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necroptosis plays a crucial role in the exacerbation of retinal injury after blunt ocular trauma

Neural Regeneration Research 2023年第4期18卷 922-928页

作者： Yu Huan Xiu-Quan Wu Tao Chen Ya-Nan Dou Bo Jia Xin He Dong-Yu Wei Zhou Fei Fei Fei Department of Neurosurgery Xijing HospitalAir Force Medical UniversityXi’anShaanxi ProvinceChina Center of Clinical Aerospace Medicine Air Force Medical UniversityXi’anShaanxi ProvinceChina Department of Aviation Medicine Xijing HospitalAir Force Medical UniversityXi’anShaanxi ProvinceChina Department of Ophthalmology Xijing HospitalAir Force Medical UniversityXi’anShaanxi ProvinceChina

Retinal injury after blunt ocular trauma may directly affect prognosis and lead to vision loss.To investigate the pathological changes and molecular mechanisms involved in retinal injury after blunt ocular trauma,we established a weight drop injury model of blunt ocular trauma in male Beagle dogs.Hematoxylin-eosin staining,immunofluorescence staining,western blotting,and TUNEL assays were performed to investigate retinal injury within 14 days after blunt ocular trauma.Compared with the control group,the thicknesses of the inner and outer nuclear layers,as well as the number of retinal ganglion cells,gradually decreased within 14 days after injury.The number of bipolar cells in the inner nuclear layer began to decrease 1 day after injury,while the numbers of cholinergic and amacrine cells in the inner nuclear layer did not decrease until 7 days after injury.Moreover,retinal cell necroptosis increased with time after injury;it progressed from the ganglion cell layer to the outer nuclear layer.Visual electrophysiological findings indicated that visual impairment began on the first day after injury and worsened over time.Additionally,blunt ocular trauma induced nerve regeneration and Müller glial hyperplasia;it also resulted in the recruitment of microglia to the retina and polarization of those microglia to the M1 phenotype.These findings suggest that necroptosis plays an important role in exacerbating retinal injury after blunt ocular trauma via gliosis and neuroinflammation.Such a role has important implications for the development of therapeutic strategies.

关键词： Beagle dogs blunt ocular trauma gliosis M1 microglia Müller cells necroptosis neuroinflammation retinal ganglion cells retinal injury weight drop injury

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necroptosis-elicited host immunity:GOx-loaded MoS_(2) nanocatalysts for self-amplified chemodynamic immunotherapy

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Nano Research 2022年第3期15卷 2244-2253页

作者： Wensheng Xie Jingsong Lu Zhenhu Guo Xiaoxiao Guo Yongjiu Chi Jieling Ye Junxin Zhang Wanling Xu Lingyun Zhao Yen Wei The Key Laboratory of Bioorganic Phosphorus Chemistry&Chemical Biology(Ministry of Education) Department of ChemistryTsinghua UniversityBeijing 100084China State Key Laboratory of New Ceramics and Fine Processing School of Materials Science and EngineeringTsinghua UniversityBeijing 100084China Research Center of Magnetic and Electronic Materials College of Materials Science and EngineeringZhejiang University of TechnologyHangzhou 310014China State Key Laboratory of Powder Metallurgy Powder Metallurgy Research InstituteCentral South UniversityChangsha 410083China Department of Chemistry Tsinghua UniversityBeijing 100084China.

Nanoparticles induced potent antitumor immunotherapy plays a significant role for enhancing conventional therapeutic effectiveness.However,revealing the pathway of how nanoagents themselves trigger the host immunity or how to maximize the immunotherapy efficacy still needs further exploration.Herein,rose-like MoS2 nanoflowers modified with 2-deoxy-D-glucose(2-DG)and glucose oxidase(GOx)(MPGGFs)have been successfully fabricated via a one-pot hydrothermal reaction and following one-by-one surface modification as a multifunctional nanocatalyst for photothermal therapy enhanced self-amplified chemodynamic immunotherapy(PTT-co-CDT).By introducing GOx,the obtained MPGGFs exhibited self-amplified chemodynamic therapeutic efficacy under hypoxia tumor microenvironment(TME)because of the raised intracellular H2O2 level via enzyme-catalysis of oxygen.Furthermore,combined with the intrinsic excellent photothermal conversion efficiency of MoS2 nanoflowers,PTT-co-CDT performances by MPGGFs could effectively induce the necroptosis of tumor cells both in vitro and in vivo.Then the induced necroptosis via PTT-co-CDT by MPGGFs could directly trigger host immunity by activating the antigen-specific T-cells(CD4^(+) and CD8^(+)).Finally,the excellent in vivo safety of MPGGFs makes us believe that the successful construction of rose-like multifunctional nanocatalyst not only has great potentials for self-amplified chemodynamic immunotherapy,but also provides a paradigm for exploring necroptosis triggered host immunity for cancer treatment.

关键词： chemodynamic immunotherapy necroptosis nanocatalyst photothermal therapy self-amplified

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Molybdenum and cadmium co-induce necroptosis through Th1/Th2 imbalance-mediated endoplasmic reticulum stress in duck ovaries

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Journal of Environmental Sciences 2024年第8期142卷 92-102页

作者： Ting Cui Xueyan Dai Huiling Guo Dianyun Wang Bingyan Huang Wenjing Pu Xuesheng Chu Caiying Zhang Jiangxi Provincial Key Laboratory for Animal Health Institute of Animal Population HealthCollege of Animal Science and TechnologyJiangxi Agricultural UniversityNanchang 330045China

Cadmium(Cd)and excess molybdenum(Mo)pose serious threats to animal health.Our previous study has determined that Cd and/or Mo exposure can cause ovarian damage of ducks,while the specific mechanism is still obscure.To further investigate the toxic mechanism of Cd and Mo co-exposure in the ovary,forty 8-day-old female ducks were randomly allocated into four groups for 16 weeks,and the doses of Cd and Mo in basic diet per kg were as follows:control group,Mo group(100 mg Mo),Cd group(4 mg Cd),and Mo+Cd group(100 mg Mo+4 mg Cd).Cadmium sulfate 8/3-hydrate(CdSO_(4)·8/3H_(2)O)and hexaammonium molybdate((NH_(4))_(6)Mo_(7)O_(24)·4H_(2)O)were the origins of Cd and Mo,respectively.At the 16th week of the experiment,all ovary tissues were collected for the detection of related indexes.The data indicated that Mo and/or Cd induced trace element disorders and Th1/Th2 balance to divert toward Th1 in the ovary,which activated endoplasmic reticulum(ER)stress and then provoked necroptosis through triggering RIPK1/RIPK3/MLKL signaling pathway,and eventually caused ovarian pathological injuries and necroptosis characteristics.The alterations of above indicators were most apparent in the joint group.Above all,this research illustrates that Mo and/or Cd exposure can initiate necroptosis through Th1/Th2 imbalance-modulated ER stress in duck ovaries,and Mo and Cd combined exposure aggravates ovarian injuries.This research explores the molecular mechanism of necroptosis caused by Mo and/or Cd,which reveals that ER stress attenuation may be a therapeutic target to alleviate necroptosis.

关键词： Molybdenum Cadmium Th1/Th2 imbalance Endoplasmic reticulum stress necroptosis Ovary

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necroptosis was found in a rat ischemia/reperfusion injury flap model

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Chinese Medical Journal 2019年第1期132卷 42-50页

作者： Hao Uu Ming-Zi Zhang Yi-Fang Liu Xin-Hang Dong Yan Hao You-Bin Wang Department of Plastic Surgery Peking Union Medical College HospitalBeijing 100005China Chinese Academy of Medical Sciences & Peking Union Medical College Beijing 100005China International Education College Beijing Vocational College of AgricultureBeijing 100012China

Background:necroptosis is a new form of cell death that has been identified as a third pathway causing cell death.In this study,necrostatin-1 (Nec-1) was used to determine whether necroptosis exists in a rat ischaemia/reperfusion injury flap model.Methods:In this study,twenty male Sprague-Dawley rats were divided randomly into two groups:a control group (CTL group) and a Nec-1 group.Each abdominal skin flap underwent 3 h of ischaemia and then reperfusion.Fifteen minutes before and after reperfusion,phosphate buffer saline (PBS) was administered intraperitoneally to the CTL group,while Nec-1 was administered intraperitoneally to the Nec-1 group.Twenty-four hours after reperfusion,the whole flap was divided equally into 54 sections.Flap blood perfusion was measured.One sample was taken randomly from each row.Morphological changes,apoptosis,receptor-interacting protein-1 (RIP-1) expression and caspase-3 activity were observed and detected.The measurements between the two groups were compared with the independentt-test,and aPvalue of necroptosis was present in a rat abdominal ischaemia/reperfusion injury flap model.

关键词： Necrostatin-1 necroptosis cell death ischaemia/reperfusion injury skin flap

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Artemisia vulgaris Induces Tumor-Selective Ferroptosis and necroptosis via Lysosomal Ca2+ Signaling

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CHINESE JOURNAL OF INTEGRATIVE MEDICINE 2023年第6期30卷 525-533页

作者： Zamarioli, Lucas dos Santos Santos, Michele Rosana Maia Erustes, Adolfo Garcia Meccatti, Vanessa Marques Pereira, Thais Cristine Smaili, Soraya S. Marcucci, Maria Cristina Oliveira, Carlos Rocha Pereira, Gustavo J. S. Bincoletto, Claudia Univ Fed Sao Paulo Paulista Sch Med Dept Pharmacol BR-04044020 Sao Paulo SP Brazil Anhembi Morumbi Univ Sch Hlth Sci Res Grp Phytocomplexes & Cell Signaling BR-03164000 Sao Paulo SP Brazil Sao Paulo State Univ ICT UNESP Inst Sci & Technol Dept Biosci & Oral Diag BR-12231280 Sao Paulo SP Brazil

Objective: To evaluate the chemical composition and effects of Artemisia vulgaris (AV) hydroalcoholic extract (HEAV) on breast cancer cells (MCF-7 and SKBR-3), chronic myeloid leukemia (K562) and NIH/3T3 fibroblasts. Methods: Phytochemical analysis of HEAV was done by high-performance liquid chromatography-mass (HPLC) spectrometry. Viability and cell death studies were performed using trypan blue and Annexin/FITC-7AAD, respectively. Ferrostatin-1 (Fer-1) and necrostatin-1 (Nec-1) were used to assess the mode of HEAV-induced cell death and acetoxymethylester (BAPTA-AM) was used to verify the involvement of cytosolic calcium in this event. Cytosolic calcium measurements were made using Fura-2-AM. Results: HEAV decreased the viability of MCF-7, SKBR-3 and K562 cells (P<0.05). The viability of HEAV-treated K562 cells was reduced compared to HEAV-exposed fi broblasts (P<0.05). Treatment of K562 cells with HEAV induced cell death primarily by late apoptosis and necrosis in assays using annexin V-FITC/7-AAD (P<0.05). The use of Nec-1 and Fer-1 increased the viability of K562 cells treated with HEAV relative to cells exposed to HEAV alone (P<0.01). HEAVinduced Ca2+ release mainly from lysosomes in K562 cells (P<0.01). Furthermore, BAPTA-AM, an intracellular Ca2+ chelator, decreased the number of non-viable cells treated with HEAV (P<0.05). Conclusions: HEAV is cytotoxic and activates several modalities of cell death, which are partially dependent on lysosomal release of Ca2+. These effects may be related to artemisinin and caffeoylquinic acids, the main compounds identifi ed in HEAV.

关键词： Artemisia vulgaris necroptosis ferroptosis late apoptosis Ca2+ signaling CANCER-CELLS APOPTOSIS EXTRACTS DEATH K562 LINE

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Do pyroptosis, apoptosis, and necroptosis (PANoptosis) exist in cerebral ischemia? Evidence from cell and rodent studies

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Neural Regeneration Research 2022年第8期17卷 1761-1768页

作者： Wei-Tao Yan Yan-Di Yang Xi-Min Hu Wen-Ya Ning Lyu-Shuang Liao Shuang Lu Wen-Juan Zhao Qi Zhang Kun Xiong Department of Neurobiology and Human Anatomy School of Basic Medical ScienceCentral South UniversityChangshaHunan ProvinceChina Department of Dermatology Xiangya HospitalCentral South UniversityChangshaHunan ProvinceChina Department of Human Resources Third Xiangya Hospital of Central South UniversityChangshaHunan ProvinceChina Hunan Key Laboratory of Ophthalmology ChangshaHunan ProvinceChina

Some scholars have recently developed the concept of PANoptosis in the study of infectious diseases where pyroptosis,apoptosis and necroptosis act in consort in a multimeric protein complex,PANoptosome.This allows all the components of PANoptosis to be regulated simultaneously.PANoptosis provides a new way to study the regulation of cell death,in that different types of cell death may be regulated at the same time.To test whether PANoptosis exists in diseases other than infectious diseases,we chose cerebral ischemia/reperfusion injury as the research model,collected articles researching cerebral ischemia/reperfusion from three major databases,obtained the original research data from these articles by bibliometrics,data mining and other methods,then integrated and analyzed these data.We selected papers that investigated at least two of the components of PANoptosis to check its occurrence in ischemia/reperfusion.In the cell model simulating ischemic brain injury,pyroptosis,apoptosis and necroptosis occur together and this phenomenon exists widely in different passage cell lines or primary neurons.Pyroptosis,apoptosis and necroptosis also occurred in rat and mouse models of ischemia/reperfusion injury.This confirms that PANoptosis is observed in ischemic brain injury and indicates that PANoptosis can be a target in the regulation of various central nervous system diseases.

关键词： apoptosis brain central nervous system ischemia/reperfusion middle cerebral artery occlusion necroptosis oxygen and glucose deprivation PANoptosis pyroptosis regulated cell death

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Necrostatin-1 decreases necroptosis and inflammatory markers after intraventricular hemorrhage in mice

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Neural Regeneration Research 2022年第12期17卷 2710-2716页

作者： Chang Liu Yi Cao Hao-Xiang Wang Long Zhao Ya-Xing Chen Kun-Hong Zhong Gao-Wei Li Guo-Qing Wang Ke-Ru Huang Ai-Ping Tong Liang-Xue Zhou Department of Neurosurgery West China Medical SchoolWest China HospitalSichuan UniversityChengduSichuan ProvinceChina Department of Neurosurgery Chengdu Second People’s HospitalChengduSichuan ProvinceChina Department of Neurosurgery Affiliated Hospital of North Sichuan Medical CollegeNanchongSichuan ProvinceChina State Key Laboratory of Biotherapy West China Medical SchoolSichuan UniversityChengduSichuan ProvinceChina

Necrostatin-1,an inhibitor of necroptosis,can effectively inhibit necrotic apoptosis in neurological diseases,which results in the inhibition of inflammation,endoplasmic reticulum stress,and reactive oxygen species production and substantial improvement of neurological function.However,the effects of necrostatin-1 on intraventricular hemorrhage(IVH)remain unknown.In this study,we established a mouse model of IVH by injecting autologous blood into the lateral ventricle of the brain.We also injected necrostatin-1 into the lateral ventricle one hour prior to IVH induction.We found that necrostatin-1 effectively reduced the expression levels of the necroptosis markers receptor-interacting protein kinase(RIP)1,RIP3,mixed lineage kinase domain-like protein(MLKL),phosphorylated(p)-RIP3,and p-MLKL and the levels of interleukin-1β,interleukin-6,and tumor necrosis factor-αin the surrounding areas of the lateral ventricle.However,necrostatin-1 did not reduce ependymal ciliary injury or brain water content.These findings suggest that necrostatin-1 can prevent local inflammation and microglial activation induced by IVH but does not greatly improve prognosis.

关键词： ependymal cilia hydrocephalus inflammation intraventricular hemorrhage microglia MLKL necroptosis necrostatin-1 RIP1 RIP3

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Bufalin Induces Programmed necroptosis in Triple-Negative Breast Cancer Drug-Resistant Cell Lines through RIP1/ROS-Mediated Pathway

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Chinese Journal of Integrative Medicine 2022年第10期28卷 900-908页

作者： LIU Xiao-dan SONG Cheng-yang KONG Cui-cui TIAN Xin Department of Breast Surgery the Fourth Affiliated Hospital of China Medical UniversityShenyang(110032)China Department of Thoracic Surgery the Fourth Affiliated Hospital of China Medical UniversityShenyang(110032)China Molecular Oncology Laboratory of Cancer Research Institute the First Affiliated Hospital of China Medical UniversityShenyang(110001)China

Objective: To explore the effect and mechanism of action of bufalin in triple-negative breast cancer(TNBC) drug-resistant cell lines. Methods: The normal human mammary epithelial cell line, TNBC cell line, TNBC adriamycin-resistant cell line, and TNBC docetaxel-resistant cell line were treated with different doses of bufalin(0–1,000 nmol/L) at different time points(0–72 h). Propidium iodide staining, AV-FITC/PI double staining, Hoechst 33342/PI double staining and transmission electron microscopy(TEM) were used to evaluate the death patterns of the cell lines. Results: Bufalin killed the TNBC cell line and its drug-resistant cell lines in a dose/time-dependent manner(all Pnecroptosis and apoptosis. However, at 48 h, necroptosis was the main manifestation. After treatment with bufalin, the expressions of tumor necrosis factor α, phospho-tumor necrosis factor receptor 1, phospho-receptor interacting protein 1 and c-caspase 3 increased(all Pnecroptosis characteristic after 48 h of bufalin treatment under TEM. Conclusions: Bufalin could induce necroptosis through RIP1/ROS-mediated pathway to kill the drug-resistant TNBC cell lines. This finding provides critical experimental data and theoretical basis for the clinical application of bufalin to overcome the difficulties in the treatment of TNBC.

关键词： bufalin necroptosis drug resistant reactive oxygen species pathway triple-negative breast cancer

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Protocatechuic acid and quercetin attenuate ETEC-caused IPEC-1 cell inflammation and injury associated with inhibition of necroptosis and pyroptosis signaling pathways

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Journal of Animal Science and Biotechnology 2023年第4期14卷 1551-1568页

作者： Kan Xiao Mohan Zhou Qingqing Lv Pengwei He Xu Qin Dan Wang Jiangchao Zhao Yulan Liu Hubei Key Laboratory of Animal Nutrition and Feed Science Wuhan Polytechnic UniversityWuhan 430023People’s Republic of China Department of Animal Science Division of AgricultureUniversity of ArkansasFayettevilleAR 72701USA

Background:necroptosis and pyroptosis are newly identified forms of programmed cell death,which play a vital role in development of many gastrointestinal disorders.Although plant polyphenols have been reported to protect intestinal health,it is still unclear whether there is a beneficial role of plant polyphenols in modulating necroptosis and pyroptosis in intestinal porcine epithelial cell line(IPEC-1)infected with enterotoxigenic Escherichia coli(ETEC)K88.This research was conducted to explore whether plant polyphenols including protocatechuic acid(PCA)and quercetin(Que),attenuated inflammation and injury of IPEC-1 caused by ETEC K88 through regulating necroptosis and pyroptosis signaling pathways.Methods:IPEC-1 cells were treated with PCA(40μmol/L)or Que(10μmol/L)in the presence or absence of ETEC K88.Results:PCA and Que decreased ETEC K88 adhesion and endotoxin level(P<0.05)in cell supernatant.PCA and Que increased cell number(P<0.001)and decreased lactate dehydrogenases(LDH)activity(P<0.05)in cell supernatant after ETEC infection.PCA and Que improved transepithelial electrical resistance(TEER)(P<0.001)and reduced fluorescein isothiocyanate-labeled dextran(FD4)flux(P<0.001),and enhanced membrane protein abundance of occludin,claudin-1 and ZO-1(P<0.05),and rescued distribution of these tight junction proteins(P<0.05)after ETEC infection.PCA and Que also declined cell necrosis ratio(P<0.05).PCA and Que reduced mRNA abundance and concentration of tumor necrosis factor-α(TNF-α),interleukin(IL)-6 and IL-8(P<0.001),and down-regulated gene expression of toll-like receptors 4(TLR4)and its downstream signals(P<0.001)after ETEC infection.PCA and Que down-regulated protein abundance of total receptor interacting protein kinase 1(t-RIP1),phosphorylated-RIP1(p-RIP1),p-RIP1/t-RIP1,t-RIP3,p-RIP3,mixed lineage kinase domain-like protein(MLKL),p-MLKL,dynamin-related protein 1(DRP1),phosphoglycerate mutase 5(PGAM5)and high mobility group box 1(HMGB1)(P<0.05)after ETEC infection.Moreover,PCA and Que reduced protein abundance of

关键词： Cell damage ETEC K88 Intestinal inflammation necroptosis Protocatechuic acid Pyroptosis Quercetin

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Identification of necroptosis-related lncRNAs for prognosis prediction and screening of potential drugs in patients with colorectal cancer

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World Journal of Gastrointestinal Oncology 2023年第11期15卷 1951-1973页

作者： Zhi-Hua Chen Yi-Lin Lin Shao-Qin Chen Xiao-Yu Yang Department of Gastrointestinal Surgery The First Affiliated Hospital of Fujian Medical UniversityFuzhou 350005Fujian ProvinceChina Department of Gastrointestinal Surgery National Regional Medical CenterBinhai Campus of the First Affiliated HospitalFujian Medical UniversityFuzhou 350212Fujian ProvinceChina Peking University People’s Hospital Beijing 100044China School of Basic Medicine Sciences Fujian Medical UniversityFuzhou 350122Fujian ProvinceChina

BACKGROUND Tumor recurrence and metastasis lead to a poor prognosis in colorectal cancer(CRC).necroptosis is closely related to the tumor microenvironment(TME)and affects tumor recurrence and metastasis.We aimed to stratify CRC patients according to necroptosis-related long noncoding RNAs(lncRNAs),which can be used to not only evaluate prognosis and improve precision medicine in clinical practice but also screen potential immunotherapy drugs.AIM To stratify CRC patients according to necroptosis-related lncRNAs(NRLs),which can be used to not only evaluate prognosis and improve precision medicine in clinical practice but also screen potential immunotherapy drugs.METHODS LncRNA expression profiles were collected from The Cancer Genome Atlas.NRLs were identified by coexpression analysis.Cox regression analysis identified a NRL signature.Then,the value of this signature was comprehensively and multidimensionally evaluated,and its reliability for CRC prognosis prediction was assessed with clinical CRC data and compared with that of six other lncRNA were also performed according to the risk score(RS)of the signature.RESULTS An 8-lncRNA signature significantly associated with overall survival(OS)was constructed,and its reliability was validated with clinical CRC data.Most of the areas under the receiver operating characteristic curves(AUCs)values for 1-,3-and 5-year OS for this signature were higher than those for the other six lncRNA signatures.OS,disease-specific survival and the progression-free interval were all significantly poorer in the high-risk group.The RS of the signature showed good concordance with the predicted prognosis,with AUCs for 1-,3-and 5-year OS of 0.79,0.81 and 0.77,respectively.Additionally,the calibration plots for this signature combined with clinical factors showed that this combination could effectively improve the ability to predict OS.The RS was correlated with tumor stage,lymph node metastasis and distant metastasis.Most of the enriched Kyoto Encyclopedia of Genes and Genomes and Gene Ontol

关键词： Long noncoding RNA necroptosis Immunotherapy Prognosis Colorectal cancer

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