Table 1.
Mouse models in ARDS research.
| Direct Lung Damage [17,22,23] | Route of Application | ARDS-Like Affects | Antioxidant Approaches Already Used |
Ref. |
|---|---|---|---|---|
| LPS [24,25,26] | intranasal/intratracheal instillation |
lung accumulation of neutrophils, induction of proinflammatory cytokines | NAC, SAMC | [27,28,29] |
| Bacteria [30,31,32] | intratracheal instillation | lung accumulation of neutrophils, induction of proinflammatory cytokines | CDC | [33] |
| HCl [34,35,36] | intratracheal instillation | neutrophil infiltration, damage of alveolar/ vascular barrier |
apocynin, MitoTempo | [37,38] |
| Hyperoxia (HALI) [39,40,41] | intratracheal | damage of epithelial cells, neutrophil infiltration | AA, BNF, SFN, MnSOD | [42,43,44] |
| MV (VILI) [45,46,47,48] | intratracheal | inflammasome-mediated proinflammatory cytokine expression | NAC, Nrf2+/+, Nrf2−/−, PIP-2; PC-SOD |
[49,50,51,52] |
| Bleomycin [53,54,55] | intratracheal instillation | invertible fibrosis | BRNPs, adelmidrol, EC-SOD |
[56,57,58] |
| Pulmonary ischemia/reperfusion [59,60,61] |
surgery; mesenteric artery clamping or hilar ligation and reperfusion | neutrophil infiltration, damage of alveolar/ vascular barrier |
irisin | [60] |
| Indirect lung damage [17,22,23] | ||||
| Sepsis (live bacteria, CASP, CLP, CSI) [62,63,64,65,66,67] |
i.p.¸ peritonitis | damage of alveolar/ vascular barrier |
PC-SOD, SOD mimetic, Prdx6−/− | [51,68,69] |
| Endotoxemia [70,71,72] | i.v. or i.p. | damage of alveolar/ vascular barrier |
NAC, EUK-8, CypD | [73,74,75] |
| Oleic acid [70,76,77] | i.v. | mimics fat embolism | BAY 60-6583, leptin | [76,78] |
| Multiple transfusions (TRALI) [79,80,81,82] | i.v.; syngeneic or allogenic | acute onset; underlying a 2-hit onset, pulmonary neutrophil sequestration, involvement of MΦ |
MΦ depletion, C3−/−, C5−/−, C5aR−/− | [83,84,85] |
| Multiple trauma [86,87,88] |
externally received | neutrophil infiltration, complement activation | p47phox−/− | [89] |
| H2O2 [90,91,92] | i.v. | increased vascular permeability and fluid retention, edema formation | AA, TP | [93] |
| Nonpulmonary ischemia/reperfusion [94,95,96] | surgery; liver, gut, kidney | neutrophil sequestration, acceleration of microvascular permeability | CypDPlt−/−, SB239063, FK866, LY333531 | [97,98] |
| Two-hit models | ||||
| LPS + MV [99,100,101] | intratracheal, i.v., i.p. | inflammasome-dependent | ATF3 OE/KD; HIF1α−/−, enoxaparin, DJ-1, paracoxib |
[102,103,104,105] |
| Sepsis + MV [106,107,108] | i.p., peritonitis, intratracheal | augment sepsis-mediated organ damage | AM | [109] |
| HCl + MV [100,110,111,112] |
intratracheal | enhanced HCl impact | IL-6−/− | [113] |
+/+, wild-type mice; −/−, knockout mice; AA, ascorbic acid; AM, adrenomedullin; ATF3, activating transcription factor 3; BAY 60-6583, adenosine A2B receptor agonist; BNF, β-naphthoflavone; BRNPs, bilirubin-derived nanoparticles; C, complement; CASP, colon ascendens stent peritonitis; CDC, water-soluble curcumin formulation; CLP, cecal ligation and puncture; CSI, cecal slurry injection; CybD, cyclophilin D; DJ-1, Daisuke-Junko protein 1; EC-SOD, extracellular SOD; R, receptor; FK866, competitive visfatin inhibitor; HALI, hyperoxia-induced lung injury; HIF, hypoxia-inducible factor; IL, interleukin; i.p., intraperitoneal; i.v., intravenously; KD, knock-down; LPS, lipopolysaccharide; LY333531, PKCβ inhibitor; MΦ, macrophage; MV, mechanical ventilation; NAC, N-acetylcysteine; OE, overexpression; PCI, peritoneal cavity infection; PC-SOD, lecithinized SOD; PIP-2, peroxiredoxin 6 inhibitor peptide-2; PLT−/−, platelet-conditional knockout mice; SAMC, S-allylmercaptocysteine; SB239063, p38 MAPK inhibitor; SFN, sulforaphane; TP, α-tocopherol; TRALI, transfusion-induced acute lung injury; VILI, ventilator-induced lung injury.