Table 8.
Interaction between miRNAs, hazardous compounds, as well as antioxidants.
| Type | miRNA | Human/Animal Study | Dose | Other treatments (Source of antioxidants) | Cell line | Dose of hazardous materials | Targets or Pathways | Results | Ref |
|---|---|---|---|---|---|---|---|---|---|
| CdCl2 | miR-21a (Up) | Male Wistar rats | 10 moml/L, 5 months | Quercetin; 50 mg/kg, 5 months | – | – | NF-kB P65, Nrf2, Smad3, SREBP1, TGF-β1 | Treatment with quercetin via inhibiting miR-21 could attenuate liver fibrosis and steatosis induced by cadmium. | [116] |
| CdCl2 | miR-26a-5p (Down) | Hy-Line Brown strain | 150 mg/kg, 42 days | Selenium yeast (Se–Y); 0.5 mg/kg, 42 days | – | – | HSP60/80/90, PTEN, PI3K/AKT, RIP1/3 | Se–Y via increasing the expression of miR-26a-5p could act against necroptosis induced by CdCl2 in the kidney of the chicken. | [117] |
| CdCl2 | miR-30a (Down) | Hy-Line Brown chickens | 150 mg/kg, 3 months | Se; (0.2 mg/kg of Na2SeO3), 3 months | – | – | GRP78, JNK, IRE-1, ATG5, LC-3I/II, Beclin-1 | In the chicken kidneys, CdCl2 via mediating GRP78 and miR-30a could cause JNK-dependent autophagy. | [118] |
| CdCl2 | miR-125a, miR-125b, (Down) | – | – | Selenium; 5–20 μM, 0.5 h before the Cd administration | LLC-PK1 | 20 μM, 12 h, | Bax, Bak, Caspase-3 | Treatment with selenium via targeting miR-125a/b could inhibit apoptosis induced by CdCl2. | [119] |
| CdCl2 | miR-146a (Up) | Male albino rats | 3 mg/kg, daily, 2 months | N-acetylcysteine (NAC); 100 mg/kg, daily, 2 months | – | – | NF-κB p65, TNF-α, IL-1β, TRAF6 | NAC could attenuate Cd-induced hepatotoxicity by decreasing the expression of miR-146a and inflammation. | [120] |
| CdCl2 | miR-182-5p (Down) | male Kunming mice | 1.5 mg/kg, | CAPE; 10 μmol/kg body weight |
– | – | TLR4, IL-1β, IL-6, TNF-α, PI3K/AKT, mTOR, Caspase-3 | CAPE could downregulate hepatotoxicity induced by CdCl2. | [121] |
| CdCl2 | miR-216a (Up) | common carps | – | Se; (10−6 mol/L of Na2SeO3), 6 h | Lymphocyte | 4 × 10−5 mol/L, 6 h | PI3K/AKT, Bax, Bcl-2, Caspase-3/9, RIP3, MLKL | Se could act against the promotion of the miR-216a, necrosis, and apoptosis induced by CdCl2 in the lymphocytes of common carp. | [122] |
| CdCl2 | miR-661 (Down) | – | – | Caffeic acid phenethyl ester (CAPE); 10 μM | HepG2 | 0–30 μM, 24 h | Caspase-9 | CAPE could downregulate apoptosis induced by CdCl2. | [123] |
| Pb | miR-16-5p (Up) | Hy-Line Brown chickens | – | Se; (1 μM of Na2SeO3) | Neutrophil | 12.5 μM | IGF1R, PiK3R1, p53, Bcl-2, Bax, Caspase-3/8/9 | In chicken neutrophil cells, Se via targeting miR-16-5p had an antagonistic impact against lead-induced apoptosis. | [73] |
| Pb | miR-224 (Up) | Male Wistar rats | 30 mg/kg, once every 2 days, less than 4 months | Selenium nanoparticles (Se-NPs); 0.5 mg/kg, less than 4 months | – | – | ID1 | Se-NPs via inhibiting miR-224 could attenuate adverse effects of Pb on thyroid tissues. | [124] |
| ATO | miR-182-5p (down) | – | – | NAC; 10 mM, 4h | U87MG, S1 GBM primary cells, A549, H1299 | 0–5 μM | SESN2, HO-1 | ATO via inhibiting miR-182-5p and increasing SESN2 could impede oxidative stress. | [125] |