到2015年12月保定市第-医院收治的40例未经治疗的JAK2V617F阳性MPN患者，以15名健康志愿者为对照组。免疫组化法检测两组骨髓活检组织中磷酸化JAK2（p-JAK2）、基质金属蛋白酶2（MMP-2）、MMP．9的表达水平。选取JAK2V617F阳性MPN患者骨髓细胞，体外应用ruxolitinib干预，测定干预前后细胞迁移力和MMP-2、MMP-9表达。②不同浓度ruxolitinib（0、50、100、250、500、1000nmol／L）作用于人红白血病细胞株HEL细胞不同时间后CCK-8检测细胞活力，Tanswell小室检测细胞迁移，荧光定量PCR检测JAK2、MMP-2、MMP-9mRNA水平变化，Westernblot检测P—JAK2、MMP．2、MMP-9蛋白表达。结果①MPN组p-JAK2、MMP-2、MMP-9蛋白表达均高于对照组[（78．56±24．55）％对（41．59±17．29）％、（48．25±18．74）％对（22．79±13．89）％、（53．29±19．28）％对（15．56±14．96）％，P值均〈0．05]。Spearman相关分析显示MMP-2、MMP-9蛋白水平与JAK2V617F突变量呈正相关（r=0．526，P=0．001；r=0．543，p=-0．001）。②ruxolitinib能够呈时间和剂量依赖性抑制HEL细胞增殖。③迁移实验结果显示5nmol／Lruxolitinib作用MPN原代细胞及HEL细胞24h后迁移至下室细胞数均少于无ruxolitinib组（154．7±27．5对320．3±67．3，t=13．47，P=0．001；70．7±10．5对135．3±16．7，t=13．89，P=0．001）。④JAK2、MMP-2、MMP-9mRNA及蛋白表达随ruxolitinib剂量增加而降低。结论ruxolitinib通过调控JAK2信号通路抑制MMP-2、MMP．9表达而抑制MPN细胞迁移能力。

关键词：骨髓增殖性肿瘤 ruxolitinib 基质金属蛋白酶2 基质金属蛋白酶9 细胞迁移分析

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ruxolitinib对人红白血病HEL细胞VEGF、HIF-1α表达的影响

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四川大学学报（医学版） 2016年第5期47卷 669-673页

作者：徐倩刘贵敏王凤云张丽军梁文同成志勇保定市第一医院血液内科保定071000 南京市红十字医院南京210001 承德医学院研究生院承德067000

目的探讨JAK2抑制剂ruxolitinib对人红白血病HEL细胞血管内皮生长因子(VEGF)、缺氧诱导因子-1α(HIF-1α)分泌的影响。方法用不同浓度ruxolitinib(1、5、10、50、100、500nmol/L)处理HEL细胞24、48、72h,通过CCK-8法观察其对HEL细胞增... 详细信息

目的探讨JAK2抑制剂ruxolitinib对人红白血病HEL细胞血管内皮生长因子(VEGF)、缺氧诱导因子-1α(HIF-1α)分泌的影响。方法用不同浓度ruxolitinib(1、5、10、50、100、500nmol/L)处理HEL细胞24、48、72h,通过CCK-8法观察其对HEL细胞增殖的抑制作用;不同浓度ruxolitinib处理细胞24、48、72h,RT-PCR检测Jauns激酶2基因(JAK2)mRNA水平,Western blot检测p-JAK2、VEGF、HIF-1α蛋白表达;鸡胚绒毛尿囊膜(CAM)体内血管生长实验检测ruxolitinib对血管生成的影响。结果不同浓度ruxolitinib(除外1nmol/L作用24h)均可抑制HEL细胞增殖。不同浓度ruxolitinib处理HEL细胞24、48、72h后,RT-PCR结果显示JAK2mRNA表达较对照组降低(Pruxolitinib处理细胞72h后血管数目明显减少。结论 ruxolitinib可能通过抑制JAK2通路,抑制HEL细胞VEGF、HIF-1α表达进而抑制血管新生。

关键词：骨髓增殖性肿瘤 ruxolitinib 血管新生 VEGF HIF-1α

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