Three sunflower head pectin (SFHP) with different molecular weights
(Mw = 4.50, 97.23, and 254.64 kDa) were
obtained by enzyme-assisted extraction and characterized by FTIR and 1H NMR spectroscopy. The corrosion inhibition of mild steel
in 1 M HCl solution was evaluated by the weight loss measurement.
The inhibition efficiency (IE%) increased as its concentration increases
and decreased as the temperature increases. The SFHP with the lowest Mw of 4.50 kDa exhibited an IEmax of
92.05% at the medium concentration (2.0 g L–1).
The inhibition properties of SFHP (Mw =
4.50 kDa) were investigated electrochemically and theoretically. The
electrochemical impedance spectroscopy (EIS) revealed that the charge-transfer
resistance increased as its concentration increases, the double-layer
capacitance decreased as concentration increases, and the IE% also
increased as concentration increases. The potentiodynamic polarization
(PP) revealed that the SFHP acted as mixed-type inhibitor. The IE%
reached 90.3% at the medium concentration (2.0 g L–1) of SHFP. The three-dimensional super depth digital microscopy and
scanning electron microscopy tests confirmed the formation of inhibitor
films on the surface of mild steel. The adsorption of SFHP on the
mild steel surface was proved to obey the Langmuir adsorption isotherm.
The theoretical studies via density functional theory and molecular
dynamics simulation further revealed the mechanism of corrosion inhibition.
Subcritical water extraction (SWE)
of pectin from fresh sunflower
heads was optimized using the response surface methodology (RSM).
The optimal conditions for the maximum yield of pectin (6.57 ±
0.6%) were found to be a pressure of 8 bar, temperature of 120 °C,
time of 20 min, and liquid–solid ratio (LSR) of 7 mL/g. The
degree of esterification (DE) of pectin was analyzed by titrimetry
and Fourier transform infrared (FTIR) methods, which was low methoxyl
pectin. The molecular weight (M
w), galacturonic
acid (GalA) content, and surface tension of pectin were 11.50 kDa,
82%, and 45.38 mN/m (1.5% w/v), respectively. Moreover, thermogravimetric
(TG) and differential scanning calorimetry (DSC) analysis confirmed
that pectin had excellent thermal stability. FTIR and 1H NMR spectra confirmed its structure. This study demonstrated that
SWE could be used as a productive and environmentally friendly method
for extracting pectin from fresh sunflower heads.
The aim of the present study was to examine the role of protease-activated receptor-1 (PAR1)-stimulated platelet activation in the epithelial-mesenchymal transition (EMT) and migration of colon cancer cells, and to identify the underlying mechanisms. TFLLR-NH2, a PAR1 agonist, was used to activate platelets and the platelet supernatants were used to treat the SW620 colon cancer cell line. Expression of E-cadherin and vimentin on SW620 cells was detected by immunofluorescence and western blotting, and the level of the transforming growth factor β1 (TGF-β1) was measured using ELISA following the activation of platelets by TFLLR-NH2. miR-200b expression was detected using quantitative PCR in SW620 cells. In order to investigate the chemotactic ability of the SW620 cells, the expression of CXC chemokine receptor type 4 (CXCR4) was measured by flow cytometry. Transwell migration assays were performed following exposure of the cells to the supernatant of PAR1-activated platelets. SW620 cells cultured in the supernatant of TFLLR-NH2-activated platelets upregulated E-cadherin expression and downregulated the vimentin expression. In the in vitro platelet culture system, a TFLLR-NH2 dose-dependent increase of secreted TGF-β1 was detected in the supernatant. The activation of PAR1 on the platelets led to the inhibition of miR-200b expression in the SW620 cells that were cultured in platelet-conditioned media. The number of SW620 cells that penetrated through the Transwell membrane increased with the dose of TFLLR-NH2 used to treat the platelets. The percentage of CXCR4-positive SW620 cells was significantly higher when they were exposed to the supernatant of platelets cultured for 24 h with PAR1 agonist than when cultured in non-conditioned media (40.89±6.74 vs. 3.47±1.40%, P<0.01). Platelet activation with a PAR1 agonist triggered TGF-β secretion, which induced EMT of SW620 human colon cancer cells via the downregulation of miR-200b expression, and activated platelets had a chemotactic effect on colon cancer cells mediated by the upregulation of CXCR4 on the cell surface.
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