Table 1.
Summary of representative applications of inorganic NPs in aging and AAD.
| NPs type | Diseases | Model | Dose | Time | Outcomes | References |
|---|---|---|---|---|---|---|
| RGD-Au NPs | Neurodegenerative diseases | Hutchinson Gilford progeria syndrome mouse model | / | 3 weeks | Enhance hippocampal neurogenesis | [157] |
| Au NPs | Ovarian cancer | Patient-derived xenograft mouse model | 100–300 μg per mice | 14 days | Inhibited the growth of ovarian cancer | [158] |
| Au NPs (5 nm, 20 nm) | Ischemic injury | Oxygen-glucose deprivation/reperfusion cell model | 200–240 µg/L | 48h | Neuroprotective efects | [160] |
| Au NPs (5, 50, 100 nm) | Aging | PC12 cells | 3.12–100 µM | 24h | Au NPs at 100 nm could maintain maximum neuronal activity | [161] |
| Au NPs (5, 40, 100 nm) | Heart disease | Isoproterenol-induced hyperthyroid heart disease in Sprague-Dawley rats | 0.1 mM | 7 days | Size-dependent cardiac protective effect | [163] |
| H9c2 cell | 10 µg/mL | 24h | Decreased autophagy | |||
| Ag NPs | Obesity | High-fat diet mice | 100, 300 mg/kg | 2 weeks | Accelerated formation of steatohepatitis | [164] |
| Ag NPs | Myocardial infarction | Isoproterenol-induced myocardial infarction rat model | 2.5 mg/kg | 14 days | Cardioprotective effects | [165] |
| Ag NPs | Aging | Drosophila | 10–5 µg/mL | 14 days | Shorten lifespan | [166] |
| Ag NPs | Aging | Drosophila | 0.1, 1 µg/mL | 10 days | Shorten lifespan | [167] |
| Ag NPs | Aging | Endothelial cells | 3, 3.6, and 16 μg/mL | 24h | Significant reduced the cells elasticity | [168] |
| Ag NPs | Lung disease | MRC5 cells | 4 µg/mL | 10 days | Accelerated lung cellular senescence | [169] |
| C57BL/6 mice | 0.7 mg/m3 | 4 days | ||||
| Ag NPs | Cancer | MCF-7, A549 and Hep2 cell lines | 10–100 µg/mL | 48h | Good cytotoxicity in all cancer lines | [170] |
| Ag NPs | MCF-7 cell | 12.5 100 mg/mL | 48h | Remarkable cytotoxicity | [171] | |
| ZnO NPs (10–30 and 35–45 nm) |
Aging | Mesenchymal stem cells | 0–5 µg/mL | 24, 48, 72h | Size-dependent cytotoxicity | [172] |
| ZnO NPs | Aging | Drosophila | 0.1, 1, and 10 mM | 48 days | Induced aberrant phenotype in the progeny. | [174] |
| ZnO NPs | Neurodegenerative diseases | Adult and old male mice | 5.6 mg/kg | 4 weeks | Induced neurotoxicity | [175] |
| ZnO NPs | Colon cancer | Human HT29 colon cancer cell | 10–25 µg/mL | 48h | Inhibiting HT29 cell proliferation | [176] |
| ZnO NPs | Skin tumor | Primary mouse keratinocytes | 0.5–8 µg/mL | 48h | Induced cell death | [177] |
| SKH-1 mice | 10 % w/w | h | ||||
| ZnO NPs | Lung cancer | A549 human lung cancer cells | 2.5–7.5 µg/mL | 24h | Decreased cell viability | [178] |
| Fe3O4 NPs | Neurodegenerative diseases | L929 cells | 10 and 100 µg/mL | 24h | Largely reduced the level of H2O2 | [179] |
| Drosophila | 20 µg/mL | 8 days | Prolonged lifespan to 57 days | |||
| Glioma stem cells | 10 µg | 24, 48, 72h | Inhibits the tumourigenicity | [180] | ||
| SPIONs | Cancer | SCC-7 or 4T1 cells | 80–320 µM | 24h | Killed cancer cells under the influence of blue light | [181] |
| Tumor-bearing mouse model | 20–80 mM Fe | 20 days | Prevented cancer development | |||
| SPIONs | Obesity | Human primary adipocytes | / | / | Reduced adipocytes | [182] |
| IONPs | Nonalcoholic fatty liver disease | HepG2 | 5–10 µg/mL | 24h | Aggravated hepatic steatosis and liver injury | [183] |
| C57BL/6J mice | 5 mg Fe/kg | 8 weeks | ||||
| Fe2O3 NPs | Cardiovascular disease | Mice | 25, 5 mg/kg | 30 days | Cardiac dysfunction | [184] |
| TiO2 NPs | Cardiovascular disease | Sprague-Dawley rats | 2–50 mg/kg | 30, 90 days | Induced adverse cardiovascular effects | [185] |
| TiO2 NPs | Cardiovascular disease | H9c2 cell | 20, 40 µg/cm2 | 72h | Reduced metabolic activity and cell proliferation | [186] |
| TiO2 NPs | Gestational diabetes mellitus | Gestational diabetes mellitus mice | 10–250 mg/kg | 20 days | Reproductive toxicity | [187] |
| TiO2 NPs | Cancer | HCT-116 and Caco-2 cell lines | 0.01–1000 mg/L | 72h | Low genotoxicity | [188] |
| TiO2 NPs | Cancer | Liver and lung cancer metastasis mice model | 20 mg/kg | 21 days | Suppressed lung and liver cancer metastasis | [189] |
| TiO2 NPs | Cancer | 4T1 cells | 0.5–32 µg/mL | 2, 4, 6, 12h | Concentration-dependent cytotoxicity | [190] |
| BALB/c Model of 4T1 Mammary Carcinoma |
5 mg/kg | 21 days | Decreased tumor size | |||
| TiOx NPs | Cancer | Cancer stem cells | 200, 400 µg/mL | 48h | Inhibited migration and invasion of pancreatic cancer cells | [191] |
| BALB/c nude mouse tumors |
3 mg/mL | 30 days | Significantly reduced tumor size | |||
| TiO2 NPs | Skin | HaCat keratinocytes | 0.007–50 µg/cm2 | 24, 48, 7 days | Low cytotoxicity | [192] |
| Thallium acetate | Cancer | C6 and U373 cell lines | 5, 10, 50, 100, 200 µM | 24h | Antiproliferative effects in glioblastoma cells | [193] |
| Platinum | Lung cancer | A549 cells | 0.5 µM | 72h | Compound 15 exerted the most cytotoxicity | [199] |
| BALB/c nude mouse tumors |
5, 11.5 mg/kg | 28 days | Markedly inhibited tumor growth | |||
| Platinum complexes | Cancer | HepG2, MCF-7, SGV-7901 cell lines | 1–100 µM | 72h | Potent cytotoxicity | [202] |
| Platinum | Blind retinal diseases | Light-induced retinal degeneration mouse model | 0.3, 1 µM | 3 days | Maintained retinal function | [205] |
| 661 W cells | 1–1 nM | 24, 48h | ||||
| CeO2 NPs | Neurodegenerative diseases | Rat hippocampal culture neurons | 1 µM | 24h | Neuroprotective properties | [206] |
| CeO2 NPs | Neurodegenerative diseases | Scopolamine-induced Alzheimer rat model | 1–10 | 14 days | Enhanced cognitive ability | [207] |
| CeO2 NPs | Cancer | YM1, cancer stem cell like cell lines | 200–100 µg/mL | 24, 48h | Inhibited cell viability | [210] |
| CeO2 NPs | Cancer | MKN28 and BGC823 | 0.01–10 µg/mL | 72h | Suppressed gastric cancer | [211] |
| CeO2 NPs | Cancer | HT-29, NCI-H460, MRC-5, 518A2, HaCaT, DLD1 | 50–500 µM | 72h | Sensitive in HT-29 and 518A2 cell lines | [212] |
| CeO2 NPs | Heart failure | Isoproterenol-induced cardiac toxicity rats model | 0.5, 5 µg/kg | 5 weeks | Cardio protective effect | [213] |
| CeO2 NPs | Diabetes | Streptozotocin-induced rat model | 30 mg/kg | weeks | Attenuate detrimental effects of diabetes | [214] |
| CeO2 NPs | Diabetes | Diabetic mice | 60 mg/kg | 16 days | Reduce fetal abnormalities | [215] |
| CuO NPs | Neurodegenerative diseases | SH-SY5Y cell line | 1, 10, 50 µg/mL | 24h | Adverse effects | [217] |
| Cu/CuO NPs | Cancer | A549 cell line | 0.5–10 ng/mL–10 µg/mL | 72h | Cytotoxicity | [219] |
| Cu NPs | Cancer | SW480 cell line | 4–125 µg/mL | 24h | Significantly inhibited cell viability | [220] |
| Cu NPs | Cancer | MCF-7 and LoVo cell line | 1–50 µg/mL | 48h | Induced apoptosis | [221] |
| CuO NPs | Cardiovascular diseases | EA.hy 926 cell line | 5, 7.5, 10 and 15 µg/mL | 24h | Induced cell death | [224] |
| CuO NPs |
Cardiovascular diseases | Human umbilical vein endothelial cells |
10, 20, 40 µg/mL | 24h | Vascular toxicity | [225] |