In vitro antioxidant, anti-diabetic and antilipemic potentials of quercetagetin extracted from marigold (Tagetes erecta L.) inflorescence residues.

Quercetagetin, the major flavonoid in marigold (Tagetes erecta L.) inflorescence residues was extracted and purified. The content of quercetagetin after the purification was 89.91 ± 0.26 %. The in vitro antioxidant activity of quercetagetin and its potential in controlling diabetes mellitus and obesity were investigated and compared to quercetin and rutin. The 50 % inhibitory concentration (IC50) values of quercetagetin on scavenging 1, 1-diphenyl-2-picrylhydrazyl (DPPH), 2,2-azinobis-(3-ethylbenzothiazolin-6-sulfonic acid) (ABTS) and hydroxyl radicals were 27.12 ± 1.31 µmol/L, 12.16 ± 0.56 µmol/L and 1833.97 ± 6.66 µmol/L, respectively. The IC50 values of quercetagetin on α-glucosidase, α-amylase and pancreatic lipase were 180.11 ± 3.68 µmol/L, 137.71 ± 3.55 µmol/L and 2327.58 ± 12.37 µmol/L, respectively. These results indicated that quercetagetin exhibited strong in vitro antioxidant, anti-diabetic and antilipemic activities. Lineweaver-Burk plots analysis elucidated that quercetagetin inhibited α-glucosidase and α-amylase non-competitively, while its inhibition against pancreatic lipase was involved in a mixed-type pattern. Moreover, strong correlations were found between ABTS(·+)/DPPH(·) scavenging activities and lipase inhibitory activity (R (2) > 0.90), as well as ·OH scavenging activity and α-amylase inhibitory activity (R (2) = 0.8967).

Subcritical water extraction and antioxidant activity evaluation with on-line HPLC-ABTS(·+) assay of phenolic compounds from marigold (Tagetes erecta L.) flower residues.

Subcritical water extraction (SWE) of phenolics was investigated from marigold (Tagetes erecta L.) flower residues. The total phenolics content (TPC), total flavonoids content (TFC) and antioxidant capacities of extracts were determined, furthermore, antioxidant activities of individual compounds were evaluated with on-line HPLC-ABTS(•+) system. The optimum SWE time was 45 min, solid-to-liquid ratio was 1:50, and the highest TPC and TFC were obtained at 220 °C respectively. The effect of SWE temperature on TPC and TFC was significant (p < 0.05), and TPC was ranged from 28.42 ± 0.94 to 124.27 ± 1.94 (mg GAE/g), and TFC ranged from 34.21 ± 0.36 to 133.22 ± 1.57 (mg GAE/g) between 80 and 220 °C. On-line HPLC-ABTS(•+) profiles revealed that quercetagetin from SWE at 200 °C had nearly twofold radical scavenging activities than that by leaching extraction.

Cell-cell and cell-matrix adhesion regulated by Piezo1 is critical for stiffness-dependent DRG neuron aggregation.

The dorsal root ganglion (DRG) is characterized by the dense clustering of primary sensory neuron bodies, with their axons extending to target tissues for sensory perception. The close physical proximity of DRG neurons facilitates the integration and amplification of somatosensation, ensuring normal physiological functioning. However, the mechanism underlying DRG neuron aggregation was unclear. In our study, we culture DRG neurons from newborn rats on substrates with varying stiffness and observe that the aggregation of DRG neurons is influenced by mechanical signals arising from substrate stiffness. Moreover, we identify Piezo1 as the mechanosensor responsible for DRG neurons' ability to sense different substrate stiffness. We further demonstrate that the Piezo1-calpain-integrin-ß1/E-cadherin signaling cascade regulates the aggregation of DRG neurons. These findings deepen our understanding of the mechanisms involved in histogenesis and potential disease development, as mechanical signals arising from substrate stiffness play a crucial role in these processes.

Development of a soy protein isolate-carrageenan-quercetagetin non-covalent complex for the stabilization of ß-carotene emulsions.

The current study investigated the application of a soy protein isolate (SPI), κ-carrageenan (CG) and quercetagetin (Qut) non-covalent complex in stabilizing ß-carotene emulsions. The ternary complex was formed through a mild mixing and incubation process. FTIR measurement indicated the formation of hydrogen bonds in the non-covalent complex. SPI-CG and SPI-CG-Qut complexes had a much smaller particle size when redispersed in water after spray drying, compared to those in the original dispersions (p < 0.05). Dynamic light scattering analysis revealed that the emulsion stabilized with the ternary complex had a bigger particle size, higher surface charge, and improved creaming stability compared to those stabilized with SPI or SPI-Qut (p < 0.05). The ternary complex allowed less degradation of ß-carotene in the emulsions when exposed to light or thermally treated at 37 °C or 55 °C. Therefore, the SPI-CG-Qut non-covalent complex might work as a novel ingredient in designing delivery systems for ß-carotene.

MicroRNA-1907 enhances atherosclerosis-associated endothelial cell apoptosis by suppressing Bcl-2.

Injury and endothelial cell apoptosis are hall marks of atherosclerosis (AS). However, the mechanisms underlying its pathogenesis remain ill-defined. Recent evidence of a role for microRNAs in AS-associated endothelial cell apoptosis encouraged us to address this question. Here, AS was developed in ApoE (-/-) mice supplied with a high-fat diet (HFD), compared to ApoE (-/-) mice supplied with a normal diet (ND). Mouse endothelial cells were isolated from the aortic arch using flow cytometry based on their expression of CD31. Human aortic endothelial cells (HAECs) were treated with oxidized low-density lipoprotein (ox-LDL) as an in vitro model for AS. Gene expression was quantified by RT-qPCR and protein levels were analyzed by Western blotting. Apoptosis was evaluated by FITC Annexin V Apoptosis assay and by TUNEL staining. Predicting binding patterns between miRNAs and the 3'-UTR of mRNA from the target gene was performed by bioinformatics analyses and confirmed by a dual luciferase reporter assay. We found that HFD mice, but not ND mice, developed AS in 12 weeks. A significant reduction in endothelial cells and a significant increase in mesenchymal cells were detected in the aortic arch of the HFD mice, compared to those of ND mice. Endothelial cell apoptosis was significantly higher in HFD mice, seemingly due to functional suppression of protein translation of anti-apoptotic Bcl-2 protein through upregulation of miR-1907, confirmed by in vitro analysis. Moreover, inhibition of miR-1907 abolished the effects of ox-LDL-induced apoptotic cell death on HAECs. Thus, AS-associated endothelial cell apoptosis may partially result from downregulation of Bcl-2, via upregulation of miR-1907 which binds and suppresses the translation of Bcl-2 mRNA.