Objective: To investigate the effect of Gynura divaricata aqueous extract on foot injury in diabetic foot (DF) model rats

and explore its possible mechanism. Method: A total of 80 SD rats were included in the study. Among them

8 rats were randomly selected as control group

while the other rats were given with high-fat and glucose feed and intraperitoneally injected with low-dose streptozotocin (STZ) to establish the rat model of diabetes; then

the model of DF was established by ligating their lower extremity vascular and making foot surgery. The model rats (n=40) were randomly divided into model group

metformin group (0.2 g · kg-1)

and Gynura divaricata aqueous extract groups (16

8

4 g · kg-1). The healing of ulcer were observed on day 1

4

7

14

21.After 28 days

the immunohistochemical method was used to observe the angiogenesis of the ischemic lower limb muscles. The content of intercellular cell adhesion molecule-1(ICAM-1)

C-reactive protein(CRP)

interleukin-6(IL-6)

IL-1β

tumor necrosis factor-α(TNF-α)

endothelin-1(ET-1) and thromboxane A2(TXA2) were determined by ELISA

and NO and nitric oxide synthase(NOS) content were determined by nitric acid reduction method. Real-time PCR and Western blot were used to determine vascular endothelial growth factor(VEGF) mRNA and protein expressions in ischemic lower limb muscles. Result: Compared with the normal group

the wound healing in the model group was delayed

while that of the G.divaricata aqueous extract group; Compared with the normal group

the microangiogenesis

serum NO and NOS levels

and VEGF mRNA and protein expressions in the model group decreased

whereas serum NO and NOS levels

and VEGF mRNA and protein expressions in the G. divaricata aqueous extract groups increased (P<0.05

P<0.01); compared with the normal group

ICAM-1

CRP

IL-6

IL-1β

TNF-α

ET-1

TXA2 levels in the model group significantly increased (P<0.01)

while those in the G. divaricata aqueous extract groups decreased(P<0.05

P<0.01). Conclusion: G.divaricata aqueous extract could promote the foot wound healing of DF model rats

and its mechanism may be related to the inhibition of inflammation

the regulation of vascular endothelial function

the increase in the expression of VEGF

the promotion of the angiogenesis in ischemic tissues

and the improvement of the blood supply of the lower extremity.