TABLE 2.
Studies of miRNAs modulated by respective nutrient and bioactive compounds.
| Experiment | Consequences | Reference/s |
|---|---|---|
| THP-1 cells were incubated with Resveratrol (30 or 50 µM) for 14 h | Anti-inflammatory miR-663 up-regulated, which targets two AP-1 factors (Jun B and Jun D) reducing AP-1 activity. Pro-inflammatory miR-155 down-regulated and miR-663 up-regulated | Tili et al. (2010) |
| THP-1 cells were incubated with resveratrol (25, 50, 100, and 200 mM) for 48 h | Upregulation of miR-Let7A in treated cells compared to non-treated cells. Resveratrol and/ormiR-Let7A target mRNA of TNF-α and IL-6 and amplified IL-10 after stimulation of cells with LPS. | Song et al. (2016) |
| Human glioblastoma (U251) cells were treated with 10 or 50 µM resveratrol for 12 h to check the effect of resveratrol on the expression of miR-21 | The phenolic compound resveratrol inhibited and reduced expression of pro-inflammatory miR-21 in-turn causing a reduction in the activity of IkB phosphorylation and NF-kB | Li et al. (2013) |
| Macrophages (RAW 264.7) incubated with concentrations of resveratrol, hydroxytyrosol, and oleuropein compatible with plasma physiological concentrations (5 and 10 µM) | Resveratrol and hydroxytyrosol (at 10 µM) downregulated miR-146a which targets the nuclear factor (erythroid-derived 2)–like 2 (Nfr2) transcription factor with a role in the inhibition of pro-inflammatory mediators. Nfr2 was positively modulated by resveratrol and hydroxytyrosol after macrophage stimulation with LPS. | Bigagli et al. (2017) |
| Randomized placebo-controlled study on 35 type-2 diabetic and hypertensive men who consumed capsules with placebo (maltodextrin), grape extract (devoid of resveratrol) (GE), and grape extract with over 8 mg of resveratrol (GE-RES) during 1 year | In the group supplemented with GE-RES, miR-21, miR -181b, miR-663, and miR -30c2 were upregulated and miR-155 and miR-34a were downregulated as compared to the control group | Tomé-Carneiro et al. (2013) |
| Treatment of human myocytes (L6 GLUT4myc) with palmitic acid | MiR-29a levels enhanced causing posttranscriptional inhibition of insulin receptor substrate (IRS)-1 and reducing protein concentration | Yang et al. (2014) |
| EPA- and DHA-induced stimulation of macrophages (RAW 264.7) and epithelial (TIME) cells with LPS and pro-inflammatory cytokines (IL-1β, TNF-α, and IFN-γ) and the treatment of these cells with DHA (C22:6n3) or arachidonic acid (AA, C20:4n6) | The anti-inflammatory action of PUFAs was mediated by downregulation of miR-146a, miR-146b, miR-21, miR-125a, and miR-155 linked with pro-inflammatory response triggered by NF-kB signaling | Roessler et al. (2017) |
| The treatment of mouse cardiomyocytes (HL-1 cells) with palmitic acid | Stimulation of miR-27b expression signifying an enhanced vulnerability to atrial arrhythmia | Takahashi et al. (2016) |
| Leukotriene B4 synthesized from arachidonic acid in mice macrophages | Stimulated the inflammatory response by increasing MyD88 via upregulation of miR-155 and miR -146b, which are responsible for SOCS-1 mRNA degradation and MyD88 inhibition | Wang et al. (2014) |
| Treatment of hepatocytes with oleic acid | Reduced PTEN expression by upregulating miR-21 via a direct effect of NF-kB p65 on the miR-21 promoter | Vinciguerra et al. (2009) |
| Humans(30) consumed 30 g/day of almonds and nut sources of polyunsaturated fatty acids (PUFA) for 8 weeks | miR-328, miR-330-3p, miR-221, and miR-125a-5p had their expressions reduced, while miR-192, miR-486-5p, miR-19b, miR-106a, miR-130b, miR-18a, and miR-769-5p displayed increased levels after the intervention. miR-221 and miR-130b were associated with positive variations in plasma protein C-reactive (PCR) levels | Ortega et al. (2015) |
| Treatment of breast cancer cells with curcumin | The upregulation of miR-181b is related to a down-modulation of pro-inflammatory cytokines CXCL1 and -2, causing an inhibitory effect on the metastatic process of these cells | Kronski et al. (2014) |
| Treatment of breast stromal fibroblast with curcumin | Tumor suppressor p16INK4A protein inhibits carcinogenic effects of cells by repressing IL-6 expression and secretion. This process is mediated by miR-146b-5p which inhibits the expression of cytokines at a specific sequence at IL-6 3′UTR. After curcumin treatment, p16INK4A and miR-146b-5p levels increase and suppress IL-6 | Al-Ansari and Aboussekhra, (2015) |
| Female mice consumed quercetin-enriched diets (2 mg/g), compared to controls with the control diet | Hepatic levels of miR-125b (negatively regulates inflammation) and miR-122 (regulates lipid homeostasis) showed upregulation in female mice fed on quercetin-enriched diets. | Boesch-Saadatmandi et al. (2012) |
| A harvested heart of a rat model with selenium deficiency | MiR-374, miR-16, miR-199a-5p, miR-195, and miR-30e involved in cell differentiation, signal transduction, and stress-response were upregulated >5-fold in the deficiency group than the selenium-supplemented group. The miR-3571, miR-675, and miR-450a were downregulated | Xing et al. (2015) |
| Humans consumed a zinc depletion dietary regimen | Dietary zinc depletion–responsive 20 miRNAs were shown and reversed by succeeding zinc repletion. Highly downregulated miR-204 and miR-296-5p suppress oncogene expression | Ryu et al. (2011) |