Table 2.

The potential mechanisms of the four main compounds in the treatment of DPN.

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]