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Hydrotreating renewable oils over sulfided metal catalysts is commercially applied to produce green diesel, but it requires a continuous sulfur replenishment to maintain catalyst activity, which inevitably results in sulfur contamination and increases production costs. We report a robust P-doped NiAl-oxide catalyst with frustrated Lewis pairs (i.e., P atom bonded with the O atom acts as an electron donor, while the spatially separated Ni atom acts as an electron acceptor) that allows efficient green diesel production without sulfur replenishment. The catalyst runs more than 500 h at a weight hourly space velocity (WHSV) of 28.3 h-1 without deactivation (methyl laurate as a model compound), and is able to completely convert a real feedstock of soybean oil to diesel-range hydrocarbons with selectivity >90% during 500 h of operation. This work is expected to open up a new avenue for designing non-sulfur catalysts that can make the green diesel production greener.
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Four undescribed coumarin derivatives, ficusalt A (1) and ficusalt B (2), a pair of racemic coumarins, (±) ficudimer A (3a/3b), along with ten known amides, were isolated from the roots of Ficus hirta. Their structures were elucidated by several spectroscopic data analyses, including HRESIMS, NMR, and X-ray single-crystal diffraction. The cytotoxic activities of all compounds against HeLa, HepG2, MCF-7, and H460 cell lines were detected using the MTT assay. Among these, 5 showed the highest activity against HeLa cells. Subsequently, the apoptotic, anti-invasive, and anti-migration effects of 5 on HeLa cells were determined by flow cytometer, transwell invasion assay, and wound-healing assay, respectively. The result suggested that 5 distinctly induced the apoptosis in HeLa cells and inhibited their invasion and migration. Further studies on anticancer mechanisms were conducted using Western blotting. As a result, 5 increased the cleavage of PARP and the expression of pro-apoptotic protein Bax. Moreover, 5 notably upregulated the phosphorylation of p38 and JNK, whereas inhibited the expression of p-ERK and p-AKT. Our results demonstrated that 5 could be a potential leading compound for further application in the treatment of cervical cancer.
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Antineoplásicos , Ficus , Femenino , Humanos , Células HeLa , Ficus/química , Amidas/farmacología , Cumarinas/farmacología , Antineoplásicos/farmacología , Antineoplásicos/química , ApoptosisRESUMEN
Parkinson's disease (PD) is a common neurodegenerative motor disorder characterized by a dramatic reduction in pars compacta of substantia nigra dopaminergic neurons and striatal dopamine (DA) levels. Mutations or deletions in the PARK7/DJ-1 gene are associated with an early-onset familial form of PD. DJ-1 protein prevents neurodegeneration via its regulation of oxidative stress and mitochondrial function as well as its roles in transcription and signal transduction. In this study, we investigated how loss of DJ-1 function affected DA degradation, ROS generation and mitochondrial dysfunction in neuronal cells. We showed that loss of DJ-1 significantly increased the expression of monoamine oxidase (MAO)-B but not MAO-A in both neuronal cells and primary astrocytes. In DJ-1-knockout (KO) mice, MAO-B protein levels in the substantia nigra (SN) and striatal regions were significantly increased. We demonstrated that the induction of MAO-B expression by DJ-1 deficiency depended on early growth response 1 (EGR1) in N2a cells. By coimmunoprecipitation omics analysis, we found that DJ-1 interacted with receptor of activated protein C kinase 1 (RACK1), a scaffolding protein, and thus inhibited the activity of the PKC/JNK/AP-1/EGR1 cascade. The PKC inhibitor sotrastaurin or the JNK inhibitor SP600125 completely inhibited DJ-1 deficiency-induced EGR1 and MAO-B expression in N2a cells. Moreover, the MAO-B inhibitor rasagiline inhibited mitochondrial ROS generation and rescued neuronal cell death caused by DJ-1 deficiency, especially in response to MPTP stimulation in vitro and in vivo. These results suggest that DJ-1 exerts neuroprotective effects by inhibiting the expression of MAO-B distributed at the mitochondrial outer membrane, which mediates DA degradation, ROS generation and mitochondrial dysfunction. This study reveals a mechanistic link between DJ-1 and MAO-B expression and contributes to understanding the crosslinks among pathogenic factors, mitochondrial dysfunction and oxidative stress in PD pathogenesis.
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Enfermedades Neurodegenerativas , Enfermedad de Parkinson , Ratones , Animales , Enfermedad de Parkinson/metabolismo , Monoaminooxidasa/genética , Monoaminooxidasa/metabolismo , Monoaminooxidasa/farmacología , Regulación hacia Arriba , Especies Reactivas de Oxígeno/metabolismo , Neuronas Dopaminérgicas/metabolismo , Transducción de Señal , Enfermedades Neurodegenerativas/metabolismo , Receptores de Cinasa C Activada/genética , Receptores de Cinasa C Activada/metabolismo , Receptores de Cinasa C Activada/farmacología , Proteína Desglicasa DJ-1/genética , Proteína Desglicasa DJ-1/metabolismoRESUMEN
[This corrects the article DOI: 10.3389/fpsyg.2023.1030043.].
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Workplace ostracism is an essential predictor of knowledge-sharing behaviors, but few studies have explored the influence of this mechanism in higher education. According to the conservation of resources theory, this study elucidated the roles of job burnout and job satisfaction as sequential mediators of the link between workplace ostracism and knowledge-sharing behaviors in a sample of 388 university teachers. The results of the study were analyzed via structural equation modeling (SEM). Higher knowledge-sharing behaviors were associated with lower workplace ostracism, lower job burnout, and more job satisfaction. Furthermore, increased workplace ostracism was associated with more job burnout, but job satisfaction was not related to workplace ostracism. The relationship between workplace ostracism and knowledge-sharing behaviors was mediated by job burnout and was sequentially mediated by job burnout and job satisfaction. These findings help to clarify the mechanisms underlying the association between workplace ostracism and knowledge-sharing behaviors in university teachers. The theoretical and practical implications of the findings are discussed.
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Metal nanoparticles confined in porous carbon materials have been widely used in various heterogeneous catalytic processes due to their enhanced activity and stability. However, fabrication of such catalysts in a facile and scalable way remains challenging. Herein, we report a general and scalable thiol-assisted strategy to synthesize sulfur-doped mono-/bi-/trimetallic nanoparticles confined in mesoporous carbon (S-M@MC, M = Pt, Pd, Rh, Co, Zn, etc.), involving only two synthetic steps, i.e., a hydrothermal process and pyrolysis. The strategy is based on coordination chemistry and hydro-phobic interaction that the metal precursors coordinated with the hydrophobic thiol ligands are located at the hydrophobic core of micelles, in situ confined in the hydrothermally prepared mesostructured polymer, and then converted into sulfur-doped metal nanoparticles confined in MC after pyrolysis. It is demonstrated that the S-PtCo@MC exhibits enhanced catalytic activity and improved durability toward acidic hydrogen evolution reaction due to the confinement effect and S-doping.
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Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic (DA) neurons and the accumulation of Lewy bodies (LB) in the substantia nigra (SN). Evidence shows that microglia-mediated neuroinflammation plays a key role in PD pathogenesis. Using TNF-α as an indicator for microglial activation, we established a cellular model to screen compounds that could inhibit neuroinflammation. From 2471 compounds in a small molecular compound library composed of FDA-approved drugs, we found 77 candidates with a significant anti-inflammatory effect. In this study, we further characterized pazopanib, a pan-VEGF receptor tyrosine kinase inhibitor (that was approved by the FDA for the treatment of advanced renal cell carcinoma and advanced soft tissue sarcoma). We showed that pretreatment with pazopanib (1, 5, 10 µM) dose-dependently suppressed LPS-induced BV2 cell activation evidenced by inhibiting the transcription of proinflammatory factors iNOS, COX2, Il-1ß, and Il-6 through the MEK4-JNK-AP-1 pathway. The conditioned medium from LPS-treated microglia caused mouse DA neuronal MES23.5 cell damage, which was greatly attenuated by pretreatment of the microglia with pazopanib. We established an LPS-stimulated mouse model by stereotactic injection of LPS into mouse substantia nigra. Administration of pazopanib (10 mg·kg-1·d-1, i.p., for 10 days) exerted significant anti-inflammatory and neuronal protective effects, and improved motor abilities impaired by LPS in the mice. Together, we discover a promising candidate compound for anti-neuroinflammation and provide a potential repositioning of pazopanib in the treatment of PD.
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Enfermedades Neurodegenerativas , Enfermedad de Parkinson , Ratones , Animales , Neuronas Dopaminérgicas/metabolismo , Lipopolisacáridos/farmacología , Factor de Transcripción AP-1/metabolismo , Enfermedades Neurodegenerativas/tratamiento farmacológico , Enfermedad de Parkinson/tratamiento farmacológico , Enfermedad de Parkinson/metabolismo , Microglía/metabolismo , Antiinflamatorios/farmacología , Antiinflamatorios/uso terapéutico , Antiinflamatorios/metabolismoRESUMEN
Objective: T cells represent a predominant cell type in autoimmune disease. However, their exact roles are not fully clear in systemic sclerosis (SSc). This study aimed to mainly investigate the alteration in the absolute numbers of T-lymphocyte subsets and the serum levels of cytokines in SSc patients. Methods: A total of 76 patients with SSc and 76 age- and sex-matched healthy controls (HCs) were enrolled. The levels of circulating T cell subsets and serum cytokines were measured by flow cytometry. T cell subsets or serum cytokines correlations with disease activity and organ involvement were analyzed. Results: The absolute numbers of Th2 and Treg cells in SSc patients were lower than those in HCs (p < 0.05), resulting in the ratios of Th1/Th2 [25.01 (12.24, 38.61) vs. 11.64 (6.38, 20.34)] and Th17/Treg [0.42 (0.17, 0.66) vs. 0.17 (0.13, 0.29)] were increased significantly (p < 0.001). The absolute numbers of total T, Th, and Treg cells were negatively correlated with CRP (r = -0.406, p = 0.002; r = -0.263, p < 0.05; r = -0.367 p < 0.01). The serum levels of IL-2, SIL-2R, IL-6, IL-10, INF-γ, and TNF-α were significantly higher than those in HCs (p < 0.001). Increasing IL-2 in the wake of the augment of ESR (r = 0.671, p = 0.004), so did IL-6 (r = 0.378, p < 0.05). The ratio of Th17/Treg in SSc-ILD patients had lower levels than that in other patients [0.35 (0.14, 0.53) vs. 0.64 (0.26, 0.93) p = 0.028]; Treg cells were lessened in patients with Raynaud's phenomenon relative to controls [3.00 (2.41, 4.28) vs. 3.55 (2.86, 4.53) p < 0.05]. The levels of IL-2, IL-10 and INF-γ [3.32 (1.05,11.73) vs. 2.32 (0.44,6.45), p = 0.045], [8.08 (3.63, 355,77) vs. 4.89 (0.78, 21.44), p = 0.02], [6.31 (2.66, 44.03) vs. 4.03 (0.22, 16.96), p = 0.009] were elevated in patients with arthralgia, while the level of Th17 was decreased [0.62 (0.20,2.16) vs. 1.26 (0.22,10.93), p = 0.026]. ROC curve analysis yielded an optimal cut-off IL-2, IL-10, and INF-γ levels of 2.67, 5.93, and 5.32 pg/ml for the presence of arthralgia. Conclusion: We exhibited abnormalities in T subsets and the production of their cytokines in SSc, as compared with those in HCs. This may allow the pathogenesis of SSc and the development of novel therapeutic interventions aimed at targeting these cells and the cytokines they produce.
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Four undescribed seco-polyprenylated acylphloroglucinols (seco-PAPs), elodeoidesones A-D (1-4), were characterized from Hypericum elodeoides. Compound 1 represents the 1,6-seco-PAPs with fascinating 5/5 fused ring, while 2-4 possess a 1,2-seco-PAPs skeleton with a five-membered lactone core. Their structures including absolute configurations were established by spectroscopic analyses and quantum chemical computations. A possible biosynthetic pathway of 1-4 from normal PAPs was proposed. All the isolates were investigated for their cytotoxicity against tumor cells. Notably, 1 inhibited the proliferation of MCF-7 cells with the IC50 value of 7.34 µM. Mechanism investigation indicated that 1 induced MCF-7 cells apoptosis by blocking cell cycle at S phase via inducing oxidative DNA damage.
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Hypericum , Apoptosis , Puntos de Control del Ciclo Celular , Humanos , Hypericum/química , Células MCF-7 , Estructura Molecular , Estrés Oxidativo , Floroglucinol/químicaRESUMEN
CONTEXT: M2 phenotype macrophage polarization is an attractive target for therapeutic intervention. Asiaticoside (ATS) has multiple pharmacological functions. OBJECTIVE: This study investigates the effect of ATS on M2 phenotype macrophage polarization in osteosarcoma. MATERIALS AND METHODS: The differentiation of human THP-1 monocytes into M0 phenotype macrophages was induced by 100 nM phorbol myristate acetate for 24 h, and treated with 20 ng/mL IL-4 and 20 ng/mL IL-13 for 48 h to obtain M2 phenotype macrophages. The function of ATS on the growth and invasion was investigated by cell counting kit-8, transwell, and western blot under the co-culture of M2 phenotype macrophages and osteosarcoma cells for 24 h. The mechanism of ATS on osteosarcoma was assessed using molecular experiments. RESULTS: ATS reduced the THP-1 cell viability with an IC50 of 128.67 µM. Also, ATS repressed the M2 phenotype macrophage polarization induced by IL-4/IL-13, and the effect was most notably at a 40 µM dose. ATS (40 µM) restrained the growth and invasion of osteosarcoma cells induced by M2 phenotype macrophages. In addition, ATS reduced the tumour necrosis factor receptor-associated factor 6 (TRAF6)/NF-κB activity in osteosarcoma cells and the TRAF6 knockdown reduced the growth and invasion of osteosarcoma cells induced by M2 phenotype macrophages. TRAF6 (2 µg/mL) attenuated the inhibitory effect of ATS on the growth and invasion of osteosarcoma cells caused by M2 phenotype macrophages. In vivo studies further confirmed ATS (2.5, 5, or 10 mg/kg) repressed osteosarcoma tumour growth. DISCUSSION AND CONCLUSIONS: ATS reversed M2 phenotype macrophage polarization-evoked osteosarcoma cell malignant behaviour by reducing TRAF6/NF-κB activity, suggesting ATS might be a promising drug for the clinical treatment of osteosarcoma.
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Osteosarcoma , Factor 6 Asociado a Receptor de TNF , Humanos , Interleucina-13/farmacología , Interleucina-4/farmacología , Macrófagos , FN-kappa B , Osteosarcoma/tratamiento farmacológico , Osteosarcoma/patología , Fenotipo , Factor 6 Asociado a Receptor de TNF/farmacología , TriterpenosRESUMEN
Four new sesquiterpene quinone meroterpenoids, dysideanones F-G (1-2) and dysiherbols D-E (3-4), were isolated from the marine sponge Dysidea avara collected from the South China Sea. The new structures were elucidated by extensive analysis of spectroscopic data including HR-MS and 1D and 2D NMR spectra, and their absolute configurations were assigned by single-crystal X-ray diffraction and ECD calculations. Anti-inflammatory evaluation showed that dysiherbols D-E (3-4) exhibited moderate inhibitory activity on TNF-α-induced NF-κB activation in human HEK-293T cells with IC50 values of 10.2 and 8.6 µmol·L-1, respectively.
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Dysidea , Poríferos , Sesquiterpenos , Animales , Dysidea/química , Quinonas/química , Quinonas/farmacología , Sesquiterpenos/química , Sesquiterpenos/farmacología , EsqueletoRESUMEN
Atmospheric reaction mechanism and dynamics of phenol with nitrogen dioxide dimer were explored by the density functional theory and high-level quantum chemistry combined with statistical kinetic calculations within 220-800 K. The nitric acid and phenyl nitrite, the typical aerosol precursors, are the preponderant products because of the low formation free energy barrier (â¼8.7 kcal/mol) and fast rate constants (â¼10-15 cm3 molecule-1 s-1 at 298 K). Phenyl nitrate is the minor product and it would be also formed from the transformation of phenyl nitrite in NO2-rich environment. More importantly, kinetic effects and catalytic mechanism of a series of metal-free catalysts (H2O, NH3, CH3NH2, CH3NHCH3, HCOOH, and CH3COOH) on the title reaction were investigated at the same level. The results indicate that CH3NH2 and CH3NHCH3 can not only catalyze the title reaction by lowering the free energy barrier (about 1.4-6.5 kcal/mol) but also facilitate the production of organic ammonium nitrate via acting as a donor-acceptor of hydrogen. Conversely, the other species are non-catalytic upon the title reaction. The stabilization energies and donor-acceptor interactions in alkali-catalyzed product complexes were explored, which can provide new insights to the properties of aerosol precursors. Moreover, the lifetime of phenol determined by nitrogen dioxide dimer in the presence of dimethylamine may compete with that of determined by OH radicals, indicating that nitrogen dioxide dimer is responsible for the elimination of phenol in the polluted atmosphere. This work could help us thoroughly understand the removal of nitrogen oxides and phenol as well as new aerosol precursor aggregation in vehicle exhaust.
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Dióxido de Nitrógeno , Fenol , Aerosoles , Catálisis , Nitratos , FenolesRESUMEN
One undescribed lignan, one new natural product, along with fourteen known compounds, were isolated from the roots of Ficus hirta. The structures of the isolates were elucidated by comprehensive spectroscopic technologies, including UV, IR, HRESIMS, and NMR. The absolute configuration of 1 was determined by comparison of experimental and calculated ECD data. The cytotoxicity of all the compounds against HeLa and HepG2 cell lines was evaluated and compound 7 showed considerable cytotoxic effect towards HepG2 cells. Also, the apoptotic effect of 7 on HepG2 cells and the effect of 7 on the key proteins (p-JNK and p-p38) in MAPK (Mitogen-activated protein kinases) pathways were studied by flow cytometry and western blotting experiment. As a result, compound 7 induced the apoptosis of HepG2 cells, and dose-dependently increased the phosphorylation of JNK and p38. Thus, 7 might trigger HepG2 cells apoptosis via JNK/p38 MAPK signaling pathway.
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Antineoplásicos , Ficus , Lignanos , Antineoplásicos/farmacología , Apoptosis , Ficus/química , Células Hep G2 , Humanos , Lignanos/análisis , Lignanos/farmacología , Raíces de Plantas/química , Proteínas Quinasas p38 Activadas por Mitógenos/análisis , Proteínas Quinasas p38 Activadas por Mitógenos/metabolismo , Proteínas Quinasas p38 Activadas por Mitógenos/farmacologíaRESUMEN
(±)-Hypersines A-C (1-3), the three pairs of enantiomerically pure monoterpenoid polyprenylated acylphloroglucinols with an unprecedented 6/6/5/4 fused ring system, were isolated from Hypericum elodeoides. Their structures, including absolute configurations, were elucidated by comprehensive spectroscopic data, single-crystal X-ray diffraction, and quantum chemical calculations. The plausible, biosynthetic pathway of 1-3 was proposed. Moreover, the bioactivity evaluation indicated that 1a might be a novel DNA damage response inhibitor, and could enhance MCF-7 cell sensitivity to the anticancer agent, camptothecin.
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Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Although its pathogenesis remains unclear, a number of studies indicate that microglia-mediated neuroinflammation makes a great contribution to the pathogenesis of PD. Melatonin receptor 1 (MT1) is widely expressed in glia cells and neurons in substantia nigra (SN). Neuronal MT1 is a neuroprotective factor, but it remains largely unknown whether dysfunction of microglial MT1 is involved in the PD pathogenesis. Here, we found that MT1 was reduced in microglia of SN in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model. Microglial MT1 activation dramatically inhibited lipopolysaccharide (LPS)-induced neuroinflammation, whereas loss of microglial MT1 aggravated it. Metabolic reprogramming of microglia was found to contribute to the anti-inflammatory effects of MT1 activation. LPS-induced excessive aerobic glycolysis and impaired oxidative phosphorylation (OXPHOS) could be reversed by microglial MT1 activation. MT1 positively regulated pyruvate dehydrogenase alpha 1 (PDHA1) expression to enhance OXPHOS and suppress aerobic glycolysis. Furthermore, in LPS-treated microglia, MT1 activation decreased the toxicity of conditioned media to the dopaminergic (DA) cell line MES23.5. Most importantly, the anti-inflammatory effects of MT1 activation were observed in LPS-stimulated mouse model. In general, our study demonstrates that MT1 activation inhibits LPS-induced microglial activation through regulating its metabolic reprogramming, which provides a mechanistic insight for microglial MT1 in anti-inflammation.
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Microglía/metabolismo , Enfermedades Neurodegenerativas/metabolismo , Enfermedad de Parkinson/metabolismo , Receptor de Melatonina MT1/metabolismo , Animales , Modelos Animales de Enfermedad , Indenos/farmacología , Lipopolisacáridos/antagonistas & inhibidores , Lipopolisacáridos/farmacología , Masculino , Ratones , Ratones Endogámicos C57BL , Microglía/efectos de los fármacos , Microglía/patología , Enfermedades Neurodegenerativas/tratamiento farmacológico , Enfermedades Neurodegenerativas/genética , Enfermedades Neurodegenerativas/patología , Enfermedad de Parkinson/tratamiento farmacológico , Enfermedad de Parkinson/genética , Enfermedad de Parkinson/patología , Receptor de Melatonina MT1/agonistasRESUMEN
A pair of undescribed enantiomers, (±) ficusflavonid A (1a/1b), along with five known analogues, were isolated from the roots of Ficus hirta. Their structures were determined by the analysis of extensive spectroscopic data (including UV, IR, HRESIMS and NMR). Two enantiomers (1a and 1b) were successfully separated by chiral chromatographic column and their absolute configurations were assigned by the comparison of experimental and calculated ECD data. The cytotoxicity of all the isolates against HeLa, MCF-7, HepG2 and H460 cell lines were evaluated by MTT assay. Among them, 4 suppressed the proliferation of HeLa cells with the IC50 value of 28.88 µM. Furthermore, the apoptotic effect of 4 on HeLa cells and the level of several crucial proteins in AKT/MAPKs signaling pathways were analyzed by flow cytometer and western blot assay. As a result, 4 induced HeLa cell apoptosis in a dose dependent manner and significantly increased the protein levels of p-JNK and p-p38, whereas distinctly reduced the expression of p-AKT, and p-ERK. Thus, compound 4 might induce HeLa cells apoptosis via MAPK and AKT signaling pathways, which could be considered as a potential leading compound for the development of anticancer drugs.
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Antineoplásicos/farmacología , Apoptosis/efectos de los fármacos , Ficus/química , Flavonoides/farmacología , Proteínas Proto-Oncogénicas c-akt/antagonistas & inhibidores , Antineoplásicos/síntesis química , Antineoplásicos/química , Línea Celular Tumoral , Proliferación Celular/efectos de los fármacos , Relación Dosis-Respuesta a Droga , Ensayos de Selección de Medicamentos Antitumorales , Flavonoides/síntesis química , Flavonoides/química , Humanos , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Estructura Molecular , Proteínas Proto-Oncogénicas c-akt/metabolismo , Relación Estructura-ActividadRESUMEN
Descaudatine A (1), an undescribed phenolic glycoside, along with a known analogue (2) and ten flavonoids (3-12), were isolated from the whole plant of Desmodium caudatum. Compounds 1 and 4 exhibited potent antioxidant activities with the IC50 of 58.59 µM and 31.31 µM, respectively, which were approached to that of the positive control Vitamin C (IC50 = 46.32 µM). Meanwhile, 12 showed moderate antioxidant activity with the IC50 of 173.9 µM. Besides, compounds 3 and 6 inhibited the proliferation of HeLa cells with IC50 values of 56.14 µM and 69.04 µM, respectively. Further studies indicated that 3 and 6 could dose-dependently induce PARP cleavage and might trigger caspase-3, 8, 9 activation to induce apoptosis. RXRα is an ideal anticancer target of nuclear receptor. The reporter gene assay of RXRα indicated that 3 and 6 could inhibited the 9-cis-RA induced RXRα transcription in a concentration-dependent manner.
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Antioxidantes , Flavonoides , Antioxidantes/farmacología , Flavonoides/farmacología , Glicósidos/farmacología , Células HeLa , Humanos , Fenoles/farmacología , Extractos Vegetales/farmacologíaRESUMEN
Hyperelodione D (1), an undescribed polyprenylated phloroglucinol derivative possessing 6/6/5/5 fused tetracyclic core, together with hyperelodiones E-F (2-3), two unreported analogues bearing 6/5/5 fused tricyclic structure, were isolated from Hypericum elodeoides Choisy. Their planar structures were elucidated by spectroscopic analysis (HRESIMS, 1D and 2D NMR) and their absolute configurations were determined by comparison of experimental and calculated ECD data. The cytotoxicity and retinoid X receptor-α (RXRα) related activities of the isolates were evaluated and the plausible biogenetic pathways of 1-3 were proposed.
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Antineoplásicos Fitogénicos/farmacología , Hypericum/química , Floroglucinol/farmacología , Receptor alfa X Retinoide/antagonistas & inhibidores , Antineoplásicos Fitogénicos/química , Antineoplásicos Fitogénicos/aislamiento & purificación , Línea Celular , Supervivencia Celular/efectos de los fármacos , Teoría Funcional de la Densidad , Relación Dosis-Respuesta a Droga , Ensayos de Selección de Medicamentos Antitumorales , Humanos , Estructura Molecular , Floroglucinol/química , Floroglucinol/aislamiento & purificación , Receptor alfa X Retinoide/metabolismo , Relación Estructura-ActividadRESUMEN
Nitrogen-doped mesoporous carbon nanosphere (NMCS) with tunable sizes and uniform mesoporosity was synthesized by a facile soft-templating method. During the synthesis, F127 (PEO-PPO-PEO triblock copolymer) could be used not only as a soft template to generate the mesostructure but also as a size-control agent to tailor the size of NMCS in a relatively wide range of 100 to 700â nm. In addition, the synthesis process was simple and suitable for large-scale production. Moreover, the NMCS was used as support of ultrafine Ru nanoparticles (Ru/NMCS), which exhibited good catalytic performances for selective hydrogenation of quinolones. It is expected that the simple synthetic strategy for the NMCS can generate extensive interest in many catalysis and sorption applications.
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Two new compounds, triacremoniate (1) and dietziamide C (2) along with known compounds ß-Adenosine (3) and acrepyrone A (4) were obtained from the mangrove-derived fungus Acremonium citrinum. MMF4. Their structures were unambiguously determined by extensive spectroscopic methods, including UV, IR, HRESIMS and NMR. Triacremoniate (1) can promote apoptosis of HeLa cells by increasing the PARP cleavage and the phosphorylation of JNK and p38.