Experimental cell research最新文献_第9页

Mechanical stretch promotes the migration of mesenchymal stem cells via Piezo1/F-actin/YAP axis 机械拉伸通过Piezo1/F-actin/YAP轴促进间充质干细胞的迁移

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-21 DOI: 10.1016/j.yexcr.2025.114461

Ning Ma , Lei Huang , Qianxu Zhou , Xiaomei Zhang , Qing Luo , Guanbin Song

{"title":"Mechanical stretch promotes the migration of mesenchymal stem cells via Piezo1/F-actin/YAP axis","authors":"Ning Ma , Lei Huang , Qianxu Zhou , Xiaomei Zhang , Qing Luo , Guanbin Song","doi":"10.1016/j.yexcr.2025.114461","DOIUrl":"10.1016/j.yexcr.2025.114461","url":null,"abstract":"<div><div>Mesenchymal stem cells (MSCs) have self-renewal ability and the potential for multi-directional differentiation, and their clinical application has promising prospects, but improving the migration ability of MSCs <em>in vivo</em> is one of the challenges. We previously determined mechanical stretch at 1 Hz with 10 % strain for 8 h can significantly promote MSC migration, however, the molecular mechanism remains poorly understood. Here, we reported that the expression and activity of yes-associated protein (YAP) are upregulated after mechanical stretch. As a classical inhibitor of the YAP-TEAD activity and YAP protein, the treatment of verteporfin (VP) suppressed mechanical stretch-promoted MSC migration. We also observed F-actin polymerization after mechanical stretch. Next, we used Latrunculin A (Lat A), the most widely used reagent to depolymerize actin filaments, to treat MSCs and we found that Lat A treatment inhibits MSC migration by suppressing YAP expression and activity. In addition, the protein expression of Piezo1 was also upregulated after mechanical stretch. Knockdown of Piezo1 suppressed mechanical stretch-promoted MSC migration by restraining F-actin polymerization. Together, these findings demonstrate the role of Piezo1/F-actin/YAP signaling pathway in MSC migration under mechanical stretch, providing new experimental evidence for an in-depth understanding the mechanobiological mechanism of MSC migration.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114461"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mapping the initial effects of carcinogen-induced oncogenic transformation in the mouse bladder 绘制小鼠膀胱中致癌物质诱导的致癌转化的初始效应图

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-21 DOI: 10.1016/j.yexcr.2025.114452

Md. Kaykobad Hossain , Lucas Unger , Ulrik Larsen , Altanchimeg Altankhuyag , Thomas Aga Legøy , Joao A. Paulo , Heidrun Vethe , Luiza Ghila

{"title":"Mapping the initial effects of carcinogen-induced oncogenic transformation in the mouse bladder","authors":"Md. Kaykobad Hossain , Lucas Unger , Ulrik Larsen , Altanchimeg Altankhuyag , Thomas Aga Legøy , Joao A. Paulo , Heidrun Vethe , Luiza Ghila","doi":"10.1016/j.yexcr.2025.114452","DOIUrl":"10.1016/j.yexcr.2025.114452","url":null,"abstract":"<div><div>Characterizing the initial stages of oncogenic transformation allows the identification of tumor-promoting processes before the inherent clonal selection of the aggressive clones. Here, we used global proteomics, genetic cell tracing, and immunofluorescence to dynamically map the very early stages of cancer initiation in a mouse model of bladder cancer. We observed a very rapid and incremental proteome dysregulation, with changes in the energy metabolism, proliferation and immune signatures dominating the landscape. The changes in the lipid metabolism were immediate and defined by an increase fatty acid metabolism and lipid transport, followed by the activation of the immune landscape. Alongside the changes in the immune signature and lipid metabolism, we also mapped a clear increase in the cell cycle-related pathways and proliferation. Proliferation was mainly restricted to the basal epithelial layer rapidly leading to urothelium thickening, despite the progressive loss of the superficial layer. Moreover, we observed a tilt in the energy balance towards increased glucose metabolism, probably characterizing cells of the tumor microenvironment. All of the observed proteome signature changes were persistent, being retained and sometimes intensified or diversified along the timeline. The signatures observed in this pilot suggest these processes as potentially targetable drivers of the future neoplastic transformations in the bladder.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114452"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143474559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Activated NETosis of bone marrow neutrophils up-regulates macrophage osteoclastogenesis via cGAS-STING/AKT2 pathway to promote osteoporosis 活化的骨髓中性粒细胞NETosis通过cGAS-STING/AKT2途径上调巨噬细胞破骨生成，促进骨质疏松。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-21 DOI: 10.1016/j.yexcr.2025.114477

Yutong Guo , Hanzhang Zhou , Yixiang Wang , Yan Gu

引用次数: 0

Epic, classic, and remarkable: 75 years of Experimental Cell Research 史诗，经典，非凡：75年的实验细胞研究。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-21 DOI: 10.1016/j.yexcr.2025.114447

Ji-Long Liu (Editor-in-Chief)

引用次数: 0

Human umbilical cord mesenchymal stem cell-derived exosome ameliorate doxorubicin-induced senescence 人脐带间充质干细胞衍生的外泌体改善阿霉素诱导的衰老。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-21 DOI: 10.1016/j.yexcr.2025.114450

Zhen Yang , Feng Yan , Jiangwei Yuan , Manjun Yang , Jinyu Wang , Changqiao You , Kaiqun Ren

{"title":"Human umbilical cord mesenchymal stem cell-derived exosome ameliorate doxorubicin-induced senescence","authors":"Zhen Yang , Feng Yan , Jiangwei Yuan , Manjun Yang , Jinyu Wang , Changqiao You , Kaiqun Ren","doi":"10.1016/j.yexcr.2025.114450","DOIUrl":"10.1016/j.yexcr.2025.114450","url":null,"abstract":"<div><h3>Background</h3><div>Cellular senescence refers to a condition where cells permanently cease division while maintaining metabolic activity. Doxorubicin (Dox) is known as an agent of induction of cellular senescence. This study aimed to explore the potential role of human umbilical cord mesenchymal stem cell-derived exosomes (hucMSC-Exo) in mitigating Dox induced senescent.</div></div><div><h3>Method</h3><div>NIH3T3 cells were treated by various concentrations of Dox with or without hucMSC-Exo, cell morphology, viability, migration, senescence-associated SA-β-Gal staining were monitored. Cellular senescence was induced in C57BL/6J mice via administration of 5 mg/kg Doxorubicin, followed by treatment with hucMSC-Exo or metformin. Assessments included body weight, liver and kidney weight, colon length, SA-β-Gal staining of kidney and skin, molecular biomarkers of aging such as p16<sup>INK4A</sup>, p53, and p21<sup>Waf1/Clip1</sup> to evaluate senescence status.</div></div><div><h3>Result</h3><div>We found that after the treatment of exosomes or metformin improved several aging-related phenotypes in both mouse and cellular models, including increases in body weight, liver and kidney weights, and the reduction of SA-β-Gal positive cells in kidney and skin tissues as well as cell models. At the molecular level, hucMSC-Exo resulted in the downregulation of inflammatory factors and senescence markers in liver and kidney tissues as well as cell models.</div></div><div><h3>Conclusion</h3><div>Our study demonstrates hucMSC-Exo may ameliorate Dox induced senescence either in NIH3T3 cells or in mice.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 2","pages":"Article 114450"},"PeriodicalIF":3.3,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

microRNA-30c attenuates contrast-induced acute kidney injury by reducing renal tubular epithelial cell apoptosis via targeting SOCS1 microRNA-30c通过靶向SOCS1减少肾小管上皮细胞凋亡，减轻造影剂诱导的急性肾损伤。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-20 DOI: 10.1016/j.yexcr.2025.114456

Long Peng , Yanting Luo , Fang Tan , Qian Chen , Jiafu Wang , Xiaolan Ouyang , Bingyuan Wu , Xixiang Tang , Suhua Li

{"title":"microRNA-30c attenuates contrast-induced acute kidney injury by reducing renal tubular epithelial cell apoptosis via targeting SOCS1","authors":"Long Peng , Yanting Luo , Fang Tan , Qian Chen , Jiafu Wang , Xiaolan Ouyang , Bingyuan Wu , Xixiang Tang , Suhua Li","doi":"10.1016/j.yexcr.2025.114456","DOIUrl":"10.1016/j.yexcr.2025.114456","url":null,"abstract":"<div><div>Contrast-induced acute kidney injury (CIAKI) is a common complication after contrast media administration. Growing evidences implicate microRNA (miR)-30c has a key role in renal diseases. This study aimed to investigate the role and mechanism of miR-30c in CIAKI. CIAKI rat models were established using tail vein injection of omnipaque. MiR-30c was significantly downregulated in CIAKI models both in vivo and in vitro, concomitant with increased cell apoptosis and deteriorated renal injury. Meanwhile, the cell apoptosis, renal dysfunction and renal injury under contrast exposure were alleviated after overexpression of miR-30c. Mechanistically, we demonstrated that miR-30c directly targeted SOCS1, whose downregulation reduced contrast-induced HK-2 cell apoptosis. Furthermore, the upregulation of SOCS1 abolish the protective effect of the overexpression of miR-30c on contrast-induced cell apoptosis. In summary, overexpression of miR-30c inhibited renal tubular epithelial cell apoptosis and mitigated CIAKI via inhibiting the gene of SOCS1.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114456"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

H50Q mutation in alpha-Synuclein impairs the insulin signaling pathway and induces neuroinflammation in the Drosophila model α-Syn突变破坏胰岛素信号通路并诱导α-Syn帕金森病果蝇模型的神经炎症

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-20 DOI: 10.1016/j.yexcr.2025.114460

Pooja Rai , Rakesh Kumar

{"title":"H50Q mutation in alpha-Synuclein impairs the insulin signaling pathway and induces neuroinflammation in the Drosophila model","authors":"Pooja Rai , Rakesh Kumar","doi":"10.1016/j.yexcr.2025.114460","DOIUrl":"10.1016/j.yexcr.2025.114460","url":null,"abstract":"<div><div>H50Q mutations in the SNCA gene, also known as also known as the <em>alpha-Synuclein</em> (α-<em>Syn</em>), have been causally linked to familial Parkinson's disease (PD). PD is primarily characterized by the progressive loss of dopaminergic neurons in the substantia nigra region of the brain.α-Syn- plays a pivotal role in the formation of Lewy bodies (LB), a prominent pathological marker in PD. Growing evidence has highlighted the involvement of the insulin signaling pathway dysfunction in various neurodegenerative models. This study aimed to explore how the H50Q mutation in α-<em>Syn</em> influences the insulin signaling pathway and the overall lifespan of fruit flies afflicted with PD. It has been established that a mutation in α-<em>Syn</em> affects mitochondrial function and increases oxidative stress, ultimately contributing to the death of dopaminergic neurons. The impairment of mitochondrial function disrupts metabolism and exerts an adverse effect on the insulin signaling pathway. Furthermore, the unfolded protein response of the endoplasmic reticulum (ER) are investigated and observed a decrease in the expression of PERK (Protein kinase R-like ER kinase) during ER stress. These findings confirm the intricate interplay between the insulin signaling pathway and the activation of the PERK-ER stress pathway. However, the degeneration of neurons triggers a neuroinflammatory response, which are found to be mitigated by the improvement of insulin signaling and the PERK-ER stress-related pathway. The results of this studyshed light on the novel regulatory role of PERK within the insulin signaling pathway and suggest its potential as a therapeutic candidate for modulating neuroinflammation in the context of α-Syn -associated PD pathology.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114460"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PD98059 inhibit the proliferation and differentiation of osteoblasts in the formation of tympanosclerosis via ERK1/2-MAPK signaling pathway PD98059通过ERK1/2-MAPK信号通路抑制成骨细胞增殖和分化形成鼓膜硬化。

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-20 DOI: 10.1016/j.yexcr.2025.114437

Yu Huang, Wenxia Huang, Gengtian Liang, Dou Liu, Chenhui He, Longkai Xiao, Xianting Gao

{"title":"PD98059 inhibit the proliferation and differentiation of osteoblasts in the formation of tympanosclerosis via ERK1/2-MAPK signaling pathway","authors":"Yu Huang, Wenxia Huang, Gengtian Liang, Dou Liu, Chenhui He, Longkai Xiao, Xianting Gao","doi":"10.1016/j.yexcr.2025.114437","DOIUrl":"10.1016/j.yexcr.2025.114437","url":null,"abstract":"<div><div>Tympanosclerosis (TS) has become a common pathological condition of the middle ear, but the underlying mechanism of it is still ambiguous. It was found that osteoprotegerin/receptor activator of nuclear factor kappa B ligand (OPG/RANKL) axis played an important role in the development of TS and was regulated by the extracellular signal regulated kinase 1/2-mitogen activated protein kinase (ERK1/2-MAPK) pathway. However, whether ERK1/2-MAPK pathway mediates the occurrence of TS by regulating OPG/RANKL axis has not been reported. In this study, MAPK and calcium pathway were found significantly activated in TS model. In vivo, the expression of p-ERK1/2 in TS model was significantly increased. In vitro, osteoblasts were isolated from auditory vesicles of neonatal rats for the first time, and then cultured with ERK1/2-MAPK pathway inhibitor PD98059. As results, PD98059 showed inhibitory effects on the phosphorylation of ERK1/2 and proliferation of osteoblasts. Besides, different concentrations of PD98059 showed different inhibitory effects on mRNA expression of osteocalcin (Ocn), bone sialoprotein (Bsp), runt-related transcription factor 2 (Runx2), bone morphogenetic protein 2 (Bmp2) and OPG. Therefore, it was speculated that the ERK1/2-MAPK pathway may affect the formation of TS by regulating the proliferation and differentiation of osteoblasts, which may be helpful for the study of drug target for tympanosclerosis.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"447 1","pages":"Article 114437"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Perspectives of exosomal ncRNAs in the treatment of bone metabolic diseases: Focusing on osteoporosis, osteoarthritis, and rheumatoid arthritis 外泌体ncRNAs在骨代谢性疾病治疗中的应用前景：以骨质疏松症、骨关节炎和类风湿关节炎为重点

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-20 DOI: 10.1016/j.yexcr.2025.114457

Daodi Qiu , Binghan Yan , Haipeng Xue , Zhanwang Xu , Guoqing Tan , Yajuan Liu

{"title":"Perspectives of exosomal ncRNAs in the treatment of bone metabolic diseases: Focusing on osteoporosis, osteoarthritis, and rheumatoid arthritis","authors":"Daodi Qiu , Binghan Yan , Haipeng Xue , Zhanwang Xu , Guoqing Tan , Yajuan Liu","doi":"10.1016/j.yexcr.2025.114457","DOIUrl":"10.1016/j.yexcr.2025.114457","url":null,"abstract":"<div><div>Bone metabolic disorders, constituting a group of prevalent and grave conditions, currently have a scarcity of therapeutic alternatives. Over the recent past, exosomes have been at the forefront of research interest, owing to their nanoparticulate nature and potential for therapeutic intervention. ncRNAs are a class of heterogeneous transcripts that they lack protein-encoding capacity, yet they can modulate the expression of other genes through multiple mechanisms. Mounting evidence underscores the intricate role of exosomes as ncRNAs couriers implicated in the pathogenesis of bone metabolic disorders. In this review, we endeavor to elucidate recent insights into the roles of three ncRNAs – miRNAs, lncRNAs, and circRNAs – in bone metabolic ailments such as osteoporosis, osteoarthritis, and rheumatoid arthritis. Additionally, we examine the viability of exosomal ncRNAs as innovative, cell-free modalities in the diagnosis and therapeutic management of bone metabolic disorders. We aim to uncover the critical function of exosomal ncRNAs within the context of bone metabolic diseases.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 2","pages":"Article 114457"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Maternal protein restriction impairs intestinal morphophysiology and antioxidant system in young male offspring rats 母体蛋白质限制会损害幼年雄性后代大鼠的肠道形态生理学和抗氧化系统

IF 3.3 3区生物学

Experimental cell research Pub Date : 2025-02-20 DOI: 10.1016/j.yexcr.2025.114464

Isabela Baptista Leal dos Santos , Matheus Naia Fioretto , Miguel Silingardi Jorge , Luísa Annibal Barata , Isabelle Tenori Ribeiro , André Matheus Leandro Franzolin , Erick Guilherme Stoppa , Renato Mattos , Luiz Marcos Frediane Portela , Maycon Tavares Emílio Silva , Sérgio Alexandre Alcântara dos Santos , José Ricardo de Arruda Miranda , Clélia Akiko Hiruma Lima , Luis Antonio Justulin

{"title":"Maternal protein restriction impairs intestinal morphophysiology and antioxidant system in young male offspring rats","authors":"Isabela Baptista Leal dos Santos , Matheus Naia Fioretto , Miguel Silingardi Jorge , Luísa Annibal Barata , Isabelle Tenori Ribeiro , André Matheus Leandro Franzolin , Erick Guilherme Stoppa , Renato Mattos , Luiz Marcos Frediane Portela , Maycon Tavares Emílio Silva , Sérgio Alexandre Alcântara dos Santos , José Ricardo de Arruda Miranda , Clélia Akiko Hiruma Lima , Luis Antonio Justulin","doi":"10.1016/j.yexcr.2025.114464","DOIUrl":"10.1016/j.yexcr.2025.114464","url":null,"abstract":"<div><div>The developmental origins of health and disease (DOHaD) concept suggests that adverse conditions during gestation can influence the development and function of multiple organs, including the gastrointestinal tract. Maternal protein restriction (MPR) exposure has been associated with negative effects on reproduction, the endocrine system, and liver metabolic health. However, limited research has explored the impact of MPR on the offspring's intestinal morphophysiology. This study investigated the effects of gestational and lactational MPR on the duodenum and colon of young male offspring rats at postnatal (PND)21. We hypothesize that MPR affects intestinal morphophysiology and development early in life. Our findings revealed tachygastria in offspring exposed to MPR. The ultrastructural analysis uncovered a reduction in goblet cell numbers and changes in collagen deposition in the duodenum and colon. We also identified imbalances in inflammatory markers (IL-6 and TGF-β1) and antioxidant enzymes (CAT and SOD). These results demonstrate that MPR significantly affects gastrointestinal morphophysiology early in life by disrupting gastric motility and altering duodenal and colonic histoarchitecture, antioxidant defense, and inflammatory pathways. Such alterations may predispose the descendants to long-term gastrointestinal disorders, underscoring the importance of further research on the developmental origins of intestinal health and disease.</div></div>","PeriodicalId":12227,"journal":{"name":"Experimental cell research","volume":"446 1","pages":"Article 114464"},"PeriodicalIF":3.3,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143471263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0