We developed novel inorganic nanomaterials to combat drug-resistant bacterial infections in keratitis. These infections cause rapid severe corneal ulcers. Traditional antibiotics face challenges due to bacterial resistance. We investigated new therapies by designing nanomaterials. In an animal model of diabetic keratitis, we studied the materials’ antibacterial properties and mechanisms. In vitro, nanomaterials displayed strong antibacterial effects, confirmed by quantitative analysis. In vivo, using thermal imaging, wound closure monitoring, clinical scores, and histopathology, we demonstrated nanomaterials’ efficacy against infections. Toxicity evaluations, including weight monitoring, hemolysis, biochemical, hematological analyses, and organ histology, revealed no adverse effects on the body or organs. Confocal microscopy showed effective bacterial eradication using nanomaterials combined with near-infrared laser treatment. Minimal impact on red blood cells was observed at therapeutic concentrations. Nanomaterials, particularly gold-silver-cuprous oxide composite nanoshells, demonstrated potent resistance against drug-resistant infections. Photothermal treatment using nanomaterials and near-infrared laser showed promise without harming normal tissues, blood, or organs. Our findings offer a potential clinical solution for keratitis treatment.
{"title":"Antibacterial Effect of Nanostructured Cuprous Gold and Silver Oxide Composite Nanoshell on Keratitis","authors":"Chen Wang, Yang Liu, Mingchang Zhang","doi":"10.1166/jbn.2024.3764","DOIUrl":"https://doi.org/10.1166/jbn.2024.3764","url":null,"abstract":"We developed novel inorganic nanomaterials to combat drug-resistant bacterial infections in keratitis. These infections cause rapid severe corneal ulcers. Traditional antibiotics face challenges due to bacterial resistance. We investigated new therapies by designing nanomaterials. In\u0000 an animal model of diabetic keratitis, we studied the materials’ antibacterial properties and mechanisms. In vitro, nanomaterials displayed strong antibacterial effects, confirmed by quantitative analysis. In vivo, using thermal imaging, wound closure monitoring, clinical\u0000 scores, and histopathology, we demonstrated nanomaterials’ efficacy against infections. Toxicity evaluations, including weight monitoring, hemolysis, biochemical, hematological analyses, and organ histology, revealed no adverse effects on the body or organs. Confocal microscopy showed\u0000 effective bacterial eradication using nanomaterials combined with near-infrared laser treatment. Minimal impact on red blood cells was observed at therapeutic concentrations. Nanomaterials, particularly gold-silver-cuprous oxide composite nanoshells, demonstrated potent resistance against\u0000 drug-resistant infections. Photothermal treatment using nanomaterials and near-infrared laser showed promise without harming normal tissues, blood, or organs. Our findings offer a potential clinical solution for keratitis treatment.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139814251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kangqi Zhao, Ming Hao, Qian Xu, Hong-Xue Li, Cheng-Ye Xu, Ziyu Meng, H. Kuang
With the development of high-throughput sequencing technology, humans have been able to conduct large-scale analysis of DNA sequence, chromatin structure, RNA transcripts, proteins, metabolites and other genomes and their products. Traditional high-throughput transcriptome sequencing techniques based on tissue samples (RNA Seq) are used to centrally sequence thousands of cells, each of which varies in size, protein levels, and mRNA expression transcription. Measuring the average of multiple cells grouped together can mask significant differences in gene expression between cells. Single-cell RNA sequencing is a technique for high-throughput sequencing of the genome, transcriptome, and epigenome at the single-cell level. Based on the single cell RNA transcription map, the intraocular cells can be distinguished from other subtypes, and the different subtypes are found to have significant differences in morphology, physiology and specific expression genes. In recent years, the application of single-cell RNA sequencing technology in the field of ophthalmology has increased, mainly including cell type and cell subtype identification, retinal development process, and eye disease research. This paper systematically summarized the latest application of single-cell sequencing technology in the field of diabetic retinopathy, and summarized marker genes and potential therapeutic targets. It has guiding significance for the clinical treatment of diabetic retinopathy.
随着高通量测序技术的发展，人类已经能够对 DNA 序列、染色质结构、RNA 转录本、蛋白质、代谢物等基因组及其产物进行大规模分析。传统的基于组织样本的高通量转录组测序技术（RNA Seq）用于对成千上万个细胞进行集中测序，每个细胞的大小、蛋白质水平和 mRNA 表达转录各不相同。测量多个细胞的平均值会掩盖细胞间基因表达的显著差异。单细胞 RNA 测序是一种在单细胞水平对基因组、转录组和表观基因组进行高通量测序的技术。根据单细胞RNA转录图谱，可将眼内细胞与其他亚型细胞区分开来，并发现不同亚型细胞在形态、生理和特异性表达基因方面存在显著差异。近年来，单细胞RNA测序技术在眼科领域的应用越来越多，主要包括细胞类型和细胞亚型鉴定、视网膜发育过程和眼科疾病研究等。本文系统总结了单细胞测序技术在糖尿病视网膜病变领域的最新应用，归纳了标志基因和潜在治疗靶点。对糖尿病视网膜病变的临床治疗具有指导意义。
{"title":"Current Advances in Single-Cell RNA Sequencing in Diabetic Retinopathy","authors":"Kangqi Zhao, Ming Hao, Qian Xu, Hong-Xue Li, Cheng-Ye Xu, Ziyu Meng, H. Kuang","doi":"10.1166/jbn.2024.3770","DOIUrl":"https://doi.org/10.1166/jbn.2024.3770","url":null,"abstract":"With the development of high-throughput sequencing technology, humans have been able to conduct large-scale analysis of DNA sequence, chromatin structure, RNA transcripts, proteins, metabolites and other genomes and their products. Traditional high-throughput transcriptome sequencing\u0000 techniques based on tissue samples (RNA Seq) are used to centrally sequence thousands of cells, each of which varies in size, protein levels, and mRNA expression transcription. Measuring the average of multiple cells grouped together can mask significant differences in gene expression between\u0000 cells. Single-cell RNA sequencing is a technique for high-throughput sequencing of the genome, transcriptome, and epigenome at the single-cell level. Based on the single cell RNA transcription map, the intraocular cells can be distinguished from other subtypes, and the different subtypes are\u0000 found to have significant differences in morphology, physiology and specific expression genes. In recent years, the application of single-cell RNA sequencing technology in the field of ophthalmology has increased, mainly including cell type and cell subtype identification, retinal development\u0000 process, and eye disease research. This paper systematically summarized the latest application of single-cell sequencing technology in the field of diabetic retinopathy, and summarized marker genes and potential therapeutic targets. It has guiding significance for the clinical treatment of\u0000 diabetic retinopathy.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139820509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Min Liu, Chuanbing Xu, Huichao Dong, Dongsheng Jia, Dongfang Hao, Ruozen Rong, Yao Peng
Prostate cancer (PCa) is a common malignancy among men worldwide. Iron oxide (Fe3O4) nanoparticles (NPs) exhibit great potential in gene delivery and studies have noted the inhibitory effect of miR-124 on PCa cell growth. Herein, we identified the therapeutic effect of Fe3O4 NPs carrying miR-124 in PCa and clarified its mechanism of action in inhibiting progression of PCa. After preparation of Fe3O4 NPs carrying miR-124, human PCa cell line PC3 was treated with miR-124-Fe3O4 NPs when ferroptosis inducer FIN56, ferroptosis inhibitor Liproxstatin-1, Phosphatase and tensin homolog (PTEN) inhibitor SF1670 or PTEN activator Oroxin B were added for transfection. Afterwards, assays were conducted to evaluate PCa cell biological activities. Additionally, we determined expression of PTEN and AKT and ferroptosis-related protein GPX4 and SLC7A11 in each group. We confirmed anticancer effects of miR-124-Fe3O4 NPs in PCa, as they suppressed PC3 cell proliferation and migration, and induced apoptosis. Compared with miR-124-Fe3O4 + Liproxstatin-1 group, the expressions of GPX4 and SLC7A11 proteins in miR-124-Fe3O4 group were elevated. The advent of PTEN activator Oroxin B decreased proliferative ability of PCa cells, and SF1670 treatment decreased PTEN level and elevated AKT level. With highest apoptotic rate of PCa cells in miR-124-Fe3O4 + Oroxin B + FIN56 group, intervention of SF1670 or Liproxstatin-1 changed the cell viability, while Oroxin B caused decreased AKT level and increased level of ferroptosis-related proteins. miR-124-Fe3O4 NPs hinder PCa progression by promoting ferroptosis and cell apoptosis through regulation of PTEN/Akt pathway.
{"title":"Iron Oxide Nanoparticles Carrying microRNA-124 Promote Ferroptosis in Treatment of Prostate Cancer","authors":"Min Liu, Chuanbing Xu, Huichao Dong, Dongsheng Jia, Dongfang Hao, Ruozen Rong, Yao Peng","doi":"10.1166/jbn.2024.3782","DOIUrl":"https://doi.org/10.1166/jbn.2024.3782","url":null,"abstract":"Prostate cancer (PCa) is a common malignancy among men worldwide. Iron oxide (Fe3O4) nanoparticles (NPs) exhibit great potential in gene delivery and studies have noted the inhibitory effect of miR-124 on PCa cell growth. Herein, we identified the therapeutic effect\u0000 of Fe3O4 NPs carrying miR-124 in PCa and clarified its mechanism of action in inhibiting progression of PCa. After preparation of Fe3O4 NPs carrying miR-124, human PCa cell line PC3 was treated with miR-124-Fe3O4 NPs when ferroptosis\u0000 inducer FIN56, ferroptosis inhibitor Liproxstatin-1, Phosphatase and tensin homolog (PTEN) inhibitor SF1670 or PTEN activator Oroxin B were added for transfection. Afterwards, assays were conducted to evaluate PCa cell biological activities. Additionally, we determined expression of PTEN and\u0000 AKT and ferroptosis-related protein GPX4 and SLC7A11 in each group. We confirmed anticancer effects of miR-124-Fe3O4 NPs in PCa, as they suppressed PC3 cell proliferation and migration, and induced apoptosis. Compared with miR-124-Fe3O4 + Liproxstatin-1\u0000 group, the expressions of GPX4 and SLC7A11 proteins in miR-124-Fe3O4 group were elevated. The advent of PTEN activator Oroxin B decreased proliferative ability of PCa cells, and SF1670 treatment decreased PTEN level and elevated AKT level. With highest apoptotic rate\u0000 of PCa cells in miR-124-Fe3O4 + Oroxin B + FIN56 group, intervention of SF1670 or Liproxstatin-1 changed the cell viability, while Oroxin B caused decreased AKT level and increased level of ferroptosis-related proteins. miR-124-Fe3O4 NPs hinder PCa\u0000 progression by promoting ferroptosis and cell apoptosis through regulation of PTEN/Akt pathway.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139878141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study aims to explore the relationship between STRN, TGF-β1, Caspase-3, PD-1 expression, and myocardial fibrosis in salt-sensitive hypertensive rats. It investigates the correlation between STRN expression and myocardial fibrosis, along with the protective effects of Sacubitril/Valsartan (ARNI). Fifteen 18-week-old rats were divided into three groups: Control, high salt (SSH), and ARNI+SSH. Blood pressure was monitored weekly for 8 weeks. Echocardiography evaluated cardiac parameters, while H&E and Masson staining visualized myocardial morphology and fibrosis. Immunohistochemistry measured protein expression of collagen-1, collagen-3, TGF-β1, PD-1, Caspase-3, and STRN. Western blot assessed STRN protein levels. High-salt diet increased fibrosis, collagen expression, TGF-β1, PD-1, Caspase-3, and reduced STRN expression compared to Control (P < 0.05). ARNI treatment decreased fibrosis, collagen expression, TGF-β1, PD-1, Caspase-3 (P <0.05), and increased STRN expression compared to SSH (P <0.05). STRN expression correlated positively with myocardial fibrosis. ARNI demonstrated potential in attenuating fibrosis by modulating STRN expression and suppressing apoptosis and inflammation in salt-sensitive hypertensive rats.
{"title":"Study on the Mechanism and Protection of Salt-Sensitive Hypertensive Rats’ Myocardial Fibrosis by Regulating Striatin with Sacubatrovalsartan","authors":"Qingxian Tu, Qianhang Xia, Meihong Chen, Haiyan Zhou, Qianfeng Jiang, Wei Li","doi":"10.1166/jbn.2024.3766","DOIUrl":"https://doi.org/10.1166/jbn.2024.3766","url":null,"abstract":"This study aims to explore the relationship between STRN, TGF-β1, Caspase-3, PD-1 expression, and myocardial fibrosis in salt-sensitive hypertensive rats. It investigates the correlation between STRN expression and myocardial fibrosis, along with the protective effects of\u0000 Sacubitril/Valsartan (ARNI). Fifteen 18-week-old rats were divided into three groups: Control, high salt (SSH), and ARNI+SSH. Blood pressure was monitored weekly for 8 weeks. Echocardiography evaluated cardiac parameters, while H&E and Masson staining visualized myocardial morphology and\u0000 fibrosis. Immunohistochemistry measured protein expression of collagen-1, collagen-3, TGF-β1, PD-1, Caspase-3, and STRN. Western blot assessed STRN protein levels. High-salt diet increased fibrosis, collagen expression, TGF-β1, PD-1, Caspase-3, and reduced STRN expression\u0000 compared to Control (P < 0.05). ARNI treatment decreased fibrosis, collagen expression, TGF-β1, PD-1, Caspase-3 (P <0.05), and increased STRN expression compared to SSH (P <0.05). STRN expression correlated positively with myocardial fibrosis. ARNI\u0000 demonstrated potential in attenuating fibrosis by modulating STRN expression and suppressing apoptosis and inflammation in salt-sensitive hypertensive rats.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139881822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To enhance the treatment of acute lung injury (ALI) induced by sepsis and optimize the clinical efficacy of simvastatin (SV), we develop SV-loaded nanoliposomes (SV/NLC) as a novel drug delivery system. The NLCs exhibited a particle size of approximately 165 nm, which increased to around 195 nm upon SV loading. NLCs significantly prolonged the half-life of SV by nearly five-fold and improved its penetration into EA.hy926 cells, demonstrating excellent biocompatibility and targeted delivery for ALI therapy. In the rat model of ALI, the SV/NLC effectively reduced the lung wet/dry ratio and the levels of inflammatory factor and albumin in the alveoli, thus improving the alveolar gas exchange function and blood oxygenation. The SV/NLC group demonstrated superior suppression of oxidative stress within lung tissues compared to other groups. Notably, treatment with SV reduction in TLR4, MyD88, and NF-κB P65 levels in lung tissues from ALI rat models. This effect was particularly pronounced in the SV/NLC group. Furthermore, SV can effectively mitigate inflammatory responses and oxidative stress in ALI treatment by modulating the TLR4/NF-κB signaling pathway. In conclusion, our findings suggest that SV can exert therapeutic effects against sepsis-induced ALI through inhibition of the TLR4/NF-κ and mitigate inflammatory response and oxidative stress.
为了加强对脓毒症诱发的急性肺损伤（ALI）的治疗并优化辛伐他汀（SV）的临床疗效，我们开发了一种新型给药系统--SV负载纳米脂质体（SV/NLC）。纳米脂质体的粒径约为 165 nm，载入 SV 后粒径增至约 195 nm。NLCs 将 SV 的半衰期延长了近五倍，并提高了 SV 在 EA.hy926 细胞中的穿透力，证明了其在 ALI 治疗中出色的生物相容性和靶向递送能力。在大鼠 ALI 模型中，SV/NLC 有效降低了肺干湿比以及肺泡中的炎症因子和白蛋白水平，从而改善了肺泡气体交换功能和血氧饱和度。与其他组相比，SV/NLC 组能更好地抑制肺组织内的氧化应激。值得注意的是，SV 治疗降低了 ALI 大鼠肺组织中 TLR4、MyD88 和 NF-κB P65 的水平。这种效应在 SV/NLC 组中尤为明显。此外，SV 还能通过调节 TLR4/NF-κB 信号通路，有效缓解 ALI 治疗过程中的炎症反应和氧化应激。总之，我们的研究结果表明，SV 可通过抑制 TLR4/NF-κ 发挥治疗脓毒症诱发的 ALI 的作用，并减轻炎症反应和氧化应激。
{"title":"A Simvastatin-Loaded Nanoliposome Delivery System for Sepsis-Induced Acute Lung Injury","authors":"Jianhai Yang, Yue Yue","doi":"10.1166/jbn.2024.3805","DOIUrl":"https://doi.org/10.1166/jbn.2024.3805","url":null,"abstract":"To enhance the treatment of acute lung injury (ALI) induced by sepsis and optimize the clinical efficacy of simvastatin (SV), we develop SV-loaded nanoliposomes (SV/NLC) as a novel drug delivery system. The NLCs exhibited a particle size of approximately 165 nm, which increased to around\u0000 195 nm upon SV loading. NLCs significantly prolonged the half-life of SV by nearly five-fold and improved its penetration into EA.hy926 cells, demonstrating excellent biocompatibility and targeted delivery for ALI therapy. In the rat model of ALI, the SV/NLC effectively reduced the lung wet/dry\u0000 ratio and the levels of inflammatory factor and albumin in the alveoli, thus improving the alveolar gas exchange function and blood oxygenation. The SV/NLC group demonstrated superior suppression of oxidative stress within lung tissues compared to other groups. Notably, treatment with SV reduction\u0000 in TLR4, MyD88, and NF-κB P65 levels in lung tissues from ALI rat models. This effect was particularly pronounced in the SV/NLC group. Furthermore, SV can effectively mitigate inflammatory responses and oxidative stress in ALI treatment by modulating the TLR4/NF-κB\u0000 signaling pathway. In conclusion, our findings suggest that SV can exert therapeutic effects against sepsis-induced ALI through inhibition of the TLR4/NF-κ and mitigate inflammatory response and oxidative stress.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139822202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Caiyue Fang, Ruibo Lin, Suqin Gan, Hong Wang, Chenghui Huang
Due to the challenges in early diagnosis and lack of specific biomarkers, liver cancer remains one of the most prevalent and lethal tumor types. Numerous studies have shown that long noncoding RNA (lncRNA) plays a crucial role in the regulation of various malignant tumors, including liver cancer. Here, we discussed the function and effect of LncRNA-LHX2 in the tumorigenesis and progression of liver cancer, which was significantly upregulated in liver cancer tissues, compared to the benign liver tissues. To improve the accuracy and efficiency of tests like qRT-PCR, we employed nano-magnetic beads for nucleic acid extraction from tissues and cells. In our experiments using HepG2 cells, silencing of LncRNA-LHX2 effectively suppressed cell proliferation, migration, and invasion by interacting with miR-939-5p, which targets VEGFA. Interestingly, overexpression of miR-939-5p also impaired malignant functions of HepG2 cells. However, simultaneously inhibition of miR-939-5p expression can partially restored the inhibitory effect on HepG2 cells resulting from LncRNA-LHX2 knockdown. Consistently, our in vivo results from tumor mice model also suggested that knockout of LncRNA-LHX2 inhibited the tumor growth and suppressed epithelial mesenchymal transition (EMT) process, while silencing of miR-939-5p exhibited the opposite effect. However, when both LncRNA-LHX2 and miR-939-5p were simultaneously interfered with, the tumor growth was partially alleviated. Based on these results, our study highlights the malignant impact of LncRNA-LHX2 in the progression of liver cancer, indicating its potential as a candidate biomarker for liver cancer diagnosis.
{"title":"Upregulation of LncRNA-LHX2 Promotes Hepatocellular Carcinoma Proliferation, Migration, Invasion and Metastasis via Targeting VEGFA by Sequestering of MiR-939-5p","authors":"Caiyue Fang, Ruibo Lin, Suqin Gan, Hong Wang, Chenghui Huang","doi":"10.1166/jbn.2024.3776","DOIUrl":"https://doi.org/10.1166/jbn.2024.3776","url":null,"abstract":"Due to the challenges in early diagnosis and lack of specific biomarkers, liver cancer remains one of the most prevalent and lethal tumor types. Numerous studies have shown that long noncoding RNA (lncRNA) plays a crucial role in the regulation of various malignant tumors, including\u0000 liver cancer. Here, we discussed the function and effect of LncRNA-LHX2 in the tumorigenesis and progression of liver cancer, which was significantly upregulated in liver cancer tissues, compared to the benign liver tissues. To improve the accuracy and efficiency of tests like qRT-PCR, we\u0000 employed nano-magnetic beads for nucleic acid extraction from tissues and cells. In our experiments using HepG2 cells, silencing of LncRNA-LHX2 effectively suppressed cell proliferation, migration, and invasion by interacting with miR-939-5p, which targets VEGFA. Interestingly, overexpression\u0000 of miR-939-5p also impaired malignant functions of HepG2 cells. However, simultaneously inhibition of miR-939-5p expression can partially restored the inhibitory effect on HepG2 cells resulting from LncRNA-LHX2 knockdown. Consistently, our in vivo results from tumor mice model also\u0000 suggested that knockout of LncRNA-LHX2 inhibited the tumor growth and suppressed epithelial mesenchymal transition (EMT) process, while silencing of miR-939-5p exhibited the opposite effect. However, when both LncRNA-LHX2 and miR-939-5p were simultaneously interfered with, the tumor growth\u0000 was partially alleviated. Based on these results, our study highlights the malignant impact of LncRNA-LHX2 in the progression of liver cancer, indicating its potential as a candidate biomarker for liver cancer diagnosis.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139824092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wenfeng Liu, Meng Zhang, Xiaojie Du, Min Zhang, Weiling Wang, Zhiying Zhang
As a malignant tumor, cervical cancer (CC) seriously affects women’s life and health. Various microRNAs (miRNAs) are involved in tumorigenesis of CC. Here, we mainly paid attention to the effect of miR-153 in CC. RT-qPCR or Western blot was employed to quantify miR-153 or SATB1 expression. Molecular mechanism of miR-153/SATB1 was detected by Transwell and dual-luciferase assays. MiR-153 was downregulated in CC. Furthermore, upregulation of miR-153 restrained cell metastasis. Upregulation of SATB1 was detected in CC, and negative connected with miR-153 in CC cells. Knockdown of SATB1 suppressed cell metastasis in CC. The inhibitory effect of miR-153 was abolished by upregulation of SATB1. Besides that, miR-153 blocked EMT and downregulated p-β-catenin expression in CC cells. MiR-153 restrains cell metastasis and EMT in CC by targeting SATB1 and regulating Wnt/β-catenin pathway.
宫颈癌（CC）作为一种恶性肿瘤，严重影响着女性的生活和健康。多种微RNA（miRNA）参与了CC的肿瘤发生。在此，我们主要关注 miR-153 在 CC 中的作用。采用RT-qPCR或Western blot定量检测miR-153或SATB1的表达。通过Transwell和双荧光素酶实验检测了miR-153/SATB1的分子机制。CC中的miR-153被下调。此外，miR-153 的上调抑制了细胞的转移。在 CC 中检测到 SATB1 的上调，并且在 CC 细胞中与 miR-153 呈负相关。敲除SATB1抑制了CC细胞的转移。SATB1的上调会取消miR-153的抑制作用。此外，miR-153还能阻止EMT，并下调CC细胞中p-β-catenin的表达。MiR-153通过靶向SATB1和调节Wnt/β-catenin通路抑制CC细胞的转移和EMT。
{"title":"MicroRNA-153 Restrains Cell Metastasis and Epithelial–Mesenchymal Transition in Cervical Carcinoma by Targeting SATB1 and Regulating Wnt/β-Catenin Pathway","authors":"Wenfeng Liu, Meng Zhang, Xiaojie Du, Min Zhang, Weiling Wang, Zhiying Zhang","doi":"10.1166/jbn.2024.3761","DOIUrl":"https://doi.org/10.1166/jbn.2024.3761","url":null,"abstract":"As a malignant tumor, cervical cancer (CC) seriously affects women’s life and health. Various microRNAs (miRNAs) are involved in tumorigenesis of CC. Here, we mainly paid attention to the effect of miR-153 in CC. RT-qPCR or Western blot was employed to quantify miR-153 or SATB1\u0000 expression. Molecular mechanism of miR-153/SATB1 was detected by Transwell and dual-luciferase assays. MiR-153 was downregulated in CC. Furthermore, upregulation of miR-153 restrained cell metastasis. Upregulation of SATB1 was detected in CC, and negative connected with miR-153 in CC cells.\u0000 Knockdown of SATB1 suppressed cell metastasis in CC. The inhibitory effect of miR-153 was abolished by upregulation of SATB1. Besides that, miR-153 blocked EMT and downregulated p-β-catenin expression in CC cells. MiR-153 restrains cell metastasis and EMT in CC by targeting SATB1\u0000 and regulating Wnt/β-catenin pathway.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139824460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yu Zhang, Yuan-min Yang, Shui-qing Qu, Shuo-qiu Deng, Yu Li, Zhongyuzn Zheng, Yue Dai, Tuo Liu, Li-na Chen, Yu-jie Li
There was an investigation into the hypoglycemic effects and potential mechanisms of dihydroartemisinin (DHA) on hepatic glycometabolism of type 2 diabetes mellitus (T2DM). The db/db mice and ApoE−/− mice induced by streptozotocin (STZ) were selected as diabetes models. The levels of FBG, body weight, glucose tolerance, insulin, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were observed to evaluate the drug’s efficacy. The glycogen content, glucose-6-phosphate (G6P), hexokinase (HK) and glucose-6-phosphatase (G6pase) were detected in the livers. Histopathological studies were conducted on the pancreas and liver. Targeting proteins and signaling pathways of DHA were identified by quantitative proteomic. Western blotting examined the protein expression of forkhead box protein O1 (FOXO1) and calcium/calmodulin-dependent-protein kinase 2 (CAMK2) in the liver. This study demonstrated that DHA reduced FBG, improved insulin sensitivity, ameliorated glucose tolerance in two diabetes models while decreasing the ALT and AST levels in db/db mice. DHA promoted hepatic glucose metabolism and inhibited gluconeogenesis via CAMK2/FOXO1-mediated HK upregulation and G6pase downregulation. In conclusion, DHA exerts protective effects against T2DM related to maintain the blance of hepatic glucose.
一项研究探讨了双氢青蒿素（DHA）对2型糖尿病（T2DM）肝糖代谢的降血糖作用和潜在机制。研究选取链脲佐菌素（STZ）诱导的 db/db 小鼠和 ApoE-/- 小鼠作为糖尿病模型。通过观察 FBG、体重、糖耐量、胰岛素、丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）的水平来评估药物的疗效。还检测了肝脏中的糖原含量、葡萄糖-6-磷酸（G6P）、己糖激酶（HK）和葡萄糖-6-磷酸酶（G6pase）。对胰腺和肝脏进行了组织病理学研究。通过定量蛋白质组鉴定了 DHA 的靶蛋白和信号通路。Western印迹检测了肝脏中叉头盒蛋白O1（FOXO1）和钙/钙调蛋白依赖性蛋白激酶2（CAMK2）的蛋白表达。该研究表明，DHA 可降低两种糖尿病模型的血糖，改善胰岛素敏感性，改善葡萄糖耐量，同时降低 db/db 小鼠的谷丙转氨酶和谷草转氨酶水平。DHA 通过 CAMK2/FOXO1 介导的 HK 上调和 G6pase 下调，促进肝糖代谢并抑制葡萄糖生成。总之，DHA对T2DM的保护作用与维持肝糖平衡有关。
{"title":"The Protective Effect of Dihydroartemisinin on Type 2 Diabetic Mice via Regulating Hepatic Glucose Output","authors":"Yu Zhang, Yuan-min Yang, Shui-qing Qu, Shuo-qiu Deng, Yu Li, Zhongyuzn Zheng, Yue Dai, Tuo Liu, Li-na Chen, Yu-jie Li","doi":"10.1166/jbn.2024.3772","DOIUrl":"https://doi.org/10.1166/jbn.2024.3772","url":null,"abstract":"There was an investigation into the hypoglycemic effects and potential mechanisms of dihydroartemisinin (DHA) on hepatic glycometabolism of type 2 diabetes mellitus (T2DM). The db/db mice and ApoE−/− mice induced by streptozotocin (STZ) were selected as diabetes\u0000 models. The levels of FBG, body weight, glucose tolerance, insulin, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were observed to evaluate the drug’s efficacy. The glycogen content, glucose-6-phosphate (G6P), hexokinase (HK) and glucose-6-phosphatase (G6pase)\u0000 were detected in the livers. Histopathological studies were conducted on the pancreas and liver. Targeting proteins and signaling pathways of DHA were identified by quantitative proteomic. Western blotting examined the protein expression of forkhead box protein O1 (FOXO1) and calcium/calmodulin-dependent-protein\u0000 kinase 2 (CAMK2) in the liver. This study demonstrated that DHA reduced FBG, improved insulin sensitivity, ameliorated glucose tolerance in two diabetes models while decreasing the ALT and AST levels in db/db mice. DHA promoted hepatic glucose metabolism and inhibited gluconeogenesis via CAMK2/FOXO1-mediated\u0000 HK upregulation and G6pase downregulation. In conclusion, DHA exerts protective effects against T2DM related to maintain the blance of hepatic glucose.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139827536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lei Yang, Yue Zhang, Jiansong Wu, Lei Wang, Shan Liu, Li Zhou, Jigang Zhang, Chengxin Li
Psoriasis is a chronic and recurrent skin disease characterized by aberrant proliferation and differentiation of keratinocyte cells. Although calcipotriol has been employed in the clinical management of psoriasis, no association between the anti-inflammatory mechanism and iron death has been reported. Therefore, we assume that calcipotriol may down-regulate cell activity and suppress the expression of tissue inflammatory factors by regulating the glutathione (GSH) and glutathione peroxidase 4 (GPX4) pathway, thereby alleviating tissue inflammation and ameliorating psoriasis symptoms. The experimental groups consisted of a control group, a model group, a Calcipotriol group, and a Calcipotriol+Ferrostatin-1 group. In vitro experiments, a lipopolysaccharides-induced HaCaT cell model was established. In vivo experiments, an imiquimod-induced psoriasis mice model was constructed. The results showed that calcipotriol effectively downregulated the expression of GPX4 and GSH, thereby inhibiting HaCaT cell proliferation through modulation of Ki-67 protein expression and DNA breakage. Ferrostatin-1 could partially reverse these effects. Additionally, calcipotriol downregulated the expression of GPX4 and GSH in skin tissues and upregulated the expression of long-chain acyl-CoA synthetase 4 by suppressing the levels of SLC7A11 and ferritin, leading to promote the accumulation of ROS and ferroptosis. Moreover, calcipotriol demonstrated inhibitory effects on the inflammatory mediators and attenuated skin inflammation. Therefore, calcipotriol effectively ameliorated psoriatic lesions. In conclusion, this study revealed that calcipotriol exerts its therapeutic potential by promoting cellular clearance and suppressing tissue inflammation through upregulation of ferroptosis progression. Therefore, this study provides new therapeutic drugs and functions for the treatment of psoriasis.
{"title":"Inhibition of HaCaT Proliferation and Imiquimod-Induced Psoriasis by Calcipotriol Through Regulation of the Glutathione/Glutathione Peroxidase 4 Pathway","authors":"Lei Yang, Yue Zhang, Jiansong Wu, Lei Wang, Shan Liu, Li Zhou, Jigang Zhang, Chengxin Li","doi":"10.1166/jbn.2024.3777","DOIUrl":"https://doi.org/10.1166/jbn.2024.3777","url":null,"abstract":"Psoriasis is a chronic and recurrent skin disease characterized by aberrant proliferation and differentiation of keratinocyte cells. Although calcipotriol has been employed in the clinical management of psoriasis, no association between the anti-inflammatory mechanism and iron death\u0000 has been reported. Therefore, we assume that calcipotriol may down-regulate cell activity and suppress the expression of tissue inflammatory factors by regulating the glutathione (GSH) and glutathione peroxidase 4 (GPX4) pathway, thereby alleviating tissue inflammation and ameliorating psoriasis\u0000 symptoms. The experimental groups consisted of a control group, a model group, a Calcipotriol group, and a Calcipotriol+Ferrostatin-1 group. In vitro experiments, a lipopolysaccharides-induced HaCaT cell model was established. In vivo experiments, an imiquimod-induced psoriasis\u0000 mice model was constructed. The results showed that calcipotriol effectively downregulated the expression of GPX4 and GSH, thereby inhibiting HaCaT cell proliferation through modulation of Ki-67 protein expression and DNA breakage. Ferrostatin-1 could partially reverse these effects. Additionally,\u0000 calcipotriol downregulated the expression of GPX4 and GSH in skin tissues and upregulated the expression of long-chain acyl-CoA synthetase 4 by suppressing the levels of SLC7A11 and ferritin, leading to promote the accumulation of ROS and ferroptosis. Moreover, calcipotriol demonstrated inhibitory\u0000 effects on the inflammatory mediators and attenuated skin inflammation. Therefore, calcipotriol effectively ameliorated psoriatic lesions. In conclusion, this study revealed that calcipotriol exerts its therapeutic potential by promoting cellular clearance and suppressing tissue inflammation\u0000 through upregulation of ferroptosis progression. Therefore, this study provides new therapeutic drugs and functions for the treatment of psoriasis.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139872517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yu Zhang, Yuan-min Yang, Shui-qing Qu, Shuo-qiu Deng, Yu Li, Zhongyuzn Zheng, Yue Dai, Tuo Liu, Li-na Chen, Yu-jie Li
There was an investigation into the hypoglycemic effects and potential mechanisms of dihydroartemisinin (DHA) on hepatic glycometabolism of type 2 diabetes mellitus (T2DM). The db/db mice and ApoE−/− mice induced by streptozotocin (STZ) were selected as diabetes models. The levels of FBG, body weight, glucose tolerance, insulin, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were observed to evaluate the drug’s efficacy. The glycogen content, glucose-6-phosphate (G6P), hexokinase (HK) and glucose-6-phosphatase (G6pase) were detected in the livers. Histopathological studies were conducted on the pancreas and liver. Targeting proteins and signaling pathways of DHA were identified by quantitative proteomic. Western blotting examined the protein expression of forkhead box protein O1 (FOXO1) and calcium/calmodulin-dependent-protein kinase 2 (CAMK2) in the liver. This study demonstrated that DHA reduced FBG, improved insulin sensitivity, ameliorated glucose tolerance in two diabetes models while decreasing the ALT and AST levels in db/db mice. DHA promoted hepatic glucose metabolism and inhibited gluconeogenesis via CAMK2/FOXO1-mediated HK upregulation and G6pase downregulation. In conclusion, DHA exerts protective effects against T2DM related to maintain the blance of hepatic glucose.
一项研究探讨了双氢青蒿素（DHA）对2型糖尿病（T2DM）肝糖代谢的降血糖作用和潜在机制。研究选取链脲佐菌素（STZ）诱导的 db/db 小鼠和 ApoE-/- 小鼠作为糖尿病模型。通过观察 FBG、体重、糖耐量、胰岛素、丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）的水平来评估药物的疗效。还检测了肝脏中的糖原含量、葡萄糖-6-磷酸（G6P）、己糖激酶（HK）和葡萄糖-6-磷酸酶（G6pase）。对胰腺和肝脏进行了组织病理学研究。通过定量蛋白质组鉴定了 DHA 的靶蛋白和信号通路。Western印迹检测了肝脏中叉头盒蛋白O1（FOXO1）和钙/钙调蛋白依赖性蛋白激酶2（CAMK2）的蛋白表达。该研究表明，DHA 可降低两种糖尿病模型的血糖，改善胰岛素敏感性，改善葡萄糖耐量，同时降低 db/db 小鼠的谷丙转氨酶和谷草转氨酶水平。DHA 通过 CAMK2/FOXO1 介导的 HK 上调和 G6pase 下调，促进肝糖代谢并抑制葡萄糖生成。总之，DHA对T2DM的保护作用与维持肝糖平衡有关。
{"title":"The Protective Effect of Dihydroartemisinin on Type 2 Diabetic Mice via Regulating Hepatic Glucose Output","authors":"Yu Zhang, Yuan-min Yang, Shui-qing Qu, Shuo-qiu Deng, Yu Li, Zhongyuzn Zheng, Yue Dai, Tuo Liu, Li-na Chen, Yu-jie Li","doi":"10.1166/jbn.2024.3772","DOIUrl":"https://doi.org/10.1166/jbn.2024.3772","url":null,"abstract":"There was an investigation into the hypoglycemic effects and potential mechanisms of dihydroartemisinin (DHA) on hepatic glycometabolism of type 2 diabetes mellitus (T2DM). The db/db mice and ApoE−/− mice induced by streptozotocin (STZ) were selected as diabetes\u0000 models. The levels of FBG, body weight, glucose tolerance, insulin, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were observed to evaluate the drug’s efficacy. The glycogen content, glucose-6-phosphate (G6P), hexokinase (HK) and glucose-6-phosphatase (G6pase)\u0000 were detected in the livers. Histopathological studies were conducted on the pancreas and liver. Targeting proteins and signaling pathways of DHA were identified by quantitative proteomic. Western blotting examined the protein expression of forkhead box protein O1 (FOXO1) and calcium/calmodulin-dependent-protein\u0000 kinase 2 (CAMK2) in the liver. This study demonstrated that DHA reduced FBG, improved insulin sensitivity, ameliorated glucose tolerance in two diabetes models while decreasing the ALT and AST levels in db/db mice. DHA promoted hepatic glucose metabolism and inhibited gluconeogenesis via CAMK2/FOXO1-mediated\u0000 HK upregulation and G6pase downregulation. In conclusion, DHA exerts protective effects against T2DM related to maintain the blance of hepatic glucose.","PeriodicalId":15260,"journal":{"name":"Journal of biomedical nanotechnology","volume":null,"pages":null},"PeriodicalIF":2.9,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139887558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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