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Table 16 Anti-diabetic Effect

From: Synthesis and biomedical applications of nanoceria, a redox active nanoparticle

S. no. Particle size Model Observation References
1. 180 ± 15.54 nm by DLS and 90 ± 9.5 nm by SEM STZ-treated diabetic mice were treated with CNPs (0.2 and 2 mg/kg bw, i.p., 28 days) CNPs treatment decreased the glucose levels, lipid peroxidation, secretion of pro-inflammatory cytokines, and NF-κB protein expression and increased the insulin levels and glutathione concentrations [152]
2. HepG2 cells were treated with 50 mM CNPs against high glucose (50 mM) exposure Treatment with CNPs significantly decreased the high glucose-induced cytotoxicity, ROS formation, lipid peroxidation, and increased intracellular glutathione [153]
3. STZ-treated diabetic animals were administered CNPs (30 mg/kg bw, daily, i.p., 2 weeks) CNPs administration alleviated the plasma glucose levels and the deleterious effects of diabetes on the sperm potential fertility, sperm parameters, DNA integrity, and Nrf2 expression levels [154]
4. STZ-treated diabetic animals were administered CNPs (30 mg/kg bw, daily, i.p., 2 weeks) CNPs administration increased the total antioxidant capacity via upregulating Nrf2 mediated increase in the mRNA expressions of antioxidant genes, namely GCLC, HQ-1, and NQO1 [155]
5. STZ-treated diabetic mice were treated with CNPs (60 mg/kg bw, 16 days) CNPs treatment significantly prevented embryonic oxidative stress and pathologic changes in diabetic mice [157]
6. Isolated pancreatic islets were pre-treated with CNPs (10, 100, 1000 nM) Treatment with CNPs increased the cell viability, secretion of insulin, and ATP/ADP ratio and reduced the ROS level [158]
7. Isolated pancreatic islets were pre-treated with CNPs (200 µM) against H2O2 (50 µM, 2 h) Pre-treatment with CNPs attenuated the ROS formation, caspase-3 activity, and apoptotic cell death and increased cell viability, glucose-induced ATP production, and glucose-stimulated insulin secretion [159]