Table 2.
Nanomaterial | Synthesis Method | Morphology | Size (nm) | Model | Dosage | Route of Administration | Markers | Effects | Ref. | |
---|---|---|---|---|---|---|---|---|---|---|
Powder | Hydrodynamic Radius | |||||||||
Albumin-conjugated CNPs (A-CNP) |
Biomineralization | Spherical | 30 ± 8.9 | ND | DBA/1J mice exposed to collagen-induced arthritis (CIA) mouse as in vivo model for rheumatoid arthritis | 1 mg/kg, 2 times a week |
Intra-articular injection | ↓ iNOS ↑ Arg-1 |
M2 polarization ↓ clinical score |
[39] |
THP-1 human monocytes and RAW 264.7 murine macrophages | 0.5 μg/mL for 24 h | NA | ↓ iNOS, IL-1β ↑ Arg-1 ↓ HIF-1α |
M2 polarization ↑ antioxidant response ↓ hypoxia |
||||||
Citric-acid-coated CNPs (CA-CNPs) |
Alkaline-based precipitation | Spherical | 2.8 ± 0.4 | 3.4 ± 1.1 | HepG2 hepatocyte cells, RAW264.7 murine macrophages, Renca epithelial kidney cells and SVEC4-10EHR1 endothelial cells exposed to LPS or H2O2 |
0.1–1 mg/mL for 24 h | NA | ↑ SOD, CAT and HORAC activity ↓ ROS (OH•) ↓ TNF-α, IL-1β |
↑ cell viability ↓ oxidative stress ↓ inflammation |
[40] |
C57BL/6J mice treated with complete Freund’s adjuvant (CFA) as in vivo model for peripheral Inflammation | 100 mg/kg | Intravenous tail injection | ↓ TNF-α, IL-1β ↑ IL-10 |
↓ paw inflammation ↓ edema formation ↓ immune cell infiltration |
||||||
CNPs + Hyaluronic acid | hydrothermal | Cubic | 10–60 | ND | Chondrocytes treated with H2O2 for 30 min | 0.02 μg/mL | NA | ↑ ACAN, COL1A1, COL2A1 | ↓ cell apoptosis ↓ oxidative stress ↓ glycosaminoglycan synthesis |
[42] |
CNPs | NA | Spherical | 5 | 10 | Sprague-Dawley-rat-derived chondrocytes treated with IL-1β | 160 μg/mL | NA | ↓ ROS (O2−) ↓ NO ↑ Nrf2, HO-1, SOD, CAT, GPX ↑ ACAN, COL1A1, COL2A1 ↓ MMP13, ADAMTS4 ↓iNOS, COX-2, IL-6 |
↓ oxidative stress ↑ antioxidant response ↓ cell apoptosis ↓ ECM degradation ↓ inflammation |
[43] |
Sprague-Dawley-rat-derived condylar cartilage explants treated with IL-1β | ↓ ROS (O2−) ↓ NO |
↓ apoptosis ↓oxidative stress |
||||||||
CNPs + Lenalidomide | Precipitation | Spherical | 3–5 | 34 ± 6.8 | C57BL/6 mice treated with MOG 35–55 peptide and pertussis toxin (experimental autoimmune encephalomyelitis) as in vivo model for multiple sclerosis (MS) | 1 mg/kg, every fourth day | Intravenous injection | ↑ MBP ↓ TNF-α ↓ IL-17, INF-γ, TNF-α (mRNA) ↓ GFAP, Iba-1 ↓ CD86+ dendritic cells |
↓ clinical score ↑ body weight ↓ ventricular volume ↓ myelin loss ↓ inflammation ↓ glial cell activation ↓ peripheral immune reaction |
[45] |
CNPs: cerium oxide nanoparticles; iNOS: inducible nitric oxide synthase; M1/2: macrophage 1/2; Arg-1: arginase-1; HIF-1α: hypoxia inducible factor-1 alpha; SOD: superoxide dismutase; CAT: catalase; HORAC: hydroxyl radical antioxidant capacity (HORAC) assay; ROS: reactive oxygen species; IL: interleukin; MBP: myelin basic protein; INF-γ: interferon gamma; TNF-α: tumor necrosis factor-alpha; GFAP: glial fibrillary acidic protein; Iba-1: ionized calcium-binding adapter molecule 1; ACAN: aggrecan; COL: collagen; NO: nitrite; HO-1: heme oxygenase 1; GPX: glutathione peroxidase; MMP: matrix metallopeptidase; ADAMTS4: metallopeptidase with thrombospondin type 1 motif 4; COX: cyclooxygenase; ECM: extracellular matrix; Nrf2: nuclear factor erythroid 2-related factor 2; ND: not determined; NA: not applicable. Colored areas highlight in vivo experiments.