作者
Xinyi Ma,Yi Wen Lin,Miaojie Fang,Yingying Liu,Wenjie Li,Jibing He,Dingsheng Lin
摘要
Background: Flaps are commonly used for repairing tissues and wounds in surgery. However, various factors can cause postoperative necrosis in these flaps. Catalpol is a bioactive component in extracts from Rehmannia glutinosa, which has pharmacological characteristics that may improve flap survival. Methods: The experiments were performed in 36 male Sprague–Dawley rats divided into three groups: control, low-dose catalpol, and high-dose catalpol. The flap survival rate, neutrophil density, microvessel density (MVD), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were measured; histopathological analysis was performed 7 days after surgery. Blood flow was measured by laser Doppler flowmetry (LDF) and lead oxide-gelatin angiography. The levels of vascular endothelial growth factor (VEGF), Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, Nod-like receptor 3 (NLRP3), cysteinyl aspartate specific proteinase-1 (caspase-1), IL-1β, and IL-18 were determined by immunohistochemistry. Results: Catalpol treatment increased flap survival, reduced neutrophil recruitment and release, decreased MDA levels, and increased SOD levels; thus, it effectively reduced oxidative stress, upregulated the expression of VEGF, and increased microvessel density. LDF and gelatin-lead oxide angiography showed that catalpol treatment improved angiogenesis. Immunohistochemical analyses showed that catalpol inhibited the production of inflammatory factors, such as TNF-α and IL-6, by downregulating TLR4 and NF-κB. Furthermore, catalpol reduced cell pyroptosis by inhibiting the production of NLRP3 inflammasomes, thereby downregulating the release of IL-1β and IL-18. Conclusion: Catalpol can improve the rate of flap survival.