Effects of Tuoli Xiaodusan on Ischemia-Reperfusion Injury of Rat Skin Flaps by Regulating NF-κB Signaling Pathway

  OBJECTIVE  To explore the effect of Tuoli Xiaodusan (MDX) on ischemia-reperfusion injury of rat skin flaps and its potential mechanism.

  METHODS  Rats were randomly divided into sham operation group (Sham group), Model group, MDX high-dose group (MDX-H group) and MDX low-dose group (MDX-L group), with 10 rats in each group. After the rat back skin flap model was successfully constructed, the drug was administered by gavage immediately, once a day for 14 consecutive days. The changes of rat skin flaps in each group after surgery were observed, and the survival rate of rat skin flaps in each group was measured on the 14th day after surgery; the histopathological changes of rat skin flaps were observed by HE staining; the protein expression of p-p65 and p-IκBα in the rat skin flap tissue was detected by Western blot; ELISA method was used to detect the expression of TNF-α, IL-1β, and IL-6 cytokines; Ki67 and CD31 immunohistochemical staining were used to observe epidermal basal layer cell proliferation and vascular regeneration.

  RESULTS  Compared with Model group, MDX-H group and MDX-L group had a small amount of edema and inflammatory fluid exudation after surgery, and the scab removal time was advanced; the ischemic necrosis of the skin flap was significantly improved, the area of skin flap necrosis was significantly decreased, and the survival rate of rat skin flaps was significantly increased (P < 0.01). In addition, MDX could significantly improve the pathological morphology of ischemia-reperfusion injury in rat back skin flaps, reduce the expression of p-p65 and p-IκBα proteins (P < 0.001), and decrease the levels of TNF-α, IL-1β, IL-6 inflammatory factor levels (P < 0.05, P < 0.01, P < 0.001, P < 0.000 1). The differences in Ki67 and CD31 also suggested that treatment with MDX accelerate re-epithelialization and blood vessel formation after ischemic flap injury.

  CONCLUSION  MDX plays a role in improving ischemia-reperfusion injury of skin flaps by regulating the NF-κB signaling pathway and accelerating epithelialization and angiogenesis.