Cell Biochemistry and Biophysics最新文献_第5页

Structure-Based Discovery of Phytocompounds from Azadirachta indica as Potential Inhibitors of Thioredoxin Glutathione Reductase in Schistosoma mansoni. 基于结构从 Azadirachta indica 中发现可作为曼氏血吸虫硫氧还蛋白谷胱甘肽还原酶潜在抑制剂的植物化合物

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-07 DOI: 10.1007/s12013-024-01577-2

Olugbenga Samson Onile, Omotara Raji, Victor Omoboyede, Adeyinka Ignatius Fadahunsi, Tolulope Adelonpe Onile, Abdul Onoruoiza Momoh, Samuel Olukunle, Hassan Nour, Samir Chtita

{"title":"Structure-Based Discovery of Phytocompounds from Azadirachta indica as Potential Inhibitors of Thioredoxin Glutathione Reductase in Schistosoma mansoni.","authors":"Olugbenga Samson Onile, Omotara Raji, Victor Omoboyede, Adeyinka Ignatius Fadahunsi, Tolulope Adelonpe Onile, Abdul Onoruoiza Momoh, Samuel Olukunle, Hassan Nour, Samir Chtita","doi":"10.1007/s12013-024-01577-2","DOIUrl":"https://doi.org/10.1007/s12013-024-01577-2","url":null,"abstract":"Schistosomiasis, a parasitic disease caused by Schistosoma species such as S. haematobium, S. mansoni, and S. japonicum, poses a significant global health burden. The thioredoxin glutathione reductase (TGR) enzyme, crucial for maintaining the parasite's redox balance and preventing oxidative stress, has been identified as a promising target for anti-schistosomal drug development. This study aims to identify potential TGR inhibitors from Azadirachta indica phytochemicals using molecular modeling approaches. We screened 60 compounds derived from A. indica bark and leaves through molecular docking to assess their binding affinity, followed by the evaluation of binding-free energies for the most promising candidates. Drug-likeness and pharmacokinetic properties were assessed, and molecular dynamics simulations were conducted to explore the conformational stability of the protein-ligand complexes. Our findings revealed that several A. indica compounds exhibited significantly lower docking scores (up to -9.669 kcal/mol) compared to the standard drug praziquantel (-4.349 kcal/mol). Notably, Isorhamnetin, Isomargolonone, Nimbaflavone, Quercetin, and Nimbionol demonstrated strong interactions with TGR, although Isorhamnetin showed potential mutagenicity. Further binding free energy calculations and molecular dynamics simulations confirmed the stability of Isomargolonone, Nimbionol, and Quercetin as potential TGR inhibitors. In conclusion, these findings suggest that Isomargolonone, Nimbionol, and Quercetin warrant further experimental validation as promising candidates for anti-schistosomal therapy.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

miR-378a-3p Regulates the BMP2-Smad Pathway to Promote Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells. miR-378a-3p 调控 BMP2-Smad 通路，促进滑膜衍生间充质干细胞的软骨分化

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-07 DOI: 10.1007/s12013-024-01561-w

Xiangyi Sun, Ruchao Long, Qiang Chen, Jian Feng, Yang Gao, Guangqi Zhu, Zhihua Yang

{"title":"miR-378a-3p Regulates the BMP2-Smad Pathway to Promote Chondrogenic Differentiation of Synovium-Derived Mesenchymal Stem Cells.","authors":"Xiangyi Sun, Ruchao Long, Qiang Chen, Jian Feng, Yang Gao, Guangqi Zhu, Zhihua Yang","doi":"10.1007/s12013-024-01561-w","DOIUrl":"https://doi.org/10.1007/s12013-024-01561-w","url":null,"abstract":"This study aims to elucidate the role of miR-378a-3p in facilitating the proliferation and differentiation of synovium-derived mesenchymal stem cells (SMSCs) into chondrocytes. The effects of overexpressing miR-378a-3p on SMSCs were investigated through histological analysis, quantitative PCR, and western blotting. Then we identified binding sites of miR-378a-3p with BMP2 through Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses and predictions from the RegRNA 2.0 database. Subsequently, BMP2 was confirmed as the target by which miR-378a-3p promotes the chondrogenic differentiation of SMSCs using a luciferase reporter gene assay and an miR-378a-3p RNA interference plasmid. Finally, by constructing a rat model with articular cartilage damage, we detected the reparative effects of miR-378a-3p overexpression on cartilage damage. Additionally, we verified the mechanism by which miR-378a-3p promotes chondrogenic differentiation in SMSCs. MiR-378a-3p enhances the proliferation and differentiation of SMSCs into chondrocytes by modulating the BMP2-Smad signaling pathway, thereby facilitating repair processes for articular cartilage injuries in rats. Notably, knockdown of BMP2 diminished the reparative efficacy of miR-378a-3p on articular cartilage damage. Upregulation of miR-378a-3p promotes chondrogenic differentiation in SMSCs through activation of the BMP2-Smad pathway, positioning it as a potential therapeutic target for osteoarthritis.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142379815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Understanding the intricate impacts and mechanism of actions of adaptogens on reproductive function. 了解适应原对生殖功能的复杂影响和作用机制。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-06 DOI: 10.1007/s12013-024-01565-6

Precious Adeoye Oyedokun, Victory Jesutoyosi Ashonibare, Fidelis Batale Fabrael, Tunmise Maryanne Akhigbe, Marvelous Dasola Akangbe, Roland Eghoghosoa Akhigbe

{"title":"Understanding the intricate impacts and mechanism of actions of adaptogens on reproductive function.","authors":"Precious Adeoye Oyedokun, Victory Jesutoyosi Ashonibare, Fidelis Batale Fabrael, Tunmise Maryanne Akhigbe, Marvelous Dasola Akangbe, Roland Eghoghosoa Akhigbe","doi":"10.1007/s12013-024-01565-6","DOIUrl":"https://doi.org/10.1007/s12013-024-01565-6","url":null,"abstract":"Adaptogens, comprising plants and mushrooms, modulate the immune system, energy balance, and various physiological processes, including reproduction. Despite their potential benefits, the impact of adaptogens on reproductive function remains understudied. This review examines the effects of common adaptogens on male and female reproductive functions, highlighting their regulation of neuro-endocrine-immune interactions crucial for reproduction. While existing literature reveals varying impacts on reproductive function, most adaptogens exhibit beneficial effects, modulating neuroimmunology and promoting gonadal steroidogenesis, spermatogenesis, and folliculogenesis through direct mechanisms or suppression of oxidative stress and inflammation. Further experimental research is necessary to elucidate the mechanisms of action of adaptogens, which would significantly advance the management of reproductive disorders and other diseases. Validating these findings in clinical trials is also essential.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142378907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Molecular Mechanism of lncRNAs in Regulation of Breast Cancer Metastasis; a Comprehensive Review. lncRNAs调控乳腺癌转移的分子机制；全面综述。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-05 DOI: 10.1007/s12013-024-01535-y

Shokoufeh Ahmadi, Farzaneh Yazdi, Sahar Khastar, Irwanjot Kaur, Mareb Hamed Ahmed, Abhishek Kumar, Gulshan Rathore, Parjinder Kaur, Mohammad Shahsavan, Mahmoud Dehghani-Ghorbi, Reza Akhavan-Sigari

{"title":"Molecular Mechanism of lncRNAs in Regulation of Breast Cancer Metastasis; a Comprehensive Review.","authors":"Shokoufeh Ahmadi, Farzaneh Yazdi, Sahar Khastar, Irwanjot Kaur, Mareb Hamed Ahmed, Abhishek Kumar, Gulshan Rathore, Parjinder Kaur, Mohammad Shahsavan, Mahmoud Dehghani-Ghorbi, Reza Akhavan-Sigari","doi":"10.1007/s12013-024-01535-y","DOIUrl":"https://doi.org/10.1007/s12013-024-01535-y","url":null,"abstract":"Although the number of breast cancer deaths has decreased, and there have been developments in targeted therapies and combination treatments for the management of metastatic illness, metastatic breast cancer is still the second most common cause of cancer-related deaths in U.S. women. Numerous phases and a vast number of proteins and signaling molecules are involved in the invasion-metastasis cascade. The tumor cells penetrate and enter the blood or lymphatic vessels, and travel to distant organs via the lymphatic or blood vessels. Tumor cells enter cell cycle arrest, adhere to capillary beds in the target organ, and then disseminate throughout the organ's parenchyma, proliferating and enhancing angiogenesis. Each of these processes is regulated by changes in the expression of different genes, in which lncRNAs play a role in this regulation. Transcripts that are longer than 200 nucleotides and do not translate into proteins are called RNAs. LncRNA molecules, whose function depends on their unique molecular structure, play significant roles in controlling the expression of genes at various epigenetic levels, transcription, and so on. LncRNAs have essential functions in regulating the expression of genes linked to cell development in healthy and pathological processes, specialization, programmed cell death, cell division, invasion, DNA damage, and spread to other parts of the body. A number of cancer types have been shown to exhibit aberrant expression of lncRNAs. In this review, we describe the general characteristics, potential molecular mechanisms and targeted therapy of lncRNAs and discuss the emerging functions of lncRNAs in breast cancer.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142374943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Olfactory Receptors and Tumorigenesis: Implications for Diagnosis and Targeted Therapy. 嗅觉受体与肿瘤发生：诊断和靶向治疗的意义》。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-04 DOI: 10.1007/s12013-024-01556-7

Yi Tang, Ye Tian, Chun-Xia Zhang, Guo-Tai Wang

引用次数: 0

COL6A1 Inhibits the Malignant Development of Bladder Cancer by Regulating FBN1. COL6A1 通过调节 FBN1 抑制膀胱癌的恶性发展

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-04 DOI: 10.1007/s12013-024-01573-6

Tineng Yang, Xiaoyang Peng, Xi Huang, Peng Cao, Hualei Chen

{"title":"COL6A1 Inhibits the Malignant Development of Bladder Cancer by Regulating FBN1.","authors":"Tineng Yang, Xiaoyang Peng, Xi Huang, Peng Cao, Hualei Chen","doi":"10.1007/s12013-024-01573-6","DOIUrl":"https://doi.org/10.1007/s12013-024-01573-6","url":null,"abstract":"Bladder cancer (BLCA) is a prevalent malignancy worldwide with a high recurrence rate. Collagen Type VI Alpha 1 (COL6A1) plays a key role in several cancer types. In this study, we aimed to explore the role of COL6A1 in BLCA. COL6A1 expression in BLCA was determined using The Cancer Genome Atlas database and real-time quantitative polymerase chain reaction (RT-qPCR). Counting Kit-8, wound-healing, and transwell assays were used to assess the effect of COL6A1 on T24 and 5637 cells. Apoptosis in BLCA cell lines was explored using western blotting and flow cytometry. Co-immunoprecipitation was performed to determine interactions between proteins. The role of COL6A1 in tumor growth in nude mice was evaluated by hematoxylin-eosin, immunohistochemical, and terminal deoxynucleotidyl transferase dUTP Nick-End Labeling. In BLCA, COL6A1 expression was downregulated. Moreover, the COL6A1 overexpression suppressed the viability, migration, and invasion, while promoting apoptosis of BLCA cell lines, with increased Caspase-3, Bax, and p53, and decreased Bcl-2. Conversely, silencing of COL6A1 promoted proliferation, migration, and invasion, while inhibiting apoptosis in BLCA cell lines. In vivo, COL6A1 inhibits tumor growth and progression. Fibrillin-1 (FBN1) was positively correlated with COL6A1 expression. COL6A1 could bind to FBN1 in BLCA cell lines. The expression of FBN1 in BLCA cell lines decreased after COL6A1 silencing, whereas COL6A1 overexpression upregulated FBN1 expression. COL6A1 was downregulated and exerted an inhibitory effect on the development of BLCA, and its expression was positively correlated with the expression of FBN1.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Blocking GATA6 Alleviates Pyroptosis and Inhibits Abdominal Wall Endometriosis Lesion Growth Through Inactivating the PI3K/AKT Pathway. 阻断 GATA6 可通过抑制 PI3K/AKT 通路缓解脓毒症并抑制腹壁子宫内膜异位症病灶生长

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-04 DOI: 10.1007/s12013-024-01583-4

Xiufang Du, Hongjie Yang, Xiaobei Kang, Changna Fu, Tao Yang

{"title":"Blocking GATA6 Alleviates Pyroptosis and Inhibits Abdominal Wall Endometriosis Lesion Growth Through Inactivating the PI3K/AKT Pathway.","authors":"Xiufang Du, Hongjie Yang, Xiaobei Kang, Changna Fu, Tao Yang","doi":"10.1007/s12013-024-01583-4","DOIUrl":"https://doi.org/10.1007/s12013-024-01583-4","url":null,"abstract":"Endometriosis is a benign gynecological disorder characterized by the abnormal presence of endometrium-like cells, referred to as ectopic tissue, located outside the uterine cavity. Beyond the abnormal proliferation of endometrium-like tissues within and beyond the pelvic cavity, compelling scientific evidence underscores the crucial involvement of the NOD-like receptor NLRP3 inflammasome and pyroptosis in the pathogenesis of EMS. Our investigation has revealed a striking upregulation of the endogenous protein GATA-binding protein 6 (GATA6) in abdominal wall EMS. Notably, the knockdown of GATA6 significantly impaired the viability and migratory potential of primary ectopic endometrial stromal cells (EESCs) while also inhibiting crucial markers of pyroptosis, such as NLRP3, the gasdermin D N-terminal fragment (GSDMD-N), and reactive oxygen species (ROS) levels within these cells. Delving deeper into the underlying mechanisms, we discovered that suppressing GATA6 mitigated the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in EESCs. The administration of 740 Y-P, an agonist of the PI3K/AKT pathway, mitigated the inhibitive actions of GATA6 knockdown on EESCs' growth, migration, and pyroptosis, highlighting the intricate crosstalk between GATA6 and this intricate signaling cascade. In vivo experiments corroborated these findings, demonstrating that reduced GATA6 expression effectively restrained the growth of endometrial lesions and concurrently suppressed pyroptosis, accompanied by a dampening of PI3K/AKT signaling within these lesions. In summary, our study underscores the pivotal role of GATA6 in modulating the growth and pyroptosis of abdominal wall EMS through its regulation of the PI3K/AKT signaling pathway. Silencing GATA6 emerges as a promising approach to alleviate pyroptosis and potentially offers a novel therapeutic angle for managing abdominal wall EMS.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

The Therapeutic Potential of Exosome Therapy in Sepsis Management: Addressing Complications and Improving Outcomes". 外泌体疗法在败血症治疗中的治疗潜力：解决并发症和改善疗效"。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-03 DOI: 10.1007/s12013-024-01564-7

Payam Ali-Khiavi, Mahya Mohammadi, Sajjad Masoumi, Hossein Saffarfar, Reza Kheradmand, Ahmad Mobed, Faezeh Hatefnia

{"title":"The Therapeutic Potential of Exosome Therapy in Sepsis Management: Addressing Complications and Improving Outcomes\".","authors":"Payam Ali-Khiavi, Mahya Mohammadi, Sajjad Masoumi, Hossein Saffarfar, Reza Kheradmand, Ahmad Mobed, Faezeh Hatefnia","doi":"10.1007/s12013-024-01564-7","DOIUrl":"https://doi.org/10.1007/s12013-024-01564-7","url":null,"abstract":"Infection occurs when pathogens penetrate tissues, reproduce, and trigger a host response to both the infectious agents and their toxins. A diverse array of pathogens, including viruses and bacteria, can cause infections. The host's immune system employs several mechanisms to combat these infections, typically involving an innate inflammatory response. Inflammation is a complex biological reaction that can affect various parts of the body and is a key component of the response to harmful stimuli. Sepsis arises when the body's response to infection leads to widespread damage to tissues and organs, potentially resulting in severe outcomes or death. The initial phase of sepsis involves immune system suppression. Early identification and targeted management are crucial for improving sepsis outcomes. Common treatment approaches include antibiotics, intravenous fluids, blood cultures, and monitoring urine output. This study explores the potential of exosome therapy in enhancing the management and alleviation of sepsis symptoms.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142370581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

RBM15B Promotes Prostate Cancer Cell Proliferation via PCNA m6A Modification. RBM15B 通过 PCNA m6A 修饰促进前列腺癌细胞增殖

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-03 DOI: 10.1007/s12013-024-01558-5

Huan Cheng, Zeyu Chen, Yong Wang, Chengjian Ji, Junqi Wang, Ninghong Song

{"title":"RBM15B Promotes Prostate Cancer Cell Proliferation via PCNA m6A Modification.","authors":"Huan Cheng, Zeyu Chen, Yong Wang, Chengjian Ji, Junqi Wang, Ninghong Song","doi":"10.1007/s12013-024-01558-5","DOIUrl":"https://doi.org/10.1007/s12013-024-01558-5","url":null,"abstract":"Prostate cancer (PC) is the most frequently occurring cancer in men, characterized by the abnormal proliferation of cells within the prostate gland. This study explores the role of RNA binding motif protein 15B (RBM15B) in PC. RBM15B expression levels in PC patients were predicted using the Starbase database. The expression of RBM15B and proliferating cell nuclear antigen (PCNA) expression in PC cells was detected. Following RBM15B knockdown, cell proliferation assays were conducted. N6-methyladenosine (m6A) levels in PC cells were quantified, and RNA immunoprecipitation was performed to analyze the binding of m6A and YTH N-methyladenosine RNA binding protein 1 (YTHDF1) on PCNA mRNA. The stability of PCNA mRNA was assessed after treatment with actinomycin D. An in vivo nude mouse xenograft model was created to validate the role of RBM15B. The findings revealed the upregulation of RBM15B in PC. RBM15B knockdown resulted in decreased proliferation, colony formation, and EdU-positive cells. Mechanical analysis showed that RBM15B facilitated m6A modification of PCNA mRNA, leading to increasing m6A methylation. YTHDF1 bound to these m6A sites on PCNA mRNA, thus stabilizing it. Furthermore, PCNA overexpression mitigated the effects of RBM15B knockdown on PC cell proliferation. In conclusion, RBM15B promotes PC cell proliferation by enhancing the stability of PCNA mRNA through YTHDF1-mediated m6A modification.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142363902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Amentoflavone Induces Ferroptosis to Alleviate Proliferation, Migration, Invasion and Inflammation in Rheumatoid Arthritis Fibroblast-like Synoviocytes by Inhibiting PIN1. 门冬酰胺黄酮通过抑制 PIN1 诱导铁变态反应，从而缓解类风湿性关节炎成纤维细胞样滑膜细胞的增殖、迁移、侵袭和炎症。

IF 1.8 4区生物学

Cell Biochemistry and Biophysics Pub Date : 2024-10-01 DOI: 10.1007/s12013-024-01563-8

Yan Ma, Hongjun Lin, Yunman Li, Zhuoling An

{"title":"Amentoflavone Induces Ferroptosis to Alleviate Proliferation, Migration, Invasion and Inflammation in Rheumatoid Arthritis Fibroblast-like Synoviocytes by Inhibiting PIN1.","authors":"Yan Ma, Hongjun Lin, Yunman Li, Zhuoling An","doi":"10.1007/s12013-024-01563-8","DOIUrl":"https://doi.org/10.1007/s12013-024-01563-8","url":null,"abstract":"Rheumatoid arthritis (RA) is a systemic autoimmune disease that is prevalent worldwide and seriously threatens human health. RA-fibroblast-like synoviocytes (FLS) play important roles in almost all aspects of RA progression. This study aimed to study the effect of Amentoflavone (AMF), a polyphenol compound derived from extracts of Selaginella tamariscina, on the abnormal biological behaviors of RA-FLS. The immortalized human RA-FLS cell line (MH7A) was treated with AMF or transfected with small interfering RNAs (siRNAs) targeting peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (PIN1). Then, cell viability was detected by CCK-8 assay. EDU staining, wound healing and transwell assays were employed to measure the capacities of MH7A cell proliferation, migration and invasion. The levels of inflammatory factors were assessed using ELISA kits. Additionally, ferroptosis was analyzed by detecting Fe2+ content, lipid reactive oxygen species (ROS) level and expression of ferroptosis-related proteins. Pull-down assay was employed to verify the targeted binding of AMF to PIN1. Further, PIN1 overexpression or ferroptosis inhibitor Ferrostatin-1 (Fer-1) addition was conducted to elucidate the regulatory mechanism of AMF on PIN1 and ferroptosis. Results revealed that AMF intervention or PIN1 knockdown inhibited the proliferation, migration, invasion and inflammation in MH7A cells. AMF facilitated lipid peroxidation and ferroptosis in MH7A cells. Moreover, AMF targeted inhibition of PIN1 expression, and PIN1 overexpression restored the promoting effect of AMF on lipid peroxidation and ferroptosis in MH7A cells. Besides, Fer-1 reversed the impacts of AMF on the abnormal biological behaviors of MH7A cells. In summary, AMF induced ferroptosis to inhibit the proliferation, migration, invasion and inflammation in RA-FLS by inhibiting PIN1, providing a promising candidate for RA treatment.","PeriodicalId":510,"journal":{"name":"Cell Biochemistry and Biophysics","volume":null,"pages":null},"PeriodicalIF":1.8,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360885","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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