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Nano Research 2023年第2期16卷 2885-2894页

作者： Lei Zhang Jiaru Jing Lin Han Ziyan Liu Jingyu Wang Wei Zhang Ai Gao Department of Occupational Health and Environmental Health School of Public HealthCapital Medical UniversityBeijing 100069China Beijing Key Laboratory of Environmental Toxicology Capital Medical UniversityBeijing 100069China

Plastic pollution has become a non-negligible global pollution problem.Nanoplastics(NP)can reach the bone marrow with blood circulation and develop hematotoxicity,but potential mechanisms and prevention strategies are lacking.Here,we report the biological distribution of NP particles in the bone marrow of mice and hematopoietic toxicity after exposure to 60μg of 80 nm NP for 42 days.NP exposure inhibited the capability of bone marrow hematopoietic stem cells to renew and differentiate.Notably,probiotics and Melatonin supplementation significantly ameliorated NP-induced hematopoietic damage,and the former was superior to the latter.And interestingly,Melatonin and probiotic interventions may involve different microbes and metabolites.After Melatonin intervention,creatine showed a stronger correlation with NP-induced gut microbiota disorders.In contrast,probiotic intervention reversed the levels of more gut microbes and plasma metabolites.Of these,threonine,malonylcarnitine,and 3-hydroxybutyric acid might be potential performers in the regulation of hematopoietic toxicity by gut microbes,as they had a more significant relationship with the identified microbes.In conclusion,supplementation with Melatonin or probiotics may be two candidates to prevent hematopoietic toxicity attributable to NP exposure.Also,the multi-omics results may lay the foundation for future investigations into in-depth mechanisms.

关键词： gut microbiota-metabolism Melatonin probiotics nanoplastics exposure hematopoietic injury

Melatonin decreases GSDME mediated mesothelial cell pyroptosis and prevents peritoneal fibrosis and ultrafiltration failure

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Science China(Life Sciences) 2024年第2期67卷 360-378页

作者： Hongxia Ruan Xuejuan Li Lina Zhou Zihan Zheng Rulin Hua Xu Wang Yuan Wang Yujie Fan Shuwen Guo Lihua Wang Shafiq ur Rahman Ziwei Wang Yuyuan Wei Shuangyan Yu Rongzhi Zhang Qian Cheng Jie Sheng Xue Li Xiaoyan Liu Ruqiang Yuan Xiaoyan Zhang Lihong Chen Guowang Xu Youfei Guan Jing Nie Hongqiang Qin Feng Zheng Advanced Institute for Medical Sciences Dalian Medical UniversityDalian 116044China Department of Nephrology Second HospitalDalian Medical UniversityDalian 116023China CAS Key Laboratory of Separation Science for Analytical Chemistry Dalian Institute of Chemical PhysicsChinese Academy of SciencesDalian 116023China Chongqing International Institute for Immunology Chongqing 401320China Department of Nephrology Shenzhen HospitalSouthern Medical UniversityShenzhen 518101China Wuhu Hospital and Health Science Center East China Normal UniversityShanghai 200241China Peking University First Hospital Peking UniversityBeijing 100034China

Peritoneal fibrosis together with increased capillaries is the primary cause of peritoneal dialysis failure.Mesothelial cell loss is an initiating event for peritoneal fibrosis.We find that the elevated glucose concentrations in peritoneal dialysate drive mesothelial cell pyroptosis in a manner dependent on caspase-3 and Gasdermin E,driving downstream inflammatory responses,including the activation of macrophages.Moreover,pyroptosis is associated with elevated vascular endothelial growth factor A and C,two key factors in vascular angiogenesis and lymphatic vessel formation.GSDME deficiency mice are protected from high glucose induced peritoneal fibrosis and ultrafiltration failure.Application of Melatonin abrogates mesothelial cell pyroptosis through a MT1R-mediated action,and successfully reduces peritoneal fibrosis and angiogenesis in an animal model while preserving dialysis efficacy.Mechanistically,Melatonin treatment maintains mitochondrial integrity in mesothelial cells,meanwhile activating m TOR signaling through an increase in the glycolysis product dihydroxyacetone phosphate.These effects together with quenching free radicals by Melatonin help mesothelial cells maintain a relatively stable internal environment in the face of high-glucose stress.Thus,Melatonin treatment holds some promise in preserving mesothelium integrity and in decreasing angiogenesis to protect peritoneum function in patients undergoing peritoneal dialysis.

关键词： Melatonin mitochondria pyroptosis GSDME peritoneal fibrosis mTOR

Exercise-with-Melatonin therapy improves sleep disorder and motor dysfunction in a rat model of ischemic stroke

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Neural Regeneration Research 2024年第6期19卷 1336-1343页

作者： Haitao Zhao Tong Zhang Haojie Zhang Yunlei Wang Lingna Cheng School of Rehabilitation Medicine Capital Medical University Department of Neurological Rehabilitation Beijing Bo'ai Hospital China Rehabilitation Research Center 3. School of Rehabilitation Medicine University of Health and Rehabilitation Sciences 4. Laboratory of Brain Injury Repair and Rehabilitation China Rehabilitation Science Institute

Exercise-with-Melatonin therapy has complementary and synergistic effects on spinal cord injury and Alzheimer’s disease, but its effect on stroke is still poorly understood. In this study, we established a rat model of ischemic stroke by occluding the middle cerebral artery for 60 minutes. We treated the rats with exercise and Melatonin therapy for 7 consecutive days. Results showed that exercise-with-Melatonin therapy significantly prolonged sleep duration in the model rats, increased delta power values, and regularized delta power rhythm. Additionally, exercise-with-Melatonin therapy improved coordination, endurance, and grip strength, as well as learning and memory abilities. At the same time, it led to higher hippocampal CA1 neuron activity and postsynaptic density thickness and lower expression of glutamate receptor 2 than did exercise or Melatonin therapy alone. These findings suggest that exercise-withMelatonin therapy can alleviate sleep disorder and motor dysfunction by increasing glutamate receptor 2 protein expression and regulating hippocampal CA1 synaptic plasticity.

关键词： exercise glutamate receptor 2 hippocampus ischemic stroke learning Melatonin memory sleep disorder synaptic plasticity

Melatonin promotes the development of the secondary hair follicles by regulating circMPP5

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Journal of Animal Science and Biotechnology 2023年第4期14卷 1696-1712页

作者： Xiaogao Diao Lingyun Yao Tao Duan Jiaxin Qin Liwen He Wei Zhang Department of Animal Nutrition and Feed Science State Key Laboratory of Animal NutritionCollege of Animal Science and TechnologyChina Agricultural UniversityBeijing 100193China

Background The quality and yield of cashmere fibre are closely related to the differentiation and development of secondary hair follicles in the skin of cashmere goats.The higher the density of secondary hair follicles,the higher the quality and yield of cashmere from the fleece.Development of secondary hair follicles commences in the embryonic stage of life and is completed 6 months after birth.Preliminary experimental results from our laboratory showed that Melatonin(MT)treatment of goat kids after their birth could increase the density of secondary hair follicles and,thus,improve the subsequent yield and quality of cashmere.These changes in the secondary hair follicles resulted from increases in levels of antioxidant and expression of anti-apoptotic protein,and from a reduction in apoptosis.The present study was conducted to explore the molecular mechanism of MT-induced secondary hair follicle differentiation and development by using whole-genome analysis.Results MT had no adverse effect on the growth performance of cashmere kids but significantly improved the character of the secondary hair follicles and the quality of cashmere,and this dominant effect continued to the second year.Melatonin promotes the proliferation of secondary hair follicle cells at an early age.The formation of secondary hair follicles in the MT group was earlier than that in the control group in the second year.The genome-wide data results involved KEGG analysis of 1044 DEmRNAs,91 DElncRNAs,1054 DEcircRNAs,and 61 DEmiRNAs which revealed that the mitogen-activated protein kinase(MAPK)signaling pathway is involved in the development of secondary hair follicles,with key genes(FGF2,FGF21,FGFR3,MAPK3(ERK1))being up-regulated and expressed.We also found that the circMPP5 could sponged miR-211 and regulate the expression of MAPK3.Conclusions We conclude that MT achieves its effects by regulating the MAPK pathway through the circMPP5 sponged the miR-211,regulating the expression of MAPK3,to induce the differentiation and proliferation of seconda

关键词： Cashmere MAPK Melatonin miR-211 Secondary hair follicle

Pancreatic Melatonin enhances anti-tumor immunity in pancreatic adenocarcinoma through regulating tumor-associated neutrophils infiltration and NETosis

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Acta Pharmaceutica Sinica B 2023年第4期13卷 1554-1567页

作者： Yau-tuen Chan Hor-yue Tan Yuanjun Lu Cheng Zhang Chien-shan Cheng Junyu Wu Ning Wang Yibin Feng School of Chinese Medicine the University of Hong KongHong KongChina Centre for Chinese Herbal Medicine Drug Development School of Chinese MedicineHong Kong Baptist UniversityHong KongChina Department of Traditional Chinese Medicine Shanghai Jiaotong UniversitySchool of Medicine Affiliated Ruijin HospitalShanghai 200025China

Tumor microenvironment contributes to poor prognosis of pancreatic adenocarcinoma(PAAD)patients.Proper regulation could improve survival.Melatonin is an endogenous hormone that delivers multiple bioactivities.Here we showed that pancreatic Melatonin level is associated with patients'survival.In PAAD mice models,Melatonin supplementation suppressed tumor growth,while blockade of Melatonin pathway exacerbated tumor progression.This anti-tumor effect was independent of cytotoxicity but associated with tumor-associated neutrophils(TANs),and TANs depletion reversed effects of Melatonin.Melatonin induced TANs infiltration and activation,therefore induced cell apoptosis of PAAD cells.Cytokine arrays revealed that Melatonin had minimal impact on neutrophils but induced secretion of Cxcl2 from tumor cells.Knockdown of Cxcl2 in tumor cells abolished neutrophil migration and activation.Melatonin-induced neutrophils presented an N1-like anti-tumor phenotype,with increased neutrophil extracellular traps(NETs)causing tumor cell apoptosis through cell-to-cell contact.Proteomics analysis revealed that this reactive oxygen species(ROS)-mediated inhibition was fueled by fatty acid oxidation(FAO)in neutrophils,while FAO inhibitor abolished the anti-tumor effect.Analysis of PAAD patient specimens revealed that CXCL2 expression was associated with neutrophil infiltration.CXCL2,or TANs,combined with NET marker,can better predict patients'prognosis.Collectively,we discovered an anti-tumor mechanism of Melatonin through recruiting N1-neutrophils and beneficial NET formation.

关键词： Pancreatic adenocarcinoma Melatonin Anti-tumor immunity Tumor-associated neutrophils Tumor microenvironment CXCL2 Neutrophil extracellular traps NETosis

Role of selenoprotein M knockdown in the Melatonin antagonism of nickel-induced apoptosis and endoplasmic reticulum stress in mouse heart

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2023年第5期24卷 406-417页

作者： Xintong ZHANG Xiaoxue GAI Lihua XU Wenxue MA Qiaohan LIU Bendong SHI Cheng FANG Jingzeng CAI Ziwei ZHANG College of Veterinary Medicine Northeast Agricultural UniversityHarbin 150030China Suihua Agricultural and Rural Bureau Suihua 152000China College of Veterinary Medicine Northeast Agricultural UniversityHarbin 150030China4.Key Laboratory of the Provincial EducationDepartment of Heilongjiang for Common Animal Disease Prevention and TreatmentNortheast Agricultural UniversityHarbin 150030China

The aim of this study was to investigate the role of selenoprotein M(SelM)in endoplasmic reticulum stress and apoptosis in nickel-exposed mouse hearts and to explore the detoxifying effects of Melatonin.At 21 d after intraperitoneal injection of nickel chloride(NiCl_(2))and/or Melatonin into male wild-type(WT)and SelM knockout(KO)C57BL/6J mice,NiCl_(2)was found to induce changes in the microstructure and ultrastructure of the hearts of both WT and SelM KO mice,which were caused by oxidative stress,endoplasmic reticulum stress,and apoptosis,as evidenced by decreases in malondialdehyde(MDA)content and total antioxidant capacity(T-AOC)activity.Changes in the messenger RNA(mRNA)and protein expression of genes related to endoplasmic reticulum stress(activating transcription factor 4(ATF4),inositol-requiring protein 1(IRE1),c-Jun N-terminal kinase(JNK),and C/EBP homologous protein(CHOP))and apoptosis(B-cell lymphoma-2(Bcl-2),Bcl-2-associated X protein(Bax),Caspase-3,Caspase-9,and Caspase-12)were also observed.Notably,the observed damage was worse in SelM KO mice.Furthermore,Melatonin alleviated the heart injury caused by NiCl_(2)in WT mice but could not exert a good protective effect in the heart of SelM KO mice.Overall,the findings suggested that the antioxidant capacity of SelM,as well as its modulation of endoplasmic reticulum stress and apoptosis,plays important roles in nickel-induced heart injury.

关键词： Selenoprotein M(SelM) Nickel chloride(NiCl_(2)) Melatonin Apoptosis Mouse heart

Melatonin inhibits ESCC tumor growth by mitigating the HDAC7/β-catenin/c-Myc positive feedback loop and suppressing the USP10-maintained HDAC7 protein stability

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Military Medical Research 2023年第2期10卷 207-226页

作者： Zhi-Qiang Ma Ying-Tong Feng Kai Guo Dong Liu Chang-Jian Shao Ming-Hong Pan Yi-Meng Zhang Yu-Xi Zhang Di Lu Di Huang Fan Zhang Jin-Liang Wang Bo Yang Jing Han Xiao-Long Yan Yi Hu Department of Medical Oncology Senior Department of Oncologythe Fifth Medical CenterChinese PLA General HospitalBeijing 100853China Department of Thoracic Surgery Tangdu Hospitalthe Fourth Military Medical UniversityXi’an 710038China Department of Cardiothoracic Surgery the 71th Group Army Hospital of PLAthe Affiliated Huaihai Hospital of Xuzhou Medical UniversityXuzhou 221004JiangsuChina Department of Thoracic Surgery Shaanxi Provincial People’s Hospitalthe Third Affiliated Hospital of Xi’an Jiaotong UniversityXi’an 710068China State Key Laboratory of Cardiovascular Disease Fuwai HospitalNational Center for Cardiovascular DiseasesChinese Academy of Medical SciencesPeking Union Medical CollegeBeijing 100037China Department of Ophthalmology Tangdu Hospitalthe Fourth Military Medical UniversityXi’an 710038China Department of Cardiovascular Surgery Xijing Hospitalthe Fourth Military Medical UniversityXi’an 710032China

Background:Melatonin,a natural hormone secreted by the pineal gland,has been reported to exhibit antitumor properties through diverse mechanisms of action.However,the oncostatic function of Melatonin on esophageal squamous cell carcinoma(ESCC) remains elusive.This study was conducted to investigate the potential effect and underlying molecular mechanism of Melatonin as single anticancer agent against ESCC cells.Methods:ESCC cell lines treated with or without Melatonin were used in this study.In vitro colony formation and 5-Ethynyl-2’-deoxyuridine(EdU) incorporation assays,and nude mice tumor xenograft model were used to confirm the proliferative capacities of ESCC cells.RNA-seq,qPCR,Western blotting,recombinant lentivirus-mediated target gene overexpression or knockdown,plasmids transfection and co-IP were applied to investigate the underlying molecular mechanism by which Melatonin inhibited ESCC cell growth.IHC staining on ESCC tissue microarray and further survival analyses were performed to explore the relationship between target genes’ expression and prognosis of ESCC.Results:Melatonin treatment dose-dependently inhibited the proliferative ability and the expression of histone deacetylase 7(HDAC7),c-Myc and ubiquitin-specific peptidase 10(USP10) in ESCC cells(P<0.05).The expressions of HDAC7,c-Myc and USP10 in tumors were significantly higher than the paired normal tissues from 148 ESCC patients(P<0.001).Then,the Kaplan-Meier survival analysis suggested that ESCC patients with high HDAC7,c-Myc or USP10levels predicted worse overall survival(log-rank P<0.001).Co-IP and Western blotting further revealed that HDAC7physically deacetylated and activated β-catenin thus promoting downstream target c-Myc gene transcription.Notably,our mechanistic study validated that HDAC7/β-catenin/c-Myc could form the positive feedback loop to enhance ESCC cell growth,and USP10 could deubiquitinate and stabilize HDAC7 protein in the ESCC cells.Additionally,we verified that inhibition of the HDAC7/β-catenin/c-Myc axis and USP10/HDAC

关键词： Melatonin Histone deacetylase 7(HDAC7) β-catenin c-Myc Ubiquitin-specifc peptidase 10(USP10) Esophageal squamous cell carcinoma(ESCC)

A three-dimensional matrix system containing Melatonin and neural stem cells repairs damage from traumatic brain injury in rats

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Neural Regeneration Research 2022年第11期17卷 2512-2517页

作者： Xuan-Yu Fang Da-Wei Zhao Chao Zhang Hong-Fei Ge Xu-Yang Zhang Feng-Chun Zhao Yi-Bin Jiang Hua Feng Rong Hu Department of Neurosurgery and Key Laboratory of Neurotrauma Southwest HospitalArmy Medical UniversityChongqingChina

Brain lesions can cause neural stem cells to activate,proliferate,diffe rentiate,and migrate to the injured area.However,after traumatic brain injury,brain tissue defects and microenvironment changes greatly affect the survival and growth of neural stem cells;the resulting reduction in the number of neural stem cells impedes effective repair of the injured area.Melatonin can promote the survival,proliferation,and differentiation of neural stem cells under adverse conditions such as oxidative stress or hypoxia that can occur after traumatic brain injury.Therefore,we investigated the therapeutic effects of Melatonin combined with neural stem cells on traumatic brain injury in rats.First,in vitro studies confirmed that Melatonin promoted the survival of neural stem cells deprived of oxygen and glucose.Then,we established a three-dimensional Matrigel-based transplantation system containing Melatonin and neural stem cells and then used it to treat traumatic brain injury in rats.We found that treatment with the Matrigel system containing Melatonin and neural stem cells decreased brain lesion volume,increased the number of surviving neuro ns,and improved recove ry of neurological function compared with treatment with Matrigel alone,neural stem cells alone,Matrigel and neural stem cells combined,and Matrigel and Melatonin combined.Our findings suggest that the three-dimensional Matrigelbased transplantation system containing Melatonin and neural stem cells is a potential treatment for traumatic brain injury.

关键词： cell therapy magnetic resonance imaging Matrigel Melatonin neural stem cells neurological function recovery three-dimensional transplantation traumatic brain injury

Altered Retinal Dopamine Levels in a Melatonin-proficient Mouse Model of Form-deprivation Myopia

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Neuroscience Bulletin 2022年第9期38卷 992-1006页

作者： Kang-Wei Qian Yun-Yun Li Xiao-Hua Wu Xue Gong Ai-Lin Liu Wen-Hao Chen Zhe Yang Ling-Jie Cui Yun-Feng Liu Yuan-Yuan Ma Chen-Xi Yu Furong Huang Qiongsi Wang Xiangtian Zhou Jia Qu Yong-Mei Zhong Xiong-Li Yang Shi-Jun Weng State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science Institutes of Brain ScienceFudan UniversityShanghai200032China Discipline of Neuroscience and Department of Anatomy and Physiology College of Basic Medical SciencesShanghai Jiao Tong University School of MedicineShanghai200025China School of Ophthalmology and Optometry and Eye Hospital Wenzhou Medical UniversityWenzhou325027China Department of Immunology School of Basic Medical SciencesAnhui Medical UniversityHefei230032China

Reduced levels of retinal dopamine,a key regulator of eye development,are associated with experimental myopia in various species,but are not seen in the myopic eyes of C57BL/6 mice,which are deficient in Melatonin,a neurohormone having extensive interactions with dopamine.Here,we examined the relationship between form-deprivation myopia(FDM)and retinal dopamine levels in Melatonin-proficient CBA/CaJ mice.We found that these mice exhibited a myopic refractive shift in form-deprived eyes,which was accompanied by altered retinal dopamine levels.When Melatonin receptors were pharmacologically blocked,FDM could still be induced,but its magnitude was reduced,and retinal dopamine levels were no longer altered in FDM animals,indicating that Melatonin-related changes in retinal dopamine levels contribute to FDM.Thus,FDM is mediated by both dopamine level-independent and Melatonin-related dopamine level-dependent mechanisms in CBA/CaJ mice.The previously reported unaltered retinal dopamine levels in myopic C57BL/6 mice may be attributed to Melatonin deficiency.

关键词： Myopia Refractive development Dopamine Melatonin Mouse Retina

Melatonin improves the first cleavage of parthenogenetic embryos from vitrified-warmed mouse oocytes potentially by promoting cell cycle progression

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Journal of Animal Science and Biotechnology 2022年第1期13卷 106-122页

作者： Bo Pan Izhar Hyder Qazi Shichao Guo Jingyu Yang Jianpeng Qin Tianyi Lv Shengqin Zang Yan Zhang Changjun Zeng Qingyong Meng Hongbing Han Guangbin Zhou Farm Animal Genetic Resources Exploration and Innovation Key Laboratory of Sichuan Province College of Animal Science and TechnologySichuan Agricultural UniversityChengdu 611130China Department of Veterinary Anatomy and Histology Shaheed Benazir Bhutto University of Veterinary and Animal SciencesSakrandSindh 67210Pakistan State Key Laboratory of AgroBiotechnology China Agricultural UniversityBeijing 100193China National Engineering Laboratory for Animal Breeding Key Laboratory of Animal Genetics and Breeding of the Ministry of AgricultureBeijing Key Laboratory for Animal Genetic ImprovementCollege of Animal Science and TechnologyChina Agricultural UniversityBeijing 100193China

Background:This study investigated the effect of Melatonin(MT)on cell cycle(G1/S/G2/M)of parthenogenetic zygotes developed from vitrified-warmed mouse metaphase II(MII)oocytes and elucidated the potential mechanism of MT action in the first cleavage of embryos.Results:After vitrification and warming,oocytes were parthenogenetically activated(PA)and in vitro cultured(IVC).Then the spindle morphology and chromosome segregation in oocytes,the maternal mRNA levels of genes including Miss,Doc1r,Setd2 and Ythdf2 in activated oocytes,pronuclear formation,the S phase duration in zygotes,mitochondrial function at G1 phase,reactive oxygen species(ROS)level at S phase,DNA damage at G2 phase,early apoptosis in 2-cell embryos,cleavage and blastocyst formation rates were evaluated.The results indicated that the vitrification/warming procedures led to following perturbations 1)spindle abnormalities and chromosome misalignment,alteration of maternal mRNAs and delay in pronucleus formation,2)decreased mitochondrial membrane potential(MMP)and lower adenosine triphosphate(ATP)levels,increased ROS production and DNA damage,G1/S and S/G2 phase transition delay,and delayed first cleavage,and 3)increased early apoptosis and lower levels of cleavage and blastocyst formation.Our results further revealed that such negative impacts of oocyte cryopreservation could be alleviated by supplementation of warming,recovery,PA and IVC media with 10^(−9) mol/L MT before the embryos moved into the 2-cell stage of development.Conclusions:MT might promote cell cycle progression via regulation of MMP,ATP,ROS and maternal mRNA levels,potentially increasing the first cleavage of parthenogenetic zygotes developed from vitrified-warmed mouse oocytes and their subsequent development.

关键词： Cell cycle Cleavage rate Melatonin MetaphaseⅡoocyte Parthenogenetic activation Vitrification