cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.29877428.v1
title: Uncovering the mechanistic basis of <i>Rheum palmatum</i> L. (rhubarb) in the treatment of chronic kidney disease: an integrative approach using network pharmacology, molecular docking, and experimental validation

description: <i>Rheum palmatum</i> L. (Rhubarb) has shown potential in managing Chronic Kidney Disease (CKD) but its protective mechanisms remain unclear. This study investigates rhubarb’s therapeutic effects and underlying mechanisms in CKD. High-performance liquid chromatography (HPLC) established a rhubarb fingerprint to ensure quality control. Network pharmacology and Mendelian randomization identified primary CKD therapeutic targets. Inflammation, oxidative stress, and renal performance were assessed through ELISAs and biochemical tests. Renal structure and fibrosis were examined using hematoxylin-eosin and Masson staining. Protein expression related to fibrosis, apoptosis, and NF-κB pathway activity was measured <i>via</i> Western blotting. Discovery Studio 2019 (DS 2019) was used for molecular docking. HPLC fingerprinting confirmed high batch-to-batch consistency of rhubarb, identifying five key anthraquinones (aloe-emodin, rhein, emodin, chrysophanol, physcion) with similarity indices &gt;0.91. Network pharmacology identified 19 active compounds targeting 2,597 CKD-related proteins, with 47 overlapping targets including IL6, TNF, TP53, CASP3, and IL1B as core nodes. MR analysis demonstrated a statistically significant causal association between TNF and CKD (OR = 1.02, <i>p</i> &lt; 0.05), with positive trends for IL6 and CASP3. In CKD rat models, rhubarb significantly improved renal function by reducing blood urea nitrogen (BUN), serum creatinine (SCr), and uric acid (UA) levels (<i>p</i> &lt; 0.05). Histopathology showed reduced glomerulosclerosis, tubular atrophy, interstitial fibrosis, and inflammatory infiltration after treatment. Rhubarb markedly decreased renal fibrosis markers including collagen I, collagen III, α-SMA, and TGF-β (<i>p</i> &lt; 0.01). Pro-inflammatory cytokines IL-6, IL-1β, and TNF-α levels were significantly suppressed (<i>p</i> &lt; 0.001). Antioxidant enzyme activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were restored, while lipid peroxidation (LPO) was reduced (<i>p</i> &lt; 0.05). Rhubarb inhibited NF-κB pathway activation by lowering phosphorylated NF-κB and IκBα, and increasing total IκBα expression (<i>p</i> &lt; 0.01). Apoptosis-related proteins showed upregulated Bcl-2 and downregulated Bax and cleaved caspase-3 expression (<i>p</i> &lt; 0.05). Molecular docking confirmed strong binding affinities of rhubarb’s core compounds with key targets such as TNF and IL6, supporting their therapeutic roles. Rhubarb significantly reduces renal impairment, fibrosis, inflammation, and apoptosis through the NF-κB pathway, supporting its traditional use and potential as an adjunct therapy for CKD.
DOI: 10.6084/m9.figshare.29655687
title: Wen-Shen-Tong-Luo-Zhi-Tong Decoction alleviates bone loss in aged mice by suppressing LONP1-mediated macrophage senescence

description: Aging leads to senile osteoporosis (SOP), marked by bone loss and increased fracture risk. Macrophages, as active immune cells in bone tissue, play an important role in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) during aging. Wen-Shen-Tong-Luo-Zhi-Tong Decoction (WSTLZTD), a traditional Chinese herbal formula, has been clinically validated for its efficacy in treating SOP. However, the specific mechanisms by which WSTLZTD exerts its anti-SOP effects—particularly through modulating macrophage senescence—remain unclear. The study aims to elucidate the role of WSTLZTD in macrophage senescence and SOP. Aged mice received low, medium, high-dose WSTLZTD. Bone loss was evaluated via micro-computed tomography, hematoxylin and eosin staining and osteocalcin, tartrate-resistant acid phosphatase marker analysis. Macrophage senescence detection (β-galactosidase staining, p16, p21) and molecular mechanisms by Western blot, immunohistochemistry, immunofluorescence method were investigated. Macrophage-conditioned medium’s effects on BMSC osteogenesis and mitochondrial function were assessed through alkaline phosphatase, Alizarin Red S staining, reactive oxygen species and JC-1 mitochondrial membrane potential (ΔΨm) assays. <i>In vivo</i> experiments demonstrated that WSTLZTD effectively ameliorated macrophage senescence and osteoporosis in naturally aged mice. Mechanistically, high-dose WSTLZTD attenuated senescence in bone marrow-derived macrophages by mediating LONP1, concurrently suppressing the cyclic GMP-AMP synthase (cGAS)/STING signaling pathway in BMSCs, thereby enhancing osteogenic differentiation of BMSCs. <i>In vitro</i> studies further confirmed that WSTLZTD-containing serum attenuated the senescent phenotype of macrophages. Notably, the LONP1 inhibitor, LONP1-IN-2, was found to diminish the anti-senescence effects of WSTLZTD on macrophages and BMSC osteogenesis. WSTLZTD potentially modulate macrophage senescence via LONP1, which subsequently suppresses the activation of the cGAS/STING pathway in BMSCs, ultimately promoting their osteogenic differentiation and ameliorating osteoporosis.
DOI: 10.6084/m9.figshare.29655687.v1
title: Wen-Shen-Tong-Luo-Zhi-Tong Decoction alleviates bone loss in aged mice by suppressing LONP1-mediated macrophage senescence

description: Aging leads to senile osteoporosis (SOP), marked by bone loss and increased fracture risk. Macrophages, as active immune cells in bone tissue, play an important role in osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) during aging. Wen-Shen-Tong-Luo-Zhi-Tong Decoction (WSTLZTD), a traditional Chinese herbal formula, has been clinically validated for its efficacy in treating SOP. However, the specific mechanisms by which WSTLZTD exerts its anti-SOP effects—particularly through modulating macrophage senescence—remain unclear. The study aims to elucidate the role of WSTLZTD in macrophage senescence and SOP. Aged mice received low, medium, high-dose WSTLZTD. Bone loss was evaluated via micro-computed tomography, hematoxylin and eosin staining and osteocalcin, tartrate-resistant acid phosphatase marker analysis. Macrophage senescence detection (β-galactosidase staining, p16, p21) and molecular mechanisms by Western blot, immunohistochemistry, immunofluorescence method were investigated. Macrophage-conditioned medium’s effects on BMSC osteogenesis and mitochondrial function were assessed through alkaline phosphatase, Alizarin Red S staining, reactive oxygen species and JC-1 mitochondrial membrane potential (ΔΨm) assays. <i>In vivo</i> experiments demonstrated that WSTLZTD effectively ameliorated macrophage senescence and osteoporosis in naturally aged mice. Mechanistically, high-dose WSTLZTD attenuated senescence in bone marrow-derived macrophages by mediating LONP1, concurrently suppressing the cyclic GMP-AMP synthase (cGAS)/STING signaling pathway in BMSCs, thereby enhancing osteogenic differentiation of BMSCs. <i>In vitro</i> studies further confirmed that WSTLZTD-containing serum attenuated the senescent phenotype of macrophages. Notably, the LONP1 inhibitor, LONP1-IN-2, was found to diminish the anti-senescence effects of WSTLZTD on macrophages and BMSC osteogenesis. WSTLZTD potentially modulate macrophage senescence via LONP1, which subsequently suppresses the activation of the cGAS/STING pathway in BMSCs, ultimately promoting their osteogenic differentiation and ameliorating osteoporosis.
DOI: 10.6084/m9.figshare.30103563
title: Essential oils expose diverse targets on non-enveloped ScV-L-A totivirus

description: The spread of novel viruses substantiates the need for alternative antiviral agents. Plant-based extracts, such as essential oils (EOs), are highly relevant due to their generally human-friendly nature and broad spectrum of bioactive properties. Most EO antiviral activity is targeting enveloped viruses. <i>Orthototiviridae</i> family yeast virus ScV-L-A offers a novel, safe, non-enveloped virus model system for antiviral substance evaluation. This study aimed to investigate the antiviral efficacy of EOs and their constituents against non-enveloped ScV-L-A totivirus. The composition of EOs was determined using GC-MS. Native ScV-L-A viral particles were prepared from yeast cells <i>via</i> cesium chloride gradient ultracentrifugation. The antiviral effect of EOs and their principal components was evaluated by following the synthesis of radio-labeled viral transcripts. TEM was employed to investigate the impact of target substances on ScV-L-A capsid integrity. Tested EOs inhibited viral RNA polymerase activity in both liquid and vapor phases. Citral-rich EOs exhibited the strongest antiviral action, with lemon myrtle EO possessing the lowest half-maximal inhibitory concentration and highest timewise efficacy. Coriander and mandarin EOs showed the lowest polymerase-inhibiting capacity. EOs were more efficient compared to the action of single compounds. All EOs except for that of mandarin, dominated by limonene, were more effective in the liquid rather than the vapor phase. Tea tree and mandarin EOs were found to damage ScV-L-A capsid structure. This study highlighted the efficacy of EOs in targeting non-enveloped viruses and revealed their potential for sustainable control of viral infection.
DOI: 10.6084/m9.figshare.29094156
title: A triterpene-enriched natural extract from <i>Eucalyptus tereticornis</i> modulates the expression of genes involved in adipogenesis, lipolysis, and extracellular matrix remodeling in a primary human and mouse cell line adipocyte

description: Obesity induces alterations in adipocyte size, tissue inflammation, vascularization, and extracellular matrix composition. Previous studies have shown that a leaf extract of <i>Eucalyptus tereticornis</i> Sm. (Myrtaceae), with ursolic acid, oleanolic acid, and ursolic acid lactone mixed with minor metabolites, provided a superior antiobesity effect than reconstituted triterpenoid mixtures in adipocyte cell lines and a pre-diabetic mouse model. Further identification of the molecular mechanisms of action of this mixture of triterpenes is required. This study analyzes the effect of the natural extract and its components on early RNA expression profiles in human primary cultured adipocytes and a mouse cell line. RNA was sequenced using the DNBseq platform and the EnrichR software to perform gene enrichment analysis using the Gene Ontology database, Kyoto Encyclopedia of Genes and Genomes, and Reactome. To conduct clustering analysis, the normalized counts of each gene and applied k-means clustering were standardized. The combination of molecules in the natural extract has an additive or synergic effect that increases the number of genes regulated associated with the biological functionality of differentiating adipocytes, with UAL playing a central role. The natural extract modulates PPAR, Wnt, and Extracellular Matrix organization pathways significantly in both cellular models. Remarkably, the extract downregulates the expression of genes involved in lipid metabolism, adipogenesis, and adipocyte fat load, such as PRKAR2B, LPIN1, FABP4, Scd1, MC5R, CD36, PEG10, and HMGCS1. Our study shows that <i>Eucalyptus tereticornis</i> extract is a promising option for treating adipocyte tissue dysfunction derived from obesity.
DOI: 10.6084/m9.figshare.29094156.v1
title: A triterpene-enriched natural extract from <i>Eucalyptus tereticornis</i> modulates the expression of genes involved in adipogenesis, lipolysis, and extracellular matrix remodeling in a primary human and mouse cell line adipocyte

description: Obesity induces alterations in adipocyte size, tissue inflammation, vascularization, and extracellular matrix composition. Previous studies have shown that a leaf extract of <i>Eucalyptus tereticornis</i> Sm. (Myrtaceae), with ursolic acid, oleanolic acid, and ursolic acid lactone mixed with minor metabolites, provided a superior antiobesity effect than reconstituted triterpenoid mixtures in adipocyte cell lines and a pre-diabetic mouse model. Further identification of the molecular mechanisms of action of this mixture of triterpenes is required. This study analyzes the effect of the natural extract and its components on early RNA expression profiles in human primary cultured adipocytes and a mouse cell line. RNA was sequenced using the DNBseq platform and the EnrichR software to perform gene enrichment analysis using the Gene Ontology database, Kyoto Encyclopedia of Genes and Genomes, and Reactome. To conduct clustering analysis, the normalized counts of each gene and applied k-means clustering were standardized. The combination of molecules in the natural extract has an additive or synergic effect that increases the number of genes regulated associated with the biological functionality of differentiating adipocytes, with UAL playing a central role. The natural extract modulates PPAR, Wnt, and Extracellular Matrix organization pathways significantly in both cellular models. Remarkably, the extract downregulates the expression of genes involved in lipid metabolism, adipogenesis, and adipocyte fat load, such as PRKAR2B, LPIN1, FABP4, Scd1, MC5R, CD36, PEG10, and HMGCS1. Our study shows that <i>Eucalyptus tereticornis</i> extract is a promising option for treating adipocyte tissue dysfunction derived from obesity.
DOI: 10.6084/m9.figshare.30103563.v1
title: Essential oils expose diverse targets on non-enveloped ScV-L-A totivirus

description: The spread of novel viruses substantiates the need for alternative antiviral agents. Plant-based extracts, such as essential oils (EOs), are highly relevant due to their generally human-friendly nature and broad spectrum of bioactive properties. Most EO antiviral activity is targeting enveloped viruses. <i>Orthototiviridae</i> family yeast virus ScV-L-A offers a novel, safe, non-enveloped virus model system for antiviral substance evaluation. This study aimed to investigate the antiviral efficacy of EOs and their constituents against non-enveloped ScV-L-A totivirus. The composition of EOs was determined using GC-MS. Native ScV-L-A viral particles were prepared from yeast cells <i>via</i> cesium chloride gradient ultracentrifugation. The antiviral effect of EOs and their principal components was evaluated by following the synthesis of radio-labeled viral transcripts. TEM was employed to investigate the impact of target substances on ScV-L-A capsid integrity. Tested EOs inhibited viral RNA polymerase activity in both liquid and vapor phases. Citral-rich EOs exhibited the strongest antiviral action, with lemon myrtle EO possessing the lowest half-maximal inhibitory concentration and highest timewise efficacy. Coriander and mandarin EOs showed the lowest polymerase-inhibiting capacity. EOs were more efficient compared to the action of single compounds. All EOs except for that of mandarin, dominated by limonene, were more effective in the liquid rather than the vapor phase. Tea tree and mandarin EOs were found to damage ScV-L-A capsid structure. This study highlighted the efficacy of EOs in targeting non-enveloped viruses and revealed their potential for sustainable control of viral infection.
DOI: 10.6084/m9.figshare.29972940
title: The natural statin α,β-dehydromonacolin K exerts anti-secretory effect in human intestinal epithelial cells via a nonsense-mediated mRNA decay-dependent mechanism

description: cAMP-induced intestinal chloride secretion plays a pivotal role in the pathogenesis of secretory diarrheas. In this study, we investigated the antisecretory effects of α,β-dehydromonacolin K, a derivative of lovastatin from <i>Aspergillus sclerotiorum</i>, on cAMP-induced chloride secretion in human T84 cells and fluid secretion in human colonoids. Short-circuit current analyses and swelling assays were used to investigate the effects of α,β-dehydromonacolin K on chloride transport and fluid secretion, respectively. Proteomic analyses were performed to determine the potential anti-diarrheal mechanisms of α,β-dehydromonacolin K. In T84 cells, α,β-dehydromonacolin K inhibited cAMP-induced chloride secretion with an IC<sub>50</sub> of ∼ 6.32 μM. Apical chloride current analyses demonstrated that α,β-dehydromonacolin K inhibited CFTR chloride channels stimulated by cAMP agonists with an IC<sub>50</sub> of ∼ 1 μM. Basolateral potassium current analyses indicated that α,β-dehydromonacolin K had no effect on basolateral potassium channel activities. In a three-dimensional (3D) model of human colonoids, α,β-dehydromonacolin K (20 µM) suppressed both cAMP-induced and calcium-induced fluid secretion by ∼ 70%. Proteomic analyses of human colonoids revealed that α,β-dehydromonacolin K interacted with 33 proteins, including those associated with non-sense-mediated mRNA decay (NMD). Notably, the inhibitory effects of α,β-dehydromonacolin K on cAMP-induced chloride and fluid secretion were significantly diminished in the presence of SMG1i, an inhibitor of serine/threonine-protein kinase SMG1 involved in NMD, suggesting that α,β-dehydromonacolin K inhibits cAMP-induced chloride-driven fluid secretion in human intestinal epithelial cells by mechanisms involving SMG1-dependent NMD pathways. α, β-Dehydromonacolin K represents a promising class of natural compounds that exert antisecretory effects in human intestinal epithelia <i>via</i> a novel mechanism of action involving SMG1 in NMD pathways.
DOI: 10.6084/m9.figshare.29972940.v1
title: The natural statin α,β-dehydromonacolin K exerts anti-secretory effect in human intestinal epithelial cells via a nonsense-mediated mRNA decay-dependent mechanism

description: cAMP-induced intestinal chloride secretion plays a pivotal role in the pathogenesis of secretory diarrheas. In this study, we investigated the antisecretory effects of α,β-dehydromonacolin K, a derivative of lovastatin from <i>Aspergillus sclerotiorum</i>, on cAMP-induced chloride secretion in human T84 cells and fluid secretion in human colonoids. Short-circuit current analyses and swelling assays were used to investigate the effects of α,β-dehydromonacolin K on chloride transport and fluid secretion, respectively. Proteomic analyses were performed to determine the potential anti-diarrheal mechanisms of α,β-dehydromonacolin K. In T84 cells, α,β-dehydromonacolin K inhibited cAMP-induced chloride secretion with an IC<sub>50</sub> of ∼ 6.32 μM. Apical chloride current analyses demonstrated that α,β-dehydromonacolin K inhibited CFTR chloride channels stimulated by cAMP agonists with an IC<sub>50</sub> of ∼ 1 μM. Basolateral potassium current analyses indicated that α,β-dehydromonacolin K had no effect on basolateral potassium channel activities. In a three-dimensional (3D) model of human colonoids, α,β-dehydromonacolin K (20 µM) suppressed both cAMP-induced and calcium-induced fluid secretion by ∼ 70%. Proteomic analyses of human colonoids revealed that α,β-dehydromonacolin K interacted with 33 proteins, including those associated with non-sense-mediated mRNA decay (NMD). Notably, the inhibitory effects of α,β-dehydromonacolin K on cAMP-induced chloride and fluid secretion were significantly diminished in the presence of SMG1i, an inhibitor of serine/threonine-protein kinase SMG1 involved in NMD, suggesting that α,β-dehydromonacolin K inhibits cAMP-induced chloride-driven fluid secretion in human intestinal epithelial cells by mechanisms involving SMG1-dependent NMD pathways. α, β-Dehydromonacolin K represents a promising class of natural compounds that exert antisecretory effects in human intestinal epithelia <i>via</i> a novel mechanism of action involving SMG1 in NMD pathways.
DOI: 10.15468/dl.88bx36
title: Occurrence Download

description: A dataset containing 48490 species occurrences available in GBIF matching the query:
{
 "and" : [
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "OccurrenceStatus is Present",
 "TaxonKey is Pilosa"
 ]
}

 The dataset includes 48490 records from 509 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0002520-260120142942310/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.5517/ccdc.csd.cc2pbvc8
title: CCDC 2483080: Experimental Crystal Structure Determination

description: Related Article: Xiao-Lin Liu, Hao Wang, Xin-Tao Wu, Tian-Lu Sheng|2025|Chin.Chem.Lett.||112213|doi:10.1016/j.cclet.2025.112213
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2pbvd9
title: CCDC 2483081: Experimental Crystal Structure Determination

description: Related Article: Xiao-Lin Liu, Hao Wang, Xin-Tao Wu, Tian-Lu Sheng|2025|Chin.Chem.Lett.||112213|doi:10.1016/j.cclet.2025.112213
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2pbvfb
title: CCDC 2483082: Experimental Crystal Structure Determination

description: Related Article: Xiao-Lin Liu, Hao Wang, Xin-Tao Wu, Tian-Lu Sheng|2025|Chin.Chem.Lett.||112213|doi:10.1016/j.cclet.2025.112213
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2pr1q7
title: CCDC 2494809: Experimental Crystal Structure Determination

description: Related Article: Xian Xu, Shengjie Jiang, Xin Xu|2025|Macromolecules|||doi:10.1021/acs.macromol.5c03266
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2pr1r8
title: CCDC 2494810: Experimental Crystal Structure Determination

description: Related Article: Xian Xu, Shengjie Jiang, Xin Xu|2025|Macromolecules|||doi:10.1021/acs.macromol.5c03266
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2pr1s9
title: CCDC 2494811: Experimental Crystal Structure Determination

description: Related Article: Xian Xu, Shengjie Jiang, Xin Xu|2025|Macromolecules|||doi:10.1021/acs.macromol.5c03266
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.