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A novel anticancer property of Lycium barbarum polysaccharide in triggering ferroptosis of breast cancer cells

Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2022年第4期23卷 286-299页

作者： Xing DU Jingjing ZHANG Ling LIU Bo XU Hang HAN Wenjie DAI Xiuying PEI Xufeng FU Shaozhang HOU Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education School of Basic Medical SciencesNingxia Medical UniversityYinchuan 750004China Department of Clinical Pathology School of Basic Medical SciencesNingxia Medical UniversityYinchuan 750004China

Breast cancer is one of the most malignant tumors and is associated with high mortality rates among women.Lycium barbarum polysaccharide(LBP)is an extract from the fruits of the traditional Chinese herb,L.barbarum.LBP is a promising anticancer drug,due to its high activity and low toxicity.Although it has anticancer properties,its mechanisms of action have not been fully established.Ferroptosis,which is a novel anticancer strategy,is a cell death mechanism that relies on iron-dependent lipid reactive oxygen species(ROS)accumulation.In this study,human breast cancer cells(Michigan Cancer Foundation-7(MCF-7)and MD Anderson-Metastatic Breast-231(MDA-MB-231))were treated with LBP.LBP inhibited their viability and proliferation in association with high levels of ferroptosis.Therefore,we aimed to ascertain whether LBP reduced cell viability through ferroptosis.We found that the structure and function of mitochondria,lipid peroxidation,and expression of solute carrier family 7 member 11(SLC7 A11,also known as x CT,the light-chain subunit of cystine/glutamate antiporter system X_(c)^(-))and glutathione peroxidase 4(GPX4)were altered by LBP.Moreover,the ferroptosis inhibitor,Ferrostatin-1(Fer-1),rescued LBP-induced ferroptosis-associated events including reduced cell viability and glutathione(GSH)production,accumulation of intracellular free divalent iron ions and malondialdehyde(MDA),and down-regulation of the expression of x CT and GPX4.Erastin(x CT inhibitor)and RSL3(GPX4 inhibitor)inhibited the expression of x CT and GPX4,respectively,which was lower after the co-treatment of LBP with Erastin and RSL3.These results suggest that LBP effectively prevents breast cancer cell proliferation and promotes ferroptosis via the x CT/GPX4 pathway.Therefore,LBP exhibits novel anticancer properties by triggering ferroptosis,and may be a potential therapeutic option for breast cancer.

关键词： Lycium barbarum polysaccharide Ferroptosis Breast cancer cells xct Glutathione peroxidase 4(GPX4)

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Erythropoietin inhibits ferroptosis and ameliorates neurological function after spinal cord injury

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Neural Regeneration Research 2023年第4期18卷 881-888页

作者： Yu Kang Rui Zhu Shuang Li Kun-Peng Qin Hao Tang Wen-Shan Shan Zong-Sheng Yin Department of Orthopedics The First Affiliated Hospital of Anhui Medical UniversityHefeiAnhui ProvinceChina

Ferroptosis is one of the critical pathological events in spinal cord injury.Erythropoietin has been reported to improve the recovery of spinal cord injury.However,whether ferroptosis is involved in the neuroprotective effects of erythropoietin on spinal cord injury has not been examined.In this study,we established rat models of spinal cord injury by modified Allen’s method and intraperitoneally administered 1000 and 5000 IU/kg erythropoietin once a week for 2 successive weeks.Both low and high doses of erythropoietin promoted recovery of hindlimb function,and the high dose of erythropoietin led to better outcome.High dose of erythropoietin exhibited a stronger suppressive effect on ferroptosis relative to the low dose of erythropoietin.The effects of erythropoietin on inhibiting ferroptosis-related protein expression and restoring mitochondrial morphology were similar to those of Fer-1(a ferroptosis suppressor),and the effects of erythropoietin were largely diminished by RSL3(ferroptosis activator).In vitro experiments showed that erythropoietin inhibited RSL3-induced ferroptosis in PC12 cells and increased the expression of xct and Gpx4.This suggests that xct and Gpx4 are involved in the neuroprotective effects of erythropoietin on spinal cord injury.Our findings reveal the underlying anti-ferroptosis role of erythropoietin and provide a potential therapeutic strategy for treating spinal cord injury.

关键词： erythropoietin ferroptosis Gpx4 iron overload lipid peroxidation mechanism neurological function recovery spinal cord injury spinal neuron xct

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Effects of cooling rates on microporosity in DC casting Al-Li alloy

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China Foundry 2022年第2期19卷 177-190页

作者： Yu-xuan Zhang Jun-sheng Wang Dong-xu Chen Bing Wang Chi Zhang Zheng-an Wang School of Materials Science and Engineering Beijing Institute of TechnologyBeijing 100081China Advanced Research Institute of Multidisciplinary Science Beijing Institute of TechnologyBeijing 100081China Chinalco Southwest Aluminium(Group)Co. Ltd.Chongqing 401326China

During the direct chill(DC)casting process,primary cooling from the mold and bottom block,and secondary cooling from the waterjets produce a concave solid shell.The depth of this liquid pocket and mushy zone not only depends on the solidification range of the alloy but also the boundary conditions such as cooling rates.Al-Li alloys solidify in a long solidification range increasing the susceptibility of porosity nucleation in the semi-solid region.In this study,the effects of cooling rate on the porosity formation were quantified for the large ingot casting using X-ray computed tomography(xct).By characterizing pore size distributions at four different cooling conditions,the correlation between the mechanical properties at both room and high temperatures and the microstructure features was identified.The constitutive equations were constructed.It is found that increasing the cooling rate reduces the grain size,increases the number density of micropores,and minimizes the number of large pores,thereby improving the mechanical performance.Therefore,long mushy zones and deep liquid pockets in Al-Li alloys can be effectively controlled by controlling the boundary conditions of the DC casting solidification process,thereby obtaining castings with excellent mechanical properties.

关键词： Al-Li alloys microporosity cooling rate xct constitutive equation

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铁素体-贝氏体双相钢韧性断裂过程中的夹杂物临界尺寸及孔洞生长

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金属学报 2023年第5期59卷 611-622页

作者：赵亚峰刘苏杰陈云马会马广财郭翼中国科学院金属研究所、沈阳材料科学国家研究中心沈阳110016 东北大学材料科学与工程学院沈阳110819 中国科学院金属研究所沈阳110016

利用多模态关联成像方法研究了铁素体-贝氏体双相钢韧性断裂过程中局部微结构对孔洞生长的影响。首先使用X射线CT成像技术,从宏观层面量化分析了变形过程中孔洞的生长,并定位典型孔洞的空间坐标。之后对选定的目标孔洞,采用等离子体聚... 详细信息

利用多模态关联成像方法研究了铁素体-贝氏体双相钢韧性断裂过程中局部微结构对孔洞生长的影响。首先使用X射线CT成像技术,从宏观层面量化分析了变形过程中孔洞的生长,并定位典型孔洞的空间坐标。之后对选定的目标孔洞,采用等离子体聚焦离子束(PFIB)进行连续切片三维电子背散射衍射(3D-EBSD)扫描成像,从介观层面研究孔洞周围微观组织对孔洞形核与生长的影响。结果显示,夹杂物周围和贝氏体中均有孔洞形成。尽管有时促使大尺寸孔洞生长的应变比小尺寸孔洞处的应变更小,但相比于在小尺寸夹杂物或贝氏体中形核的孔洞,大尺寸夹杂物导致的孔洞体积更大。进一步对孔洞周围的位错密度研究显示,上述现象可能是由于不同尺寸的夹杂物周围应变梯度不同造成的。孔洞周围的位错密度与诱发孔洞的夹杂物尺寸成反比,存在明显的尺寸效应,表明影响孔洞生长的夹杂物存在一个临界尺寸。利用解析理论模型推测出夹杂物临界尺寸范围为1.85~2.86μm,小于该临界尺寸的夹杂物诱发的孔洞,由于局部变形梯度效应,位错塞积会阻碍孔洞的生长。孔洞的生长是非均匀的且其形状表现出各向异性,孔洞生长形貌与周围晶粒的可变形性相关,可用晶粒尺寸加权的Schmid因子描述。

关键词：铁素体-贝氏体双相钢孔洞形核与生长 3D-EBSD xct 尺寸效应

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Deferoxamine promotes recovery of traumatic spinal cord injury by inhibiting ferroptosis

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Neural Regeneration Research 2019年第3期14卷 532-541页

作者： Xue Yao Yan Zhang Jian Hao Hui-Quan Duan Chen-Xi Zhao Chao Sun Bo Li Bao-You Fan Xu Wang Wen-Xiang Li Xuan-Hao Fu Yong Hu Chang Liu Xiao-Hong Kong Shi-Qing Feng Department of Orthopedics Tianjin Medical University General Hospital State Key Laboratory of Medicinal Chemical Biology Nankai University International Science and Technology Cooperation Base of Spinal Cord Injury Department of Orthopedics Nankai Hospital Department of Orthopedic and Traumatology The University of Hong Kong Pokfulam Hong Kong Special Administrative Region School of Medicine Nankai University Tianjin Neurological Institute Key Laboratory of Post-Neuroinjury Neuro-repair and Regeneration in Central Nervous System Ministry of Education and Tianjin City

Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows:(1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group.(2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group.(3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury.(4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xct, and glutathione expression was markedly increased in the Deferoxamine group.(5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2(ACSF2) and iron-responsive element-binding protein 2(IREB2) were up-regulated in the Deferoxamine group.(6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury.

关键词： nerve regeneration iron spinal cord injury secondary injury ferroptosis deferoxamine GPX4 xct treatment astrogliosis lipid peroxidation neural regeneration

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人参皂苷Rg1通过激活Nrf2/xct/GPX4通路抑制神经元铁死亡改善缺血性脑卒中损伤

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中国药理学通报 2023年第10期39卷 1905-1913页

作者：胡凯超高岩何佳琦楚世峰张钊陈乃宏中国医学科学院药物研究所神经科学中心天然药物活性物质与功能国家重点实验室北京100050 天津中医药大学中药学院天津301617

目的研究人参皂苷Rg1对缺血性脑卒中后神经元铁死亡的抑制作用及其机制。方法细胞水平建立HT22细胞氧糖剥夺/复氧(oxygen glucose deprivation/reoxygenation,OGD/R)模型,CCK-8法检测Rg1对OGD/R损伤后HT22细胞活力的影响,试剂盒检测细... 详细信息

目的研究人参皂苷Rg1对缺血性脑卒中后神经元铁死亡的抑制作用及其机制。方法细胞水平建立HT22细胞氧糖剥夺/复氧(oxygen glucose deprivation/reoxygenation,OGD/R)模型,CCK-8法检测Rg1对OGD/R损伤后HT22细胞活力的影响,试剂盒检测细胞铁死亡标志物GSH/GSSG、SOD、MDA和Fe 2+含量的影响;Western blot检测细胞GPX4、xct和Nrf2蛋白的变化;ML385干预Nrf2验证其在Rg1调节OGD/R引起的细胞铁死亡中的作用。动物水平建立大鼠短暂性大脑中动脉阻塞(middle cerebral artery occlusion,MCAO)再灌注模型,分为假手术组、模型组、Rg1治疗组(40 mg·kg^(-1))和Fer-1铁死亡抑制剂组(0.2 mg·kg^(-1))。缺血90 min后拔栓并给药,再灌注24 h后进行Zea Longa和Garcia Test评分评估神经受损程度;透射电镜观察皮质神经元线粒体形态变化;Western blot检测GPX4和xct蛋白水平。结果Rg1能明显提高OGD/R后HT22细胞存活率,上调GSH/GSSG比值,恢复SOD活性,降低MDA和Fe 2+含量,并促进GPX4,xct和Nrf2蛋白表达,而ML385干预明显抑制了Rg1对OGD/R后HT22细胞存活率及GPX4、xct蛋白的上调作用。在体动物实验结果表明,Rg1可上调MCAO大鼠皮质组织GPX4和xct的表达,缓解神经元线粒体的形态损伤,改善神经功能。结论人参皂苷Rg1可通过促进Nrf2/xct/GPX4通路抑制缺血性脑卒中神经元铁死亡。

关键词：缺血性脑卒中人参皂苷Rg1 铁死亡 Nrf2 GPX4 xct

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NADPH debt drives redox bankruptcy:SLC7A11/xct-mediated cystine uptake as a double-edged sword in cellular redox regulation

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Genes & Diseases 2021年第6期8卷 731-745页

作者： Xiaoguang Liu Yilei Zhang Li Zhuang Kellen Olszewski Boyi Gan Department of Experimental Radiation Oncology The University of Texas MD Anderson Cancer CenterHoustonTX 77030USA Kadmon Corporation LLCNew YorkNY 10016USA The University of Texas MD Anderson UTHealth Graduate School of Biomedical SciencesHoustonTX 77030USA

Cystine/glutamate antiporter solute carrier family 7 member 11(SLC7A11;also known as xct)plays a key role in antioxidant defense by mediating cystine uptake,promoting glutathione synthesis,and maintaining cell survival under oxidative stress conditions.Recent studies showed that,to prevent toxic buildup of highly insoluble cystine inside cells,cancer cells with high expression of SLC7A11(SLC7A11high)are forced to quickly reduce cystine to more soluble cysteine,which requires substantial NADPH supply from the glucose-pentose phosphate pathway(PPP)route,thereby inducing glucose-and PPP-dependency in SLC7A11high cancer cells.Limiting glucose supply to SLC7A11high cancer cells results in significant NADPH“debt”,redox“bankruptcy”,and subsequent cell death.This review summarizes our current understanding of NADPH-generating and-consuming pathways,discusses the opposing role of SLC7A11 in protecting cells from oxidative stresseinduced cell death such as ferroptosis but promoting glucose starvationeinduced cell death,and proposes the concept that SLC7A11-mediated cystine uptake acts as a double-edged sword in cellular redox regulation.A detailed understanding of SLC7A11 in redox biology may identify metabolic vulnerabilities in SLC7A11high cancer for therapeutic targeting.

关键词： Cysteine Cystine NADPH Pentose phosphate pathway SLC7A11 xct

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Amino acid transporter SLC7A11/ xct at the crossroads of regulating redox homeostasis and nutrient dependency of cancer

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Cancer Communications 2018年第1期38卷 145-157页

作者： Pranavi Koppula Yilei Zhang Li Zhuang Boyi Gan Department of Experimental Radiation Oncology The University of Texas MD Anderson Cancer Center1515 Holcombe BlvdHoustonTX 77030USA The University of Texas Graduate School of Biomedical Sciences 6767 Bertner Ave.HoustonTX 77030USA Department of Molecular and Cellular Oncology The University of Texas MD

Cancer cells often upregulate nutrient transporters to fulfill their increased biosynthetic and bioenergetic needs,and to maintain redox homeostasis.One nutrient transporter frequently overexpressed in human cancers is the cystine/glutamate antiporter solute carrier family 7 member 11(SLC7A11;also known as xct).SLC7A11 promotes cystine uptake and glutathione biosynthesis,resulting in protection from oxidative stress and ferroptotic cell death.Recent studies have unexpectedly revealed that SLC7A11 also plays critical roles in glutamine metabolism and regulates the glucose and glutamine dependency of cancer cells.This review discusses the roles of SLC7A11 in regulating the anti-oxidant response and nutrient dependency of cancer cells,explores our current understanding of SLC7A11 regulation in cancer metabolism,and highlights key open questions for future studies in this emerging research area.A deeper understanding of SLC7A11 in cancer metabolism may identify new therapeutic opportunities to target this important amino acid transporter for cancer treatment.

关键词： SLC7A11 xct System xc− Cystine Glutamate Ferroptosis Oxidative stress Nutrient dependency Cancer metabolism

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Cystine transporter SLC7A11/xct in cancer:ferroptosis,nutrient dependency,and cancer therapy

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Protein & Cell 2021年第8期12卷 599-620页

作者： Pranavi Koppula Li Zhuang Boyi Gan Department of Experimental Radiation Oncology The University of Texas MD Anderson Cancer CenterHoustonTXUSA The University of Texas MD Anderson UTHealth Graduate School of Biomedical Sciences HoustonTXUSA

The cystine/glutamate antiporter SLC7A11(also commonly known as xct)functions to import cystine for glutathione biosynthesis and antioxidant defense and is overexpressed in multiple human cancers.Recent studies revealed that SLC7A11 overexpression promotes tumor growth partly through suppressing ferroptosis,a form of regulated cell death induced by excessive lipid peroxidation.However,cancer cells with high expression of SLC7A11(SLC7A11^(high))also have to endure the significant cost associated with SLC7A11-mediated metabolic reprogramming,leading to glucose-and glutamine-dependency in SLC7A11^(high) cancer cells,which presents potential metabolic vulnerabilities for therapeutic targeting in SLC7A11^(high) cancer.In this review,we summarize diverse regulatory mechanisms of SLC7A11 in cancer,discuss ferroptosis-dependent and-independent functions of SLC7A11 in promoting tumor development,explore the mechanistic basis of SLC7A11-induced nutrient dependency in cancer cells,and conceptualize therapeutic strategies to target SLC7A11 in cancer treatment.This review will provide the foundation for further understanding SLC7A11 in ferroptosis,nutrient dependency,and tumor biology and for developing novel effective cancer therapies.

关键词： SLC7A11 xct cystine cysteine ferroptosis nutrient dependency cancer therapy

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X-ray Microtomography of the Carbonation Front Shape Evolution of Cement Mortar and Modeling of Accelerated Carbonation Reaction

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Journal of Wuhan University of Technology(Materials Science) 2013年第2期28卷 303-308页

作者：韩建德孙伟 PAN Ganghua College of Civil Engineering Nanjing University of Technology School of Materials Science and Engineering Southeast University Jiangsu Key Laboratory of Construction Material

In situ monitoring of the microstructure evolution of cement mortar in accelerated carbonation reaction for different carbonation ages was carried out by X-ray computed tomography （xct）. And the carbonation degrees of different time were measured by the volume fraction of uncarbonated and carbonated parts. Meanwhile, we presented a model for the carbonation of cement mortar by means of X-ray computed tomography （xct）. Based on the principles of chemical engineering processes, the reacted products become a solid inert ash layer. Finally, the model was validated with results of accelerated carbonation of cement mortar. The model is thus able to reasonably predict the carbonation ohenomena for accelerated conditions.

关键词： xct cement mortar carbonation in-situ monitoring gray values model validation

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