期刊：
Diabetes, Metabolic Syndrome and Obesity: Targets and Therapy,2024年17:343-362 ISSN：1178-7007
通讯作者：
Wang, J;Kuang, TD
作者机构：
[Deng, Wenying; Wang, Jing; Zhao, Zeyi] Univ South China, Sch Basic Med Sci, Hengyang 421001, Hunan, Peoples R China.;[Zou, Tao] Univ South China, Affiliated Hosp 1, Dept Cardiovasc Med, Hengyang 421001, Hunan, Peoples R China.;[Kuang, Tongdong] Guilin Med Univ, Guangxi Key Lab Diabetic Syst Med, Guilin 541199, Guangxi, Peoples R China.
通讯机构：
[Kuang, TD ] G;[Wang, J ] U;Univ South China, Sch Basic Med Sci, Hengyang 421001, Hunan, Peoples R China.;Guilin Med Univ, Guangxi Key Lab Diabetic Syst Med, Guilin 541199, Guangxi, Peoples R China.
关键词：
Fc protein;albumin;diabetes mellitus;fusion protein;glucagon-like peptide 1 receptor agonists;transferrin
摘要：
Diabetes mellitus (DM) is a chronic metabolic disease characterized by elevated blood glucose levels, resulting in multi-organ dysfunction and various complications. Fusion proteins can form multifunctional complexes by combining the target proteins with partner proteins. It has significant advantages in improving the performance of the target proteins, extending their biological half-life, and enhancing patient drug compliance. Fusion protein-based drugs have emerged as promising new drugs in diabetes therapeutics. However, there has not been a systematic review of fusion protein-based drugs for diabetes therapeutics. Hence, we conducted a comprehensive review of published literature on diabetic fusion protein-based drugs for diabetes, with a primary focus on immunoglobulin G (IgG) fragment crystallizable (Fc) region, albumin, and transferrin (TF). This review aims to provide a reference for the subsequent development and clinical application of fusion protein-based drugs in diabetes therapeutics.
作者机构：
[周灵艳] Department of Pediatrics, The First Affiliated Hospital of Hengyang Medical College, University of South China, Hengyang 421600, Hunan Province, China;[殷小成] Department of Pediatrics, The First Affiliated Hospital of Hengyang Medical College, University of South China, Hengyang 421600, Hunan Province, China. E-mail: xcyin108@sina.com
通讯机构：
[Yin, Xiao-Cheng] D;Department of Pediatrics, The First Affiliated Hospital of Hengyang Medical College, University of South China, Hengyang 421600, Hunan Province, China. E-mail:
作者机构：
[Chuli, Xiao; Li, Huang; Ying, Lu] The Brain Cognition and Brain Disease Branch, Pu Ai Medical School, Shaoyang University, 422000, Shaoyang, China;[Wan, Fu] The First Affiliated Hospital, Department of neurology, Hengyang Medical School, University of South China, 421001, Hengyang, Hunan, China;[Shiqiao, Kang] The First Affiliated Hospital, Department of Critical Care Medicine, Hengyang Medical School, University of South China, 421001, Hengyang, Hunan, China;[Yijie, Fang] School of Nursing, Hengyang Medical School, University of South China, 421001, Hengyang, Hunan, China;[Xudong, Yu] The Brain Cognition and Brain Disease Branch, Pu Ai Medical School, Shaoyang University, 422000, Shaoyang, China. Electronic address: yxd_neuro@163.com
通讯机构：
[Xinhong, Yin] S;[Zhiyong, Xiao; Xudong, Yu] T;The Brain Cognition and Brain Disease Branch, Pu Ai Medical School, Shaoyang University, 422000, Shaoyang, China. Electronic address:;School of Nursing, Hengyang Medical School, University of South China, 421001, Hengyang, Hunan, China. Electronic address:;The First Affiliated Hospital, Department of Critical Care Medicine, Hengyang Medical School, University of South China, 421001, Hengyang, Hunan, China. Electronic address:
摘要：
Esketamine, the right-handed optical isomer of racemic ketamine, is a rapidly acting antidepressant approved by the FDA for treatment-resistant depression in 2019. However, few studies have investigated esketamine's role in learning and memory, particularly in the context of memory reconsolidation. Herein, we evaluated esketamine's role in memory reconsolidation in 7-week-old male Institute of Cancer Research mice subjected to the novel object recognition (NOR) memory task. The NOR reconsolidation procedure comprised three phases: sampling, reactivation, and testing. Esketamine-enhanced NOR memory performance when injected into mice 0 h after reactivation rather than following a 6 h delay. Conversely, administering esketamine 24 h after sampling without reactivation did not enhance NOR memory performance. Notably, esketamine exhibited no discernible effects on nonspecific responses, such as locomotor activity and exploratory behavior. Furthermore, the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type receptor antagonist NBQX effectively blocked the esketamine-induced enhancement of memory reconsolidation. In conclusion, esketamine treatment markedly improves memory reconsolidation in NOR tasks, and this effect is linked to AMPA receptor activity.
摘要：
BACKGROUND: Endothelial-mesenchymal transition (EndMT) induced by low shear stress plays an important role in the development of atherosclerosis. However, little is known about the correlation between hydrogen sulfide (H(2)S), a protective gaseous mediator in atherosclerosis and the process of EndMT. METHODS: We constructed a stable low-shear-stress-induced(2dyn/cm(2)) EndMT model, acombined with the pretreatment method of hydrogen sulfide slow release agent(GYY4137). The level of MEST was detected in the common carotid artery of ApoE(-/-) mice with local carotid artery ligation. The effect of MEST on atherosclerosis development in vivo was verified using ApoE(-/-) mice were given tail-vein injection of endothelial-specific overexpressed and knock-down MEST adeno-associated virus (AAV). RESULTS: These findings confirmed that MEST is up-regulated in low-shear-stress-induced EndMT and atherosclerosis. In vivo experiments showed that MEST gene overexpression significantly promoted EndMT and aggravated the development of atherosclerotic plaques and MEST gene knockdown significantly inhibited EndMT and delayed the process of atherosclerosis. In vitro, H(2)S inhibits the expression of MEST and EndMT induced by low shear stress and inhibits EndMT induced by MEST overexpression. Knockdown of NFIL3 inhibit the up regulation of MEST and EndMT induced by low shear stress in HUVECs. CHIP-qPCR assay and Luciferase Reporter assay confirmed that NFIL3 binds to MEST DNA, increases its transcription and H(2)S inhibits the binding of NFIL3 and MEST DNA, weakening NFIL3's transcriptional promotion of MEST. Mechanistically, H(2)S increased the sulfhydrylation level of NFIL3, an important upstream transcription factors of MEST. In part, transcription factor NFIL3 restrain its binding to MEST DNA by sulfhydration. CONCLUSIONS: H(2)S negatively regulate the expression of MEST by sulfhydrylation of NFIL3, thereby inhibiting low-shear-stress-induced EndMT and atherosclerosis.
期刊：
Microporous and Mesoporous Materials,2024年368:113027 ISSN：1387-1811
通讯作者：
Qinglai Yang<&wdkj&>Xiaofeng Tan
作者机构：
[Ximei Sun; Jieqiong Wang; Hao Xiao; Qiang Kang; Yiqian Zeng] School of Pharmaceutical Science, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China;[Feirong Wang; Xiaofeng Tan] Center for Molecular Imaging Probe, Hunan Province Key Laboratory of Tumor Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China;[Qinglai Yang] School of Pharmaceutical Science, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China<&wdkj&>Center for Molecular Imaging Probe, Hunan Province Key Laboratory of Tumor Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China
通讯机构：
[Qinglai Yang] S;[Xiaofeng Tan] C;Center for Molecular Imaging Probe, Hunan Province Key Laboratory of Tumor Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China<&wdkj&>School of Pharmaceutical Science, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China<&wdkj&>Center for Molecular Imaging Probe, Hunan Province Key Laboratory of Tumor Cellular and Molecular Pathology, Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China
摘要：
Designing the robust catalysts with a self-supported open structure and engineering surface would be beneficial for promoting intrinsic activity, increasing active sites, and enhancing electron/mass transfer during catalysis. The metallic aerogels (MAs) with hierarchical porous nanostructures and pure metal skeleton could be a favorable platform for fabricating high-performance catalysts. The introduction of an interface engineering strategy causes beneficial structural and electronic properties of MAs. Herein, the ionic liquid (IL) induced metallic Pd aerogels with well-defined nanowires are developed for the efficient catalytic reduction of 4-nitrophenol (4-NP) in the presence of NH3BH3. The engineered IL-Pd aerogels exhibit the integrated advantages of exceptional catalytic activities (including a high k value of 31.2 × 10−2 s−1 and a high turnover frequency (TOF) of 320.4 h−1), acceptable costeffectiveness with a low NH3BH3 concentration (n[NH3BH3]/n[4-NP] of 120), remarkable cyclability, and noticeable longstanding stability. This work opens a new avenue for developing high-performance MAs with improved activity and durability.
摘要：
BACKGROUND: The DLG3 gene encodes disks large membrane-associated guanylate kinase scaffold protein 3, which plays essential roles in the clustering of N-methyl-D-aspartate receptors (NMDARs) at excitatory synapses. Previously, DLG3 has been identified as the causative gene of X-linked intellectual developmental disorder-90 (XLID-90; OMIM# 300850). This study aims to explore the phenotypic spectrum of DLG3 and the genotype-phenotype correlation. METHODS: Trios-based whole-exome sequencing was performed in patients with epilepsy of unknown causes. To analyze the genotype-phenotype correlations, previously reported DLG3 variants were systematically reviewed. RESULTS: DLG3 variants were identified in seven unrelated cases with epilepsy. These variants had no hemizygous frequencies in controls. All variants were predicted to be damaging by silico tools and alter the hydrogen bonds with surrounding residues and/or protein stability. Four cases mainly presented with generalized seizures, including generalized tonic-clonic and myoclonic seizures, and the other three cases exhibited secondary generalized tonic-clonic seizures and focal seizures. Multifocal discharges were recorded in all cases during electroencephalography monitoring, including the four cases with generalized discharges initially but multifocal discharges after drug treating. Protein-protein interaction network analysis revealed that DLG3 interacts with 52 genes with high confidence, in which the majority of disease-causing genes were associated with a wide spectrum of neurodevelopmental disorder (NDD) and epilepsy. Three patients with variants locating outside functional domains all achieved seizure-free, while the four patients with variants locating in functional domains presented poor control of seizures. Analysis of previously reported cases revealed that patients with non-null variants presented higher percentages of epilepsy than those with null variants, suggesting a genotype-phenotype correlation. SIGNIFICANCE: This study suggested that DLG3 variants were associated with epilepsy with/without NDD, expanding the phenotypic spectrum of DLG3. The observed genotype-phenotype correlation potentially contributes to the understanding of the underlying mechanisms driving phenotypic variation.
作者：
Vu, Nguyen Trung;Kim, Hyeongsoon;Lee, Soohong;Hwang, In Sun;Kwon, Choon-Tak;...
期刊：
Applied Microbiology and Biotechnology,2024年108(1):17-17 ISSN：0175-7598
通讯作者：
Zeng, YH
作者机构：
[Vu, Nguyen Trung; Lee, Soohong; Kwon, Choon-Tak] Kyung Hee Univ, Dept Green Bio Sci, Yongin 17104, South Korea.;[Hwang, In Sun; Kim, Hyeongsoon; Oh, Chang-Sik] Seoul Natl Univ, Res Inst Agr & Life Sci, Seoul 08826, South Korea.;[Oh, Chang-Sik] Seoul Natl Univ, Coll Agr & Life Sci, Dept Agr Biotechnol, Seoul 08826, South Korea.;[Oh, Chang-Sik] Seoul Natl Univ, Plant Genom & Breeding Inst, Seoul 08826, South Korea.
通讯机构：
[Oh, CS ] S;Seoul Natl Univ, Res Inst Agr & Life Sci, Seoul 08826, South Korea.;Seoul Natl Univ, Coll Agr & Life Sci, Dept Agr Biotechnol, Seoul 08826, South Korea.;Seoul Natl Univ, Plant Genom & Breeding Inst, Seoul 08826, South Korea.
关键词：
Cyclophilin A;Apoptosis;Disease development;Therapeutic target for diseases
摘要：
Cyclophilin A (CypA), the first member of cyclophilins, is distributed extensively in eukaryotic and prokaryotic cells, primarily localized in the cytoplasm. In addition to acting as an intracellular receptor for cyclosporin A (CSA), CypA plays a crucial role in diseases such as aging and tumorigenesis. Apoptosis, a form of programmed cell death, is able to balance the rate of cell viability and death. In this review, we focus on the effects of CypA on apoptosis and the relationship between specific mechanisms of CypA promoting or inhibiting apoptosis and diseases, including tumorigenesis, cardiovascular diseases, organ injury, and microbial infections. Notably, the process of CypA promoting or inhibiting apoptosis is closely related to disease development. Finally, future prospects for the association of CypA and apoptosis are discussed, and a comprehensive understanding of the effects of CypA on apoptosis in relation to diseases is expected to provide new insights into the design of CypA as a therapeutic target for diseases.
作者机构：
[Jiang Xu] Molecular and Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA, 90089, USA. foxjuly@gmail.com;[Ao Li; Xiao Lei; Shuxing Li] Molecular and Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA, 90089, USA;[Jun Li] Institute of Clinical Medicine, The First Affiliated Hospital of University of South China, Hengyang, Hunan, 421001, People's Republic of China;[Lin Chen] Molecular and Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, CA, 90089, USA. linchen@usc.edu
通讯机构：
[Jiang Xu; Lin Chen] M;Molecular and Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, USA<&wdkj&>Molecular and Computational Biology, Department of Biological Sciences, University of Southern California, Los Angeles, USA
关键词：
Three finger protein;E. coli recombinant expression;Inclusion body refolding;Disulfide bond formation;Oxidation refolding
摘要：
The three-finger proteins are a collection of disulfide bond rich proteins of great biomedical interests. Scalable recombinant expression and purification of bioactive three-finger proteins is quite difficult. We introduce a working pipeline for expression, purification and validation of disulfide-bond rich three-finger proteins using E. coli as the expression host. With this pipeline, we have successfully obtained highly purified and bioactive recombinant α-Βungarotoxin, k-Bungarotoxin, Hannalgesin, Mambalgin-1, α-Cobratoxin, MTα, Slurp1, Pate B etc. Milligrams to hundreds of milligrams of recombinant three finger proteins were obtained within weeks in the lab. The recombinant proteins showed specificity in binding assay and six of them were crystallized and structurally validated using X-ray diffraction protein crystallography. Our pipeline allows refolding and purifying recombinant three finger proteins under optimized conditions and can be scaled up for massive production of three finger proteins. As many three finger proteins have attractive therapeutic or research interests and due to the extremely high quality of the recombinant three finger proteins we obtained, our method provides a competitive alternative to either their native counterparts or chemically synthetic ones and should facilitate related research and applications.
关键词：
botulinum toxin;botulinum toxin type A;cancer;pain
摘要：
BACKGROUND: Botulinum toxin type A (BTX-A) is a potential treatment for cancer pain. This study aimed to analyze the effectiveness and safety of BTX-A in the treatment of pain after cancer treatment. PATIENTS AND METHODS: Systematic searches of PubMed, Cochrane Library, and Embase databases were conducted. Randomized controlled trials evaluating the efficacy and safety of BTX-A compared with either placebo or active treatment in patients with pain after cancer treatment were included. The outcomes included pain intensity, quality of life, and adverse events. RESULTS: This systematic review included four studies of which 2 were included in the meta-analysis. Compared with a placebo, BTX-A injection in patients with pain after cancer treatment had a clinically meaningful reduction in self-reported pain post-treatment (mean difference=-1.79 [95% confidence interval (CI), -2.14 to -1.43], P＜0.00001, I²=0%). CONCLUSION: This systematic review and meta-analysis demonstrated that BTX-A is safe and effective for pain relief in patients with pain after cancer treatment.
作者机构：
[Kuang, Wending; Zhang, Yang; Yuan, Mei; Chen, Gang; Luo, Bang; Wang, Yuzheng; Chen, G] Univ South China, Affiliated Hosp 2, Hengyang Med Sch, Dept Neurol, Hengyang 421001, Hunan, Peoples R China.;[Chen, Liucui] Univ South China, Hengyang Med Sch, Sch Pharmaceut Sci, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Chen, G ] U;Univ South China, Affiliated Hosp 2, Hengyang Med Sch, Dept Neurol, Hengyang 421001, Hunan, Peoples R China.
关键词：
Early neurological deterioration;Acute ischemic stroke;Intravenous thrombolysis;Nomogram;Risk prediction
摘要：
OBJECTIVES: Intravenous thrombolysis therapy (IVT) with recombinant tissue plasminogen activator has proven to be a beneficial treatment for acute ischemic stroke (AIS) patients when administered within 4.5h after a stroke. This study aimed to investigate an available and inexpensive predictive tool for early neurological deterioration in AIS. METHODS: Patients admitted to our department with acute stroke who were given IVT with recombinant tissue plasminogen activator within 4.5h of stroke onset were included in the study. The NIH stroke scale (NIHSS) was used to assess patients' neurological state prior to IVT and for 24h after. Early neurological deterioration was defined as occurring if the NIHSS total score increased by≥4 or the NIHSS individual score increased by≥2 compared to baseline. Patients were randomly assigned to training or validation cohorts. RESULTS: Of the 266 AIS patients receiving IVT who were screened, 217 were deemed eligible for the study. Multivariate logistic regression analysis identified smoking history, NIHSS score, homocysteine level, and neutrophil to lymphocyte ratio as independent factors for predicting early neurological deterioration. ROC analysis was used to assess the quality of the resulting nomogram. The AUC for the training dataset was 0.826 (95% CI, 0.719-0.932), and for the validation dataset was 0.887 (95% CI, 0.763-1.000). CONCLUSION: The robustness of this nomogram suggests that it may be a reliable tool for evaluating the progression of AIS after IVT.
作者机构：
[Dou, Chengyun; Xie, Xia] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Infect Dis, Hengyang 421001, Hunan, Peoples R China.;[Zhu, Hongbo] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Med Oncol, Hengyang 421001, Hunan, Peoples R China.;[Cao, Chuangjie; Cao, CJ; Huang, Cuiqin] Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Pathol, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Cao, CJ ] U;Univ South China, Affiliated Hosp 1, Hengyang Med Sch, Dept Pathol, Hengyang 421001, Hunan, Peoples R China.
摘要：
Nonalcoholic fatty liver disease (NAFLD) is a prevalent global liver disorder, posing substantial health risks. Britanin, a bioactive sesquiterpene lactone extracted from Inula japonica, has demonstrated antidiabetic, hypolipidemic, and hepatoprotective attributes. Nonetheless, the precise impact of Britanin on NAFLD and the intricate biological mechanisms underpinning this interaction remain unexplored. We integrated computer-aided methods to unearth shared biological targets and signaling pathways associated with both Britanin and NAFLD. A network was constructed by compiling putative targets associated with Britanin and NAFLD, followed by a stringent screening of key targets and mechanisms through protein-protein interaction analysis along with GO and KEGG pathway enrichment analyses. Molecular docking was integrated as an evaluation tool, culminating in the identification of HO-1 as the pivotal therapeutic target, showcasing a satisfactory binding affinity. The primary mechanism was ascribed to biological processes and pathways linked to oxidative stress, as evidenced by the outcomes of enrichment analyses. Of these, the AMPK/SREBP1c pathway assumed centrality in this mechanism. Furthermore, in vivo experiments substantiated that Britanin effectively curtailed NAFLD development by ameliorating liver injury, modulating hyperlipidemia and hepatic lipid accumulation, and alleviating oxidative stress and apoptosis. In summary, this study demonstrates the potential of Britanin as a promising therapeutic drug against NAFLD.
摘要：
The immune response to Mycoplasma pneumoniae infection plays a key role in clinical symptoms. Previous investigations focused on the pro-inflammatory effects of leukocytes and the pivotal role of epithelial cell metabolic status in finely modulating the inflammatory response have been neglected. Herein, we examined how glycolysis in airway epithelial cells is affected by M. pneumoniae infection in an in vitro model. Additionally, we investigated the contribution of ATP to pulmonary inflammation. Metabolic analysis revealed a marked metabolic shift in bronchial epithelial cells during M. pneumoniae infection, characterized by increased glucose uptake, enhanced aerobic glycolysis, and augmented ATP synthesis. Notably, these metabolic alterations are orchestrated by adaptor proteins, MyD88 and TRAM. The resulting synthesized ATP is released into the extracellular milieu via vesicular exocytosis and pannexin protein channels, leading to a substantial increase in extracellular ATP levels. The conditioned medium supernatant from M. pneumoniae-infected epithelial cells enhances the secretion of both interleukin (IL)-1β and IL-18 by peripheral blood mononuclear cells, partially mediated by the P2X7 purine receptor (P2X7R). In vivo experiments confirm that addition of a conditioned medium exacerbates pulmonary inflammation, which can be attenuated by pre-treatment with a P2X7R inhibitor. Collectively, these findings highlight the significance of airway epithelial aerobic glycolysis in enhancing the pulmonary inflammatory response and aiding pathogen clearance.
期刊：
International Immunopharmacology,2024年131:111854 ISSN：1567-5769
通讯作者：
Cheng, Ailan
作者机构：
[Li, Lanxin; Zhao, Shuang; Xiong, Qinglin] Hunan Engineering Research Center for Early Diagnosis and Treatment of Liver Cancer, Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang, China;[Wang, Baiqi] The Second Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, China;[Cheng, Ailan] Hunan Engineering Research Center for Early Diagnosis and Treatment of Liver Cancer, Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang, China. Electronic address: 375355191@qq.com
通讯机构：
[Cheng, Ailan] H;Hunan Engineering Research Center for Early Diagnosis and Treatment of Liver Cancer, Cancer Research Institute, Hengyang Medical School, University of South China, Hengyang, China. Electronic address:
摘要：
Annexin A1 (ANXA1) is widely expressed in a variety of body tissues and cells and is also involved in tumor development through multiple pathways. The invasion, metastasis, and immune escape of tumor cells depend on the interaction between tumor cells and their surrounding environment. Research shows that ANXA1 can act on a variety of cells in the tumor microenvironment (TME), and subsequently affect the proliferation, invasion and metastasis of tumors. This article describes the role of ANXA1 in the various components of the tumor microenvironment and its mechanism of action, as well as the existing clinical treatment measures related to ANXA1. These findings provide insight for the further design of strategies targeting ANXA1 for the diagnosis and treatment of malignant tumors.
期刊：
Biosensors and Bioelectronics,2024年249:116002 ISSN：0956-5663
通讯作者：
Wang, WG
作者机构：
[Tan, Ting; Wang, Weiguo; Yang, Lin; Cao, Qianqian; Liu, Aizhe; Chen, Lijing; Deng, Yuqian] Univ South China, Inst Pharm & Pharmacol, Hengyang 421000, Hunan, Peoples R China.;[Li, Ranhui; Duan, Minghui] Univ South China, Inst Pathogen Biol, Hengyang Med Sch, Hengyang 421000, Hunan, Peoples R China.
通讯机构：
[Wang, WG ] U;Univ South China, Inst Pharm & Pharmacol, Hengyang 421000, Hunan, Peoples R China.
关键词：
Ferrous disulfide;Nickel doping;Oxidase mimics;Total antioxidant capacity;Transition metal sulfides
摘要：
The development of nanomaterials that mimic oxidase-like activities has recently attracted an increasing amount of attention. Obtaining highly active and cost-effective oxidase mimics has posed a significant challenge in this area of research. In this study, we successfully synthesized nickel-doped ferrous disulfide nanocubes (Ni-FeS(2)) via a facile one-step method. Characterization by scanning electron microscopy (SEM) and transmission electron microscopy (TEM) revealed that Ni was predominantly distributed within the surface layer of the Ni-FeS(2) nanocubes. The incorporation of nickel in density functional theory (DFT) calculations effectively reduced the d-band center of Fe, resulting in weakened adsorption to intermediates and thereby enhancing its catalytic efficiency. Moreover, we developed a novel approach based on Ni-FeS(2) (the Ni-FeS(2) method) for detecting reducing substances, which exhibited good sensitivity toward ascorbic acid (AA), glutathione (GSH), and cysteine (Cys). Remarkably, the established Ni-FeS(2) method was successfully employed for in vitro assessment of total antioxidant capacity (TAC) in cellular and organ samples, thereby enabling discrimination between normal, senescent, and malignant cells as well as distinguishing among healthy liver tissue, cancerous liver tissue, and metastatic organs.
摘要：
Ferroptosis is a newly recognized type of regulated cell death that is characterized by the accumulation of iron and lipid peroxides in cells. Studies have shown that ferroptosis plays a significant role in the pathogenesis of various diseases, including cardiovascular diseases. In cardiovascular disease, ferroptosis is associated with ischemia-reperfusion injury, myocardial infarction, heart failure, and atherosclerosis. The molecular mechanisms underlying ferroptosis include the iron-dependent accumulation of lipid peroxidation products, glutathione depletion, and dysregulation of lipid metabolism, among others. This review aims to summarize the current knowledge of the molecular mechanisms of ferroptosis in cardiovascular disease and discuss the potential therapeutic strategies targeting ferroptosis as a treatment for cardiovascular disease.
作者机构：
School of Pharmacy, Hengyang Medical College, University of South China, 28 Western Changsheng Road, Hengyang, Hunan, 421001, China;[Hao, Bo] Department of Pharmacy, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China;Phase I Clinical Trial Center, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China;[Yan, Ting] Department of Breast and Thyroid Surgery, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China;[Wang, Siyu] Department of Medical Oncology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China
通讯机构：
[Taolan Zhang] D;Department of Pharmacy, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China<&wdkj&>Phase I Clinical Trial Center, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, 421001, China
关键词：
Breast cancer;Immune infiltration;Malignant pericardial effusion;Prognostic model;Subtypes;Web-based tool
摘要：
BACKGROUND: Malignant pericardial effusion (MPE) is a common complication of advanced breast cancer (BRCA) and plays an important role in BRCA. This study is aims to construct a prognostic model based on MPE-related genes for predicting the prognosis of breast cancer. METHODS: The BRCA samples are analyzed based on the expression of MPE-related genes by using an unsupervised cluster analysis method. This study processes the data by least absolute shrinkage and selection operator and multivariate Cox analysis, and uses machine learning algorithms to construct BRCA prognostic model and develop web tool. RESULTS: BRCA patients are classified into three clusters and a BRCA prognostic model is constructed containing 9 MPE-related genes. There are significant differences in signature pathways, immune infiltration, immunotherapy response and drug sensitivity testing between the high and low-risk groups. Of note, a web-based tool (http://wys.helyly.top/cox.html) is developed to predict overall survival as well as drug-therapy response of BRCA patients quickly and conveniently, which can provide a basis for clinicians to formulate individualized treatment plans. CONCLUSION: The MPE-related prognostic model developed in this study can be used as an effective tool for predicting the prognosis of BRCA and provides new insights for the diagnosis and treatment of BRCA patients.
摘要：
HuR (Human antigen R) is an RNA binding protein (RBP) that specifically binds to certain RNA sequences, influencing post-transcriptional regulation. HuR is primarily involved in tumor regulation, as well as cell growth, proliferation, inflammation, and angiogenesis. HuR is implicated in endothelial activation, smooth muscle proliferation, inflammatory response, macrophage apoptosis, lipid regulation, and autophagy, playing a crucial regulatory role in atherosclerosis. Accumulating evidence suggests that HuR has dual roles in AS. On the one hand, HuR expedites the development of AS by facilitating endothelial activation, smooth muscle proliferation, and inflammation. On the contrary, it exerts beneficial effects by reducing macrophage apoptosis, regulating lipid efflux, and increasing autophagy. In this review, we aim to provide a comprehensive summary of the role of HuR in the development of AS by examining its involvement in cellular mechanisms, inflammation, autophagy, and apoptosis. Additionally, we discuss the mechanisms of drugs that target HuR, with the goal of offering new perspectives for the treatment of AS.
期刊：
JOURNAL OF NUTRITIONAL BIOCHEMISTRY,2024年126:109581 ISSN：0955-2863
通讯作者：
Huang, Shufang;Fu, Nian
作者机构：
[Deng, Yuting; Hu, Mengsi] The Affiliated Nanhua Hospital, Department of Gastroenterology, Hunan Provincial Clinical Research Center of Metabolic Associated Fatty Liver Disease, Hengyang Medical School, University of South China, Hengyang, Hunan, 421002, China;[Huang, Shufang] The Affiliated Nanhua Hospital, Hunan Provincial Clinical Research Center of Metabolic Associated Fatty Liver Disease, Hengyang Medical School, University of South China, Hengyang, Hunan, 421002, China;The Affiliated Nanhua Hospital, Institute of Clinical Research, Hengyang Medical School, University of South China, Hengyang, Hunan, 421002, China;[Fu, Nian] The Affiliated Nanhua Hospital, Department of Gastroenterology, Hunan Provincial Clinical Research Center of Metabolic Associated Fatty Liver Disease, Hengyang Medical School, University of South China, Hengyang, Hunan, 421002, China<&wdkj&>The Affiliated Nanhua Hospital, Institute of Clinical Research, Hengyang Medical School, University of South China, Hengyang, Hunan, 421002, China
通讯机构：
[Shufang Huang] T;The Affiliated Nanhua Hospital, Hunan Provincial Clinical Research Center of Metabolic Associated Fatty Liver Disease, Hengyang Medical School, University of South China, Hengyang, Hunan, 421002, China
摘要：
Non-alcoholic fatty liver disease (NAFLD), also known as metabolically associated fatty liver disease (MAFLD), is a systemic metabolic disease characterized by lipid accumulation in the liver, lipid toxicity, insulin resistance, intestinal dysbiosis, and inflammation that can progress from simple steatosis to nonalcoholic steatohepatitis (NASH) and even cirrhosis or cancer. It is the most prevalent illness threatening world health. Currently, there are almost no approved drug interventions for MAFLD, mainly dietary changes and exercise to control weight and regulate metabolic disorders. Meanwhile, the metabolic pathway involved in amino acid metabolism also influences the onset and development of MAFLD in the body, and most amino acid metabolism takes place in the liver. Essential amino acids are those amino acids that must be supplemented from outside the diet and that cannot be synthesized in the body or cannot be synthesized at a rate sufficient to meet the body's needs, including leucine, isoleucine, valine (collectively known as branched-chain amino acids), tryptophan, phenylalanine (which are aromatic amino acids), histidine, methionine, threonine and lysine. The metabolic balance of the body is closely linked to these essential amino acids, and essential amino acids are closely linked to the pathophysiological process of MAFLD. In this paper, we will focus on the metabolism of essential amino acids in the body and further explore the therapeutic strategies for MAFLD based on the studies conducted in recent years.
