ChemistrySelect
·
2026
·Vol. 11
·期 2
·e03878
·
IF 2
Wenfeng Xie,Zhongxiao Li,Yuwei Hao,Shouzheng Jiao,Siqiao Zhang,Fanghua Pan,Lu Han,Ruping Liu,Zhicheng Sun
In this study, grapefruit essential oil (GEO)-loaded microcapsules encapsulated within silver/calcium alginate (Ag/CA) composite shells were successfully fabricated through an electrostatic spray technique. First, a pre-emulsion of GEO was prepared in the presence of sodium dodecyl sulfate (SDS) and sodium alginate (SA). Subsequently, the pre-emulsion was sprayed into an aqueous calcium chloride solution using electrostatic spray technique in the form of microdroplets, yielding calcium alginate (CA) gel microcapsules encapsulating GEO. Then, the previously prepared CA@GEO microcapsules were introduced into hydroxymethyl aminomethane (Tris) buffer solution, followed by the addition of dopamine hydrochloride. This enabled dopamine adsorption onto the microcapsule surface and subsequent polymerization to form a polydopamine layer. Finally, the dopamine hydrochloride-treated CA@GEO microcapsules were placed into a silver ammonia solution, where coordination interaction occurred between the polydopamine (PDA) on the microcapsule surface and silver ammonia particles. Subsequent in situ reduction, facilitated by glucose acting as a reducing agent, resulted in the formation of a silver shell on the microcapsule surface. The morphology and structure of the microcapsules were comprehensively characterized using scanning electron microscopy (SEM), particle size distribution analysis, x-ray photoelectron spectroscopy (XPS), etc. Moreover, the sustained release and antibacterial properties of Ag/CA@GEO microcapsules were investigated. Graphical A pre-emulsion of grapefruit essential oil (GEO) was prepared with sodium dodecyl sulfate and sodium alginate as stabilizers. Calcium alginate (CA) gel microcapsules encapsulating GEO were prepared by electrostatically spraying the pre-emulsion as microdroplets into an aqueous calcium chloride solution. Subsequently, a polydopamine layer was deposited onto the microsphere surfaces; this layer chelated silver ammonia ions and facilitated in-situ reduction in the presence of glucose, ultimately yielding a dense silver shell on the microspheres.
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高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
·
2025
·
IF 4.7
Hong Yang,Yongxin Chen,Guoping Wu,Pengyan Ren,Tingting Chen,Jia Liu,Bao Zhang,Xiao Ma,Feng Jiang,Yue Li,Ling Tao,Xiangchun Shen
Fructus Alpiniae Zerumbet (FAZ), a folk medicinal herb used by the Miao people in Guizhou, China, is rich in 1,8-Cineole — a bioactive monoterpene oxide with antioxidant and neuroprotective properties. However, its therapeutic potential against pancreatic β cells dysfunction, a hallmark of type 2 diabetes mellitus (T2DM), remains unexplored. This study investigated the molecular mechanism by which 1,8-Cineole mitigates hyperglycemia induced β cells ferroptosis. Using high-fat and high-sugar diet / streptozotocin (HFSD/STZ) diabetes mellitus type 2-induced model (DM) and high glucose (HG)-treated β cells model. We demonstrated that 1,8-Cineole ameliorated pancreatic islet structural disorganization and pathological glycogen deposition in diabetic mice. Mechanistically, 1,8-Cineole suppressed lipid peroxidation and iron overload while restoring the expression of ferroptosis markers (GPX4 and COX2). It concurrently resolved autophagy deficiency, evidenced by upregulated LC3II/I ratio, enhanced Beclin-1 expression, and stabilized p62. Bioinformatic analysis of diabetic pancreatic transcriptomes (GEO dataset GSE25724) linked ferroptosis and PI3K/AKT/mTOR signaling to β cells dysfunction. Cellular thermal shift assay (CETSA) and molecular docking confirmed direct binding of 1,8-Cineole to PI3K with favorable binding energy at the catalytic site. Pharmacological validation using 740-YP (YP, a PI3K agonist) and LY294002 (LY, a PI3K inhibitor) revealed that 1,8-Cineole exerted its anti-ferroptotic effects via PI3K/AKT/mTOR pathway activation. Co-treatment with 740-YP synergistically enhanced β cells protection, whereas LY294002 abrogated 1,8-Cineole’s efficacy. Collectively, these findings unveil 1,8-Cineole as a novel PI3K/AKT/mTOR activator that rescues β cells function via coordinated regulation of autophagy and ferroptosis, thereby providing a mechanistic foundation for its therapeutic application in DM.
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PubMed
高影响因子
IONICS
·
2023
·Vol. 30
·期 2
·697-708
·
IF 2.8
Wang Guanzheng,Lei Huazhi,Wang Zheng,Yuan Zhentao,Zhan Zhaolin,Li Lu,Wang Xiao
Amorphous GeO 2 @C anode materials were successfully prepared from commercial GeO 2 and C 6 H 12 O 6 .H 2 O by a hydrothermal method combined with sintering under nitrogen atmosphere protection. The anode materials showed an ideal spherical shape of about 3 μm and their surface was uniformly covered with C. GeO 2 @C composite anodes exhibited better storage performance for Li-ion batteries. The discharge-specific capacities of GeO 2 @C-3 sample were 1143, 1049, 776, 551, and 308 mAh g -1 at current densities of 0.2, 0.5, 1, 2, and 5 A g -1 , and restored to 1136 mAh g -1 when the current density returned to 0.2 A g -1 . The reversible specific capacity was 756 mAhg -1 after 1000 cycles at a current density of 1 A g -1 . The GeO 2 @C anode was stable in the process of charge and discharge, and no obvious pulverization occurred. GeO 2 @C composites stabilized the electrochemical properties through carbon and amorphous structure to improve the overall electrical conductivity in Li + embedding/de-embedding processes.
研究领域:
材料科学
·
电化学
·
纳米技术
·
储能
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高影响因子
Experimental and Therapeutic Medicine
·
2021
·Vol. 22
·期 1
·1-8
·
IF 2.447
Peng Yi,Xiongfeng Xu,Jiawei Yao,Bo Qiu
Genetics and epigenetics are important subjects in the field of osteoarthritis (OA) research. DNA methylation may affect gene transcription, but the specific mechanisms have remained to be fully elucidated. In the present study, the ChAMP methylation analysis package was used to identify differentially methylated genes (DMGs) from the dataset GSE63695 from the Gene Expression Omnibus (GEO) database. The distribution of differentially methylated sites (DMS) and the total array sites across the genome were analyzed by enrichment analysis. Subsequently, two mRNA expression profiling datasets, GSE114007 and GSE113825, were obtained from the GEO database and common differentially expressed genes (DEGs) were identified using the Limma package. Key genes were screened by analyzing the distribution of DMS across the genome consisting of DEGs and DMGs. A total of 1,662 and 1,986 DEGs were identified between OA and normal human cartilage from the GSE113825 and GSE114007 dataset, respectively. A further screening revealed 292 genes with common differences between the two datasets. A total of 574 DMS containing 394 DMGs were observed between OA and normal cartilage. Integrative analysis revealed a corresponding subset of 15 genes. Of these, 6 genes were verified by reverse transcription‑quantitative PCR, confirming that the mRNA expression of 5 genes (MAP1B, FNDC1, ANLN, SCNN1A and STC2) in OA cartilage was consistent with the mRNA expression from the analysis of the datasets. Upon treatment with the DNA methylation inhibitor 5‑aza‑2'‑deoxycytidine, the mRNA levels of FNDC1 and SCNN1A were decreased, and no significant alteration in the mRNA levels of MAP1B, ANLN, KCNN4 and STC2 was observed. The incidence of differential methylation varied in subregions of the genome and the effects on transcription were associated with the distribution of DEGs across the genome. The regulation of this appears more complex than initially postulated. Combining the data on epigenetic differences of OA with the genome or transcriptome data for analysis may improve the understanding of the pathophysiological processes of OA. FNDC1 and SCNN1A may potentially be valuable biomarkers for OA.
研究领域:
遗传学
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表观遗传学
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骨科
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分子生物学
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PubMed
高影响因子
Frontiers in Oncology
·
2022
·
IF 5.738
Youfu Zhang,Xuyang Wang,Huaxiang Wang,Yi Jiang,Zhidan Xu,Laibang Luo
Background Elevated Small Nuclear Ribonucleoprotein Polypeptide A ( SNRPA ) can enhance tumor cell growth and proliferation in various cancers. However, rarely studies focus on the comprehensive analysis of SNRPA in hepatocellular carcinoma (HCC). Methods TCGA and GEO databases were used to analyze the mRNA expression of SNRPA in HCC. Protein expression of SNAPA was validated using immunohistochemistry. Stably transfected HCC cells were used to investigate the role of SNRPA in the progression of HCC. The functional enrichment analysis was utilized for the biological function prediction. The CIBERSORT and ssGSEA algorithms were used to evaluate the composition of the tumor microenvironment and immunocyte infiltration ratio. Results The SNRPA expression was upregulated in HCC and positively correlated with tumor stage and grade. SNRPA overexpression were independent risk factors for poor overall survival (OS) and recurrence-free survival (RFS). In patients with early-stage disease, low alpha-fetoprotein expression, and better differentiation, SNRPA still exhibited the excellent prognostic value. Knockdown of SNRPA inhibited the proliferation and migration while promoting the apoptosis of HCC cells. Higher methylation of the CpG site cg16596691 correlated with longer OS in HCC patients. Genes co-expressed with SNRPA were overexpressed in HCC and correlated with shorter OS. The GO and KEGG enrichment analysis showed that SNRPA expression was related to mRNA splicing, spliceosome signaling. GSEA demonstrated that the main enrichment pathway of SNRPA-related differential genes was spliceosome signaling, cell cycle signaling, P53 signaling pathway, T cell receptor signaling pathway, natural killer cell-mediated signaling. CIBERSORT and ssGSEA algorithm revealed that SNRPA was mainly associated with the higher proportion of CD8+T cells, T cells follicular helper, T cells regulatory, Macrophages M0, and the lower proportion of T cells CD4 memory resting, NK cells resting, Monocytes, and Mast cells resting. Conclusion Elevated SNRPA enhances tumor cell proliferation and correlated with poor prognosis and immune infiltrates in patients with HCC.
研究领域:
肿瘤学
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分子生物学
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免疫学
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生物信息学
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PubMed
高影响因子
Human Cell
·
2023
·Vol. 36
·期 3
·972-986
·
IF 4.3
Liu Naiquan,Liu Dajun,Cao Shiyu,Lei Jing
Renal fibrosis is the common final pathway in many renal diseases regardless of the underlying etiology. Adipocyte enhancer-binding protein 1 (AEBP1) was reported to play a vital role in the development of organ fibrosis, but its role in renal fibrosis has not been reported. Thus, the aim of this study was to investigate the possible function of AEBP1 in renal fibrosis and the mechanism associated with the β-catenin signaling pathway. A total of 83 genes upregulated after unilateral ureteral obstruction (UUO) were screened from two Gene Expression Omnibus (GEO) datasets and subjected to Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Among them, AEBP1 was enriched in collagen binding and the regulation of collagen fibril organization and was confirmed to be upregulated in UUO kidneys and TGF-β1-induced cells. Knockdown of AEBP1 ameliorated renal fibrosis via reducing collagen accumulation, inhibiting epithelial–mesenchymal transition and fibroblast transformation, as evidenced by decreases in the expression of collagen I and III, Col1a1, Col3a1, fibronectin, Snail, α-SMA, as well as collagen-specific staining of kidney tissues, whereas the E-cadherin was increased. Besides, AEBP1 silencing inhibited the expression of β-catenin in nucleus and β-catenin downstream proteins (Axin2, Myc, and Ccnd1). Continuously active β-catenin–S33Y further restored the inhibitory effect of AEBP1 silencing on renal fibrosis. These findings indicate that knockdown of AEBP1 could potentially slow down renal fibrosis by blocking the β-catenin signaling pathway, highlighting the potential of AEBP1 as a therapeutic target for renal fibrosis.
研究领域:
肾病学
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分子生物学
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细胞生物学
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病理生理学
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PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2024
·
IF 2.5
Shuangliu Chen,Yalan Pan,Yang Guo,Xiaoxian Sun,Xue Bai,Mengmin Liu,Lining Wang,Jiřimutu Xiao,Cheng Chen,Yong Ma
This study utilized bioinformatics and data mining techniques to explore the molecular mechanism of curcumin in treating osteoporosis (OP) through the lens of ferroptosis, thereby identifying novel therapeutic targets. The datasets GSE35958, GSE35956, GSE7429, and GSE7158 were obtained from the Gene Expression Omnibus (GEO) database. GSE35958 and GSE35956 were employed as training sets for data integration, while GSE7429 and GSE7158 served as independent validation sets. Through retrieval from the FerrDb database, iron death-related genes (FRGs) were identified, and the differentially expressed genes (DEGs) were intersected to obtain differentially expressed FRGs (DEFRGs). Subsequently, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted, followed by the construction of a Protein-Protein Interaction (PPI) network to identify Hub genes. The DGIdb database was utilized to predict candidate drugs associated with the Hub genes, and molecular docking and in vitro experiments confirmed that curcumin targets the Hub genes EGFR and PTGS2.Through in vitro testing of curcumin on BMSC cells, researchers examined cell vitality, iron death, osteogenic differentiation, mineralization, and the impact on EGFR and PTGS2 levels. The analysis yielded 2212 DEGs, 484 FRGs, with 45 FDEGs at the intersection. GO analysis revealed involvement in regulating mitochondrial proteins, amino acid transport across plasma membranes, and protein ubiquitination. KEGG pathway analysis indicated associations with iron death, FoxO signaling, mTOR signaling, cell aging, osteoclast differentiation, and GSH metabolism. Utilizing the MCC algorithm, five Hub genes were identified: MAPK3, PTGS2, TGFB1, CYBB, and EGFR, showing diagnostic potential for iron death. Curcumin displayed affinity for EGFR and PTGS2, mitigating iron-induced effects on BMSCs such as increased reactive oxygen species, Fe3+ levels, and decreased mitochondrial membrane potential. Furthermore, curcumin reversed these effects, suggesting EGFR and PTGS2 as targets for curcumin to inhibit BMSC ferroptosis and potentially delay osteoporosis development. Maintaining iron homeostasis and targeting BMSC ferroptosis could offer therapeutic avenues for iron overload-induced osteoporosis.
研究领域:
生物信息学
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药理学
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分子生物学
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医学遗传学
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PubMed
高影响因子
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