Effect of Shengji Xiangpi Mastic on IL-2 and TNF-α in Rats with Diabetic Ulcer During Wound Healing

Objective: To investigate the mechanisms of the immune-inflammatory response of the Shengji Xiangpi mastic(SM) promoting the ulcer healing in diabetic rats.Method: Wistar rats were randomly divided into four groups,one group as the normal control group,the remaining three groups rats were injected streptozotocin(STZ) into vena caudalis as the diabetic model.All the four group rats were punched in back to establish the diabetic ulcer model.The three group rats with diabetic ulcers were randomly divided into diabetic control group,vaseline group and SM group according to the blood glucose and body weight.The rats in SM group were treated with SM gauze compress,those in vaseline group treated with vaseline gauze compress,and those in normal control group and diabetic control group treated with physiological saline,then the content of serum IL-2 level and wound tumor necrosis factor-α(TNF-α) in the wound tissue were observed.Result: The diabetic ulcer wounds in the back of the rats in SM group healed faster than those in the rats in diabetic control group and vaseline group,and the difference was significant on the day 7,14,21 and 30 compared with diabetic control group,respectively;the contents of serum interleukin-2(IL-2) in the rats in SM group were lower than those in the rats in diabetic control group on the day 21 and 30,and the difference was significant;it was also lower than those in the rats in vaseline group on the day 21th and 30 and the difference was significant.The expression levels of TNF-α mRNA of the diabetic ulcer wounds in the rats in SM group were lower compared to those in the rats in diabetic control group on the day 21 and 30,and the difference was significant;it was also lower than those in the rats in vaseline group on the day,21 and 30 and the difference was significant.Conclusion: The Shengji Xiangpi mastic can promote the ulcer healing in diabetic rats,and it is closely related to regulating the immune-inflammatory response.