|
Compound | Mechanism | Model | Reference |
|
Quercetin | Increased BDNF, NGF, and Bcl-2, inhibited caspase-3 | Diabetic rats | [33] |
Maintained the density of the general neuronal population, reduced the loss of interosseous neurons, antioxidant | Diabetic rats | [34] |
Activated the Nrf-2/HO-1 pathway, inhibited the NF-κB pathway, and inhibited iNOS, COX-2, IL-6, and TNF-α | DRG cells | [35] |
Upregulated Beclin-1 and LC3 protein expression levels, increased cell proliferation, and upregulated autophagy | Schwann cells | [36] |
Reduced total cholesterol and TBARS levels, increased HDL-cholesterol, SOD, CAT, and GSH-Px activity | Db/db mice | [37] |
Luteolin | Upregulated protein levels of Nrf2 and HO-1, improved nerve conduction velocity and nerve blood flow | Diabetic rats | [38] |
Improved the levels of blood glucose, HbA 1c, insulin, and HOMR-IR | KK-Ay mice | [39] |
Reduced mRNA expression of SREBP-1c, TNF-α |
Kaempferol | Regulated oxidative and nitrosative stress and reduced the formation of AGEs | Diabetic rats | [40] |
Reduced ROS production and inhibited caspase-3 activation | PC12 cells | [41] |
Reduction IL-1β, TNF-α, IC, and ROS and inhibited neuroimmune activation of microglia | Diabetic mice | [42] |
Formononetin | Inhibited islet B cell apoptosis and promoted islet B cell regeneration, insulin secretion, hepatic glycogen synthesis, and hepatic glycolysis | Diabetic mice | [43] |
Controlled hyperglycemia and increased expression of SIRT1 and NGF | Diabetic rats | [44] |
Increased SIRT1 expression and reduced blood glucose | Diabetic rats | [45] |
|