Impact of polyphenols on mast cells with special emphasis on the effect of quercetin and luteolin

Shaik, Y.B.; Caraffa, Alessandro; Ronconi, Gianpaolo; Lessiani, Gianfranco; Conti, Pio

doi:10.5114/ceji.2018.81347

Cited by 34 publications

(34 citation statements)

References 43 publications

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“…While we did not specifically examine human mast cells or PDI expression in these cells in this study, it will be important to determine whether PDI has similar effects on IgE-mediated activation in human cells. In this context, interestingly, quercetin and other polyphenols have been shown to modulate human mast cell activity in other studies (51,52).…”

Section: Discussionmentioning

confidence: 88%

Protein Disulfide Isomerases Regulate IgE-Mediated Mast Cell Responses and Their Inhibition Confers Protective Effects During Food Allergy

et al. 2020

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The thiol isomerase, protein disulfide isomerase (PDI), plays important intracellular roles during protein folding, maintaining cellular function and viability. Recent studies suggest novel roles for extracellular cell surface PDI in enhancing cellular activation and promoting their function. Moreover, a number of food-derived substances have been shown to regulate cellular PDI activity and alter disease progression. We hypothesized that PDI may have similar roles during mast cell-mediated allergic responses and examined its effects on IgE-induced mast cell activity during cell culture and food allergy. Mast cells were activated via IgE and antigen and the effects of PDI inhibition on mast cell activation were assessed. The effects of PDI blockade in vivo were examined by treating mice with the irreversible PDI inhibitor, PACMA-31, in an ovalbumin-induced model of food allergy. The role of dietary PDI modulators was investigated using various dietary compounds including curcumin and quercetin-3-rutinoside (rutin). PDI expression was observed on resting mast cell surfaces, intracellularly, and in the intestines of allergic mice. Furthermore, enhanced secretion of extracellular PDI was observed on mast cell membranes during IgE and antigen activation. Insulin turbidimetric assays demonstrated that curcumin is a potent PDI inhibitor and pre-treatment of mast cells with curcumin or established PDI inhibitors such as bacitracin, rutin or PACMA-31, resulted in the suppression of IgE-mediated activation and the secretion of various cytokines. This was accompanied by decreased mast cell proliferation, FcεRI expression, and mast cell degranulation. Similarly, treatment of allergic BALB/c mice with PACMA-31 attenuated the development of food allergy resulting in decreased allergic diarrhea, mast cell activation, and fewer intestinal mast cells. The production of TH2-specific cytokines was also suppressed. Our observations suggest that PDI catalytic activity is essential in the regulation of mast cell activation, and that its blockade may benefit patients with allergic inflammation.

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Section: Discussionmentioning

confidence: 88%

Protein Disulfide Isomerases Regulate IgE-Mediated Mast Cell Responses and Their Inhibition Confers Protective Effects During Food Allergy

et al. 2020

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“…12,13 As a group, flavonoids tend to exert antioxidative, anti-inflammatory, and neuroprotective properties, but the substitutions can contribute differences in the functional properties. 14,15 Luteolin (3 0 ,4 0 ,5,7-tetrahydroxyflavone) is a common flavone with 2 hydroxylations each on the A and B rings. The presence of the hydroxyl groups at the C3 0 , C4 0 , C5, and C7 positions and the C2-C3 double bond is what structure-activity studies have indicated to be most critical to the bioactivities of luteolin and other flavones.…”

Section: Luteolin: Chemistry and Biochemistrymentioning

confidence: 99%

Protection against Alzheimer's disease by luteolin: Role of brain glucose regulation, anti‐inflammatory activity, and the gut microbiota‐liver‐brain axis

Daily¹,

Kang

Park

2020

BioFactors

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Luteolin is a widely distributed flavone herbs and vegetables. It has antioxidant and anti-inflammatory activities and improves glucose metabolism by potentiating insulin sensitivity and improving β-cell function and mass.Alzheimer's disease (AD) is induced by the deposition of amyloid-beta (Aβ) in the hippocampus and the formation of neurotoxic Aβ plaques. The Aβ deposition is associated with increased formation of Aβ from amyloid precursor protein by up-regulation of β-secretase and β-site amyloid precursor proteincleaving enzyme 1 (BACE1). Furthermore, Aβ accumulation is increased by brain insulin resistance. The impairment of insulin/IGF-1 signaling mainly in the hippocampus and brain insulin resistance is connected to signals originating in the liver and gut microbiota, known as the gut microbiota-liver-brain axis. This indicates that the changes in the production of short-chain fatty acids by the gut microbiota and pro-inflammatory cytokines can alter insulin resistance in the liver and brain. Luteolin is detected in the brain tissues after passing through the blood-brain barrier, where it can directly influence neuroinflammation and brain insulin resistance and modulate Aβ deposition. Luteolin (10-70 mg/kg bw for rodents) can modulate the systemic and brain insulin resistance, and it suppresses AD development directly, and it influences Aβ deposition by activation of the gut microbiota-liver-brain axis. In this review, we evaluate the potential of luteolin to mitigate two potential causes of AD, neuroinflammatory processes, and disruption of glucose metabolism in the brain. This review suggests that luteolin intake can enhance brain insulin resistance and neuroinflammation, directly and indirectly, to protect against the development of Alzheimer's-like disease, and the gut microbiota-liver-

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“…Lut administration through oral route basically diminished the LPO and OH concentration in plasma and colonic mucosa just as it extends the cell strengthening enzymes, which might be a result of the solid cancer prevention agent property of Lut . In an earlier published report, Lut was included as an anti‐inflammatory agent that regulates the inflammatory mediators . The goal of the present examination was to research the defensive impact of Lut against BPA‐incited renal toxicity through suppressing OS, inflammation, and upregulating nuclear factor‐like 2/antioxidant response element/heme oxygenase 1 (Nrf2/ARE/HO‐1) pathway.…”

Section: Introductionmentioning

confidence: 98%

Protective role of luteolin against bisphenol A‐induced renal toxicity through suppressing oxidative stress, inflammation, and upregulating Nrf2/ARE/ HO‐1 pathway

Sita¹,

Gowthami²,

Srikanth³

et al. 2019

IUBMB Life

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For the development of renal diseases, oxidative stress (OS) is reasoned to be one of the risk factors. For the treatment or prevention of the renal disease, the use of antioxidants could be a hopeful therapeutic mediation as they retard or block the oxidative reaction along with the inflammatory process. Luteolin (Lut) is a plant flavonoid, a pharmacologically active component normally found in glycosylated forms in basic perilla leaf, green pepper, celery, seed, honeysuckle bloom, and chamomile blossom; it exhibits antioxidant activity. In this investigation, we explored the nephroprotective activity of Lut on bisphenol A (BPA)‐induced nephron toxicity in rats. Orally administering Lut (100 and 200 mg/kg) diminished BPA‐induced anomalies in the kidney, blood urea nitrogen, creatinine, and serum uric acid levels. Lut therapy reduced the BPA‐influenced generation of inflammatory mediators, inclusive of tumor necrosis factor alpha, interleukin 6, and interleukin 1 beta. This was coupled with significant improvement in kidney histopathologic features. Lut enhanced the nuclear factor‐like 2 (Nrf2) and heme oxygenase 1 (HO‐1) expression, which showed protection against OS induced by BPA. The current outcomes of the study showed that Lut has a strong reactive oxygen species scavenging property and potentially decreases the lipid peroxidation as well as inhibits DNA damage in renal toxicity induced by BPA. In conclusion, the potential antioxidant effect of Lut may be because of its modulatory effect on the Nrf2/antioxidant response element (ARE)/HO‐1 pathway, which means it protects the kidney from BPA‐induced oxidative injury. © 2019 IUBMB Life, 2019

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Impact of polyphenols on mast cells with special emphasis on the effect of quercetin and luteolin

Cited by 34 publications

References 43 publications

Protein Disulfide Isomerases Regulate IgE-Mediated Mast Cell Responses and Their Inhibition Confers Protective Effects During Food Allergy

Protein Disulfide Isomerases Regulate IgE-Mediated Mast Cell Responses and Their Inhibition Confers Protective Effects During Food Allergy

Protection against Alzheimer's disease by luteolin: Role of brain glucose regulation, anti‐inflammatory activity, and the gut microbiota‐liver‐brain axis

Protective role of luteolin against bisphenol A‐induced renal toxicity through suppressing oxidative stress, inflammation, and upregulating Nrf2/ARE/ HO‐1 pathway

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