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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 ***,a JAK-STAT inhibitor,exhibits effectiveness in autoimmune diseases,arthritis,and managing inflammatory cytokine *** 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 *** 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 *** sequencing analysis showed that ruxolitinib alleviated inflammation and immune response after spinal cord injury,restored EAAT2 expression,reduced glutamate levels,and alleviated excitatory ***,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 ***,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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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 ***,the mechanism underlying microglial activation-induced neuroinflammation remains poorly ***(RUX),a selective inhibitor of JAK1/2,was recently reported to inhibit inflammatory storms caused by SARS-CoV-2 in the ***,its role in disrupting inflammation post-SCI has not been *** this study,microglia were treated with RUX for 24 hours and then activated with interferon-γfor 6 *** 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 *** 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 ***,microglia treated with RUX centripetally migrated toward injured foci,remaining limited and compacted within the glial scar,which resulted in axon preservation and less ***,the protein expression levels of tumor necrosis factor-α,interleukin-1β,and interleukin-6 were *** neuromotor function of SCI mice also *** 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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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 *** patients have steroid-refractory(SR) *** To evaluate the effect and safety of ruxolitinib add-on in the treatment of patients with SR acute (a) and chronic (c) *** We retrospectively analyzed 38 patients administered ruxolitinib add-on to standard immunosuppressive therapy for SR-aGVHD or SR-cGVHD following allogeneic hematopoietic stem cell *** was administered5-10 mg/d depending on disease severity,patient status,and the use of antifungal *** response rate,time to best response,malignancy relapse rate,infection rate,and treatment-related adverse events were *** 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 *** malignancy relapse rates for the SR-aGVHD and SR-cGVHD groups were 10.0%and 10.7%,*** 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 *** 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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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 *** are characterized by mutations in driver genes,the JAK2V617F point mutation being the most commonly detected genetic alteration in these hematological ***,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 ***,the use of ruxolitinib has been associated with a potential risk of infection,including opportunistic infections and reactivation of hepatitis ***,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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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治疗真性红细胞增多症的研究进展

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中国药房 2016年第23期27卷 3307-3309页

作者：李晓菲马满玲哈尔滨医科大学附属第一医院药学部哈尔滨150001

目的:为ruxolitinib治疗真性红细胞增多症(PV)提供参考。方法:查阅近年来国外相关文献,就ruxolitinib的作用机制、药效学、药动学、临床试验、安全性和耐受性等研究进展进行归纳和总结。结果:ruxolitinib的Ⅰ期临床试验表明其口服吸收迅... 详细信息

目的:为ruxolitinib治疗真性红细胞增多症(PV)提供参考。方法:查阅近年来国外相关文献,就ruxolitinib的作用机制、药效学、药动学、临床试验、安全性和耐受性等研究进展进行归纳和总结。结果:ruxolitinib的Ⅰ期临床试验表明其口服吸收迅速,有较高的生物利用度。ruxolitinib治疗PV可降低患者对静脉放血的依赖,控制血细胞比容,使血细胞计数正常化。尽管现有数据缺乏充足的随访时间来评估其在患者死亡率和血栓形成风险方面的临床优势,但其Ⅱ期和Ⅲ期的临床试验数据显示出ruxolitinib在控制PV相关症状负荷方面的作用,特别是在减轻对羟基脲无效或不耐受的PV患者的症状严重程度方面明显优于标准疗法,且ruxolitinib的相关药物毒性和ADR易于受控。结论:ruxolitinib为对羟基脲不耐受和抵抗的PV患者的有效治疗药物,有着独特的临床效果和良好的研究前景。

关键词：真性红细胞增多症 ruxolitinib JAK抑制剂骨髓纤维化

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ruxolitinib体外增强Kasumi-1细胞对rsTRAIL的敏感性和机制的研究

Ruxolitinib体外增强Kasumi-1细胞对rsTRAIL的敏感性和机制的研究

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作者：庄晏复旦大学

学位级别：硕士

肿瘤坏死因子相关凋亡诱导配体(Tumor necrosis factor(TNF)-related apoptosis-inducing ligand,TRAIL)是TNF超家族成员之一,可与死亡受体结合诱导细胞凋亡。与TNF家族的其他成员不同,TRAIL可诱导肿瘤细胞凋亡而对正常细胞毒性很轻,使... 详细信息

肿瘤坏死因子相关凋亡诱导配体(Tumor necrosis factor(TNF)-related apoptosis-inducing ligand,TRAIL)是TNF超家族成员之一,可与死亡受体结合诱导细胞凋亡。与TNF家族的其他成员不同,TRAIL可诱导肿瘤细胞凋亡而对正常细胞毒性很轻,使得它可能成为很有前途的特异性抗肿瘤药物。然而,研究也发现癌细胞可通过多种机制呈现出对TRAIL的耐药,制约了其临床应用。因此,探索新的克服TRAIL耐药的途径具有重要临床价值。ruxolitinib是一种JAK激酶抑制剂,具有抗肿瘤活性。我们前期的研究发现白血病细胞Kasumi一1亲本和TRAIL耐药细胞株呈现TRAIL显著耐药性,本研究将ruxolitinib和TRAIL联合应用于Kasumi-1细胞,旨在寻找对t(8;21)阳性急性白血病新的治疗方法。研究工作分为两部分完成：第一部分ruxolitinib和／或rsTRAIL对Kasumi-1细胞的体外作用。目的：观察rsTRAIL、ruxolitinib单独及其联合对Kasumi-1细胞的体外作用。方法：采用WST-8(CCK-8)比色法测定rsTRAIL单药、ruxolitinib单药及其联合应用对Kasumi-1细胞的生长抑制作用;采用DAPI染色法观察rsTRAIL单药、ruxolitinib单药及其联合作用于Kasumi-1细胞后细胞凋亡状态;用流式细胞术检测rsTRAIL单药及二者联合作用于Kasumi-1细胞后细胞的凋亡率。结果：(1)rsTRAIL和ruxolitinib在体外单用均可抑制Kasumi-1细胞的生长,luM和10uMruxolitinib分别与不同浓度rsTRAIL联合用药可增加Kasumi-1细胞的生长抑制率,且呈时间和剂量依赖性(Pruxolitinib(10uM)在体外单药及联合作用于Kasumi-1细胞,AnnexinV阳性细胞百分率分别为(30.62%±3.34%)(33.99%±3.67%)and(56.66%±4.23%)与对照组8.53%相比,差异显著(Pruxolitinib单独及联合rsTRAIL具有抑制Kasumi一1细胞生长作用且具有协同诱导Kasumi一1细胞凋亡的作用。第二部分ruxolitinib体外增强rsTRAIL诱导Kasumi-1细胞凋亡机制的研究。目的：探讨rsTRAIL、ruxolitinib在体外单独及其联合诱导Kasumi-1细胞凋亡作用的机制。方法：采用实时定量PCR法检测不同浓度ruxolitinib作用于Kasumi-1细胞,经不同作用时间后TRAIL及TRAIL受体DR4、DR5、DcR1及DcR2基因水平变化。WesternBlot法检测rsTRAIL、ruxolitinib单独及联合作用于Kasumi-1细胞后,TRAIL受体及凋亡相关蛋白变化。应用siRNA干扰Kasumi-1细胞JAK2、 STAT3基因,WesternBlot法检测TRAIL受体DR4的蛋白水平变化。WesternBlot法检测不同浓度ruxolitinib作用于Kasumi-1细胞48h和rsTRAIL、ruxolitinib单独及联合作用于Kasumi-1细胞后对NF-KB活化水平的抑制。结果：(1)实时定量PCR法检测发现ruxolitinib作用于Kasumi-1细胞,经不同作用时间后可以上调TRAIL及受体DR4、DR5、DcR1及DcR2基因水平。(2) Western Blot法检测ruxolitinib、rsTRAIL单独及联合作用于Kasumi-1细胞后,TRAIL受体DR4蛋白水平升高,而DR5、DcR1及DcR2蛋白水平无明显变化。应用转染技术沉默JAK2和STAT3基因后,Western Blot检测发现DR4蛋白水平升高。(3)Western Blot法检测ruxolitinib、rsTRAIL单独及联合作用于Kasumi-1细胞后,Caspase-8,-9无明显变化,Caspase-3蛋白水平升高,促凋亡蛋白Bax蛋白水平升高。(4)Western Blot法检测ruxolitinib、rsTRAIL单独及联合作用于Kasumi-1细胞后, NF-KB活性受抑。结论：ruxolitinib增强rsTRAIL诱导Kasumi-1细胞凋亡的作用的机制与DR4上调,激活Caspase-3,上调Bax和抑制NF-KB的活性有关。

关键词： Kasumi-1 cells ruxolitinib TRAIL DR4

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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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PD-1 antibody and ruxolitinib enhances graft-versus-lymphoma effect without increasing acute graft-versus-host disease in mice

PD-1 antibody and ruxolitinib enhances graft-versus-lymphoma...

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第十四届全国免疫学学术大会

作者： Bin Pan Longmei Shang Cong Liu Zhenyu Li Kailin Xu Department of Hematology The Affiliated Hospital of Xuzhou Medical College

Boosting T-cell immune response posttransplant with checkpoint-inhibitors increases graft-versus-lymphoma(GVL)effects at the cost of increasing acute graft-versus-host disease(a GVHD).We studied whether this competition could be avoided by giving concurrent anti-PD-1 antibody and ruxolitinib in allotransplant mouse *** alone the PD-1 antibody increased GVL but did not improve survival of recipients challenged with A20 cells because of increased deaths from *** ruxolitinib decreased levels of effector T cells and related ***-1 antibody preserved expression of granzyme B and cytotoxicity of T cells which were decreased by *** net result of combined therapy was increased GVL,no increase in aGVHD and increased *** combined therapy improved survival of recipients challenged by A20 cells which expressed high level of PD-L1,but not EL4 cells which do not express PD-L1.

关键词： graft-versus-lymphoma acute graft-versus-host disease programmed death-1 ruxolitinib

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