Table 16 Anti-diabetic Effect

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]