Abstract:BackgroundIn the present study, the phenolic compounds were prepared using ultrasonic-aid extraction from sugar beet molasses (SBM).MethodsGallic acid (GA), cyanidin-3-O-glucoside chloride (CGC) and epicatechin (EP) were produced after column chromatography from the extraction, and further detected using NMR, QTOF-MS and ESI-MS/MS.ResultsThe three compounds exhibited strong antioxidant activities including DPPH radical scavenging activities, ABTS radical scavenging activities and ORAC values. GA showed the str… Show more
“…This concentration of Que was not deemed cytotoxic in our IPEC-J2 cells. Furthermore, anti-proliferative activities of GA were observed in Caco-2, HepG2, MCF-7, and WT-F344 rat liver cells using the 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay and were suggested to be caused by the pro-oxidative effects of GA [30]. Thus, GA shows selective cytotoxicity for cancerous human cells, but, in our setting, very little toxicity for normal porcine cells.…”
Oxidative stress in the small intestinal epithelium can lead to barrier malfunction. In this study, the effect of rosmarinic acid (RA), quercetin (Que), gallic acid (GA), lipoic acid (LA), ethoxyquin (ETQ) and Se-methionine (SeMet) pre-treatments using 2 mM Trolox as a control on the viability and the generation of intracellular reactive oxygen species (iROS) of oxidatively (H2O2) stressed intestinal porcine epithelial cells (IPEC-J2) was investigated. A neutral red assay showed that RA (50–400 µM), Que (12.5–200 µM), GA (50–400 µM), ETQ (6.25–100 µM), and SeMet (125–1000 µM) pre-treatments but not LA significantly increased the viability of H2O2-stressed IPEC-J2 cells (p < 0.05). A 5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate, acetyl ester (CM-H2DCFDA) fluorescent probe showed that RA (100–600 µM), Que (25–800 µM), ETQ (3.125–100 µM) and SeMet (500–2000 µM) pre-treatments significantly reduced iROS in IPEC-J2 monolayers (p < 0.05). Moreover, RA and Que were most effective in reducing iROS. Therefore, the effects of RA and Que on barrier functioning in vitro were examined. RA and Que pre-treatments significantly decreased fluorescein isothiocyanate (FITC)-conjugated dextran-4 (4 kDa) permeability and transepithelial electrical resistance (TEER) of an IPEC-J2 cell monolayer (p < 0.05). These in vitro results of RA and Que hold promise for their use as antioxidants in pig feed.
“…This concentration of Que was not deemed cytotoxic in our IPEC-J2 cells. Furthermore, anti-proliferative activities of GA were observed in Caco-2, HepG2, MCF-7, and WT-F344 rat liver cells using the 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay and were suggested to be caused by the pro-oxidative effects of GA [30]. Thus, GA shows selective cytotoxicity for cancerous human cells, but, in our setting, very little toxicity for normal porcine cells.…”
Oxidative stress in the small intestinal epithelium can lead to barrier malfunction. In this study, the effect of rosmarinic acid (RA), quercetin (Que), gallic acid (GA), lipoic acid (LA), ethoxyquin (ETQ) and Se-methionine (SeMet) pre-treatments using 2 mM Trolox as a control on the viability and the generation of intracellular reactive oxygen species (iROS) of oxidatively (H2O2) stressed intestinal porcine epithelial cells (IPEC-J2) was investigated. A neutral red assay showed that RA (50–400 µM), Que (12.5–200 µM), GA (50–400 µM), ETQ (6.25–100 µM), and SeMet (125–1000 µM) pre-treatments but not LA significantly increased the viability of H2O2-stressed IPEC-J2 cells (p < 0.05). A 5-(and-6)-chloromethyl-2′,7′-dichlorodihydrofluorescein diacetate, acetyl ester (CM-H2DCFDA) fluorescent probe showed that RA (100–600 µM), Que (25–800 µM), ETQ (3.125–100 µM) and SeMet (500–2000 µM) pre-treatments significantly reduced iROS in IPEC-J2 monolayers (p < 0.05). Moreover, RA and Que were most effective in reducing iROS. Therefore, the effects of RA and Que on barrier functioning in vitro were examined. RA and Que pre-treatments significantly decreased fluorescein isothiocyanate (FITC)-conjugated dextran-4 (4 kDa) permeability and transepithelial electrical resistance (TEER) of an IPEC-J2 cell monolayer (p < 0.05). These in vitro results of RA and Que hold promise for their use as antioxidants in pig feed.
“…For example, structure activity relationship studies delineating the key functional groups required for exhibiting potent anti-cancer effects of phenolic compounds have identified the involvement of aromatic ring and hydroxylic groups [40, 41], (Fig. 4).…”
Section: Key Structural Features and Mechanism Of Action Of Plant Phementioning
confidence: 99%
“…In addition to hydroxylic groups and catechol ring structure, the presence of an unsaturated short fatty acid side chain also makes the phenolic compounds more potent. As an example, studies comparing the efficacy of cinnamic acid and benzoic acid for inhibiting cancer cell growth revealed that cinnamic acids that contain a unsaturated propionic acid side chain are more better anti-cancer agents [40, 41]. Thus phenolic acids i.e benzoic and cinnamic acid derivatives with higher hydroxyl substitutions could be considered as potential candidates for preventing the cancer cell proliferation.Fig.…”
Section: Key Structural Features and Mechanism Of Action Of Plant Phementioning
Plant derived phenolic compounds have been shown to inhibit the initiation and progression of cancers by modulating genes regulating key processes such as: (a) oncogenic transformation of normal cells; (b) growth and development of tumors; and (c) angiogenesis and metastasis. Recent studies focusing on identifying the molecular basis of plant phenolics-induced cancer cell death have demonstrated down-regulation of: (a) oncogenic survival kinases such as PI3K and Akt; (b) cell proliferation regulators that include Erk1/2, D-type Cyclins, and Cyclin Dependent Kinases (CDKs); (c) transcription factors such as NF-kβ, NRF2 and STATs; (d) histone deacetylases HDAC1 and HDAC2; and (e) angiogenic factors VEGF, FGFR1 and MIC-1. Furthermore, while inhibiting oncogenic proteins, the phenolic compounds elevate the expression of tumor suppressor proteins p53, PTEN, p21, and p27. In addition, plant phenolic compounds and the herbal extracts rich in phenolic compounds modulate the levels of reactive oxygen species (ROS) in cells thereby regulate cell proliferation, survival and apoptosis. Furthermore, recent studies have demonstrated that phenolic compounds undergo transformation in gut microbiota thereby acquire additional properties that promote their biological activities. In vitro observations, preclinical and epidemiological studies have shown the involvement of plant phenolic acids in retarding the cancer growth. However, to date, there is no clinical trial as such testing the role of plant phenolic compounds for inhibiting tumor growth in humans. More over, several variations in response to phenolic acid rich diets-mediated treatment among individuals have also been reported, raising concerns about whether phenolic acids could be used for treating cancers. Therefore, we have made an attempt to (a) address the key structural features of phenolic acids required for exhibiting potent anti-cancer activity; (b) review the reported findings about the mechanisms of action of phenolic compounds and their transformation by gut microbiota; and (c) update the toxicological aspects and anti-tumor properties of phenolic compounds and extracts containing phenolic compounds in animals.
“…These phytochemicals possess many biological activities and a documented positive impact on human health. There are data about the antioxidant, anti‐allergic, anti‐atherosclerotic, anti‐inflammatory, antibacterial and antithrombotic properties of phenolic compounds (Del Rio et al ., ; Chen et al ., ; Díaz‐de‐Cerio et al ., ; Marhuenda et al ., ). Most of these studies were conducted as in vitro experiments.…”
Section: Introductionmentioning
confidence: 99%
“…Many biological activities of phenolic compounds, especially antioxidant, immunological, anti‐inflammatory, antiproliferative and hypoglycaemic effects, are well documented (Chen et al ., ; Díaz‐de‐Cerio et al ., ; Marhuenda et al ., ). The stability of phenolic compounds as well as the binding or release thereof from various combinations due to in vitro digestion may influence the biological activity of these compounds measured after digestion.…”
There are many scientific reports on determination of the content and biological activity of compounds found in food. However, these analyses are not sufficient to determine their effect on the human body. During digestion of food ingredients, many changes can modify their structure and this may affect their absorption and bioactivity. Many phenolic aglycones are hydrophilic and can be absorbed through biological membranes by diffusion. However, most polyphenols occur in the glycosidic form, which undoubtedly affects their absorption in the intestine. Oligopeptides are also absorbable via secondary active transport but based on the hydrogen ion gradient or with transporter PepT1. The bioavailability of phytochemicals is determined by their molecular weight or chemical structure and the food matrix. Accordingly, the aim of this work was to present the novel scientific reports related to the influence the many factors on digestibility, bioaccessibility and activity of selected bioactive compounds of plant origin.
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