目的 探讨紫草素（SHI）能否通过调控Hippo-Yes相关蛋白（YAP）信号通路促进大鼠烧伤创面愈合。方法 构建SD大鼠烧伤模型，随机分为模型(Mod)组，低(L-SHI)、高紫草素(H-SHI)组（紫草素4、8 mg/cm2外敷），H-SHI+Verteporfin组（紫草素8 mg/cm2外敷+腹腔注射100 mg/kg Hippo-YAP通路抑制剂Verteporfin），每组10只。另取10只大鼠为对照（Ctrl）组，Ctrl组与Mod组给予等体积生理盐水外敷。分别于3、7、14 d计算创面愈合率；HE染色评估表皮修复及组织结构；免疫组织化学检测CD31阳性细胞；ELISA检测血清白细胞介素（IL）-6、肿瘤坏死因子α（TNF-α）、IL-1β水平；Western blotting检测巨噬细胞刺激 1(MST1)、p-MST1、大肿瘤抑制激酶1(LATS1)、p-LATS1、YAP、p-YAP、结缔组织生长因子(CTGF)、半胱氨酸丰富血管生成诱导因子61(CYR61)、血管内皮生长因子(VEGF)蛋白水平；Real-time PCR检测相关基因表达变化。结果 与Ctrl组相比，Mod组大鼠表皮厚度减少，真皮层纤维组织变性坏死，炎症浸润加重；创面结痂残留多；血清IL-6、IL-1β、TNF-α水平升高；CD31阳性率、p-MST1/MST1、p-LATS1/LATS1、p-YAP/YAP、CTGF、CYR61、VEGF蛋白水平及MST1、LATS1、YAP、CTGF、CYR61、VEGF mRNA水平降低（P<0.05）。与Mod组相比，L-SHI、H-SHI组可见新生表皮层，结缔组织和血管新生，结痂脱落完全；IL-6、IL-1β、TNF-α水平降低；创面愈合率、CD31阳性率、p-MST1/MST1、p-LATS1/LATS1、p-YAP/YAP、CTGF、CYR61、VEGF蛋白水平及MST1、LATS1、YAP、CTGF、CYR61、VEGF mRNA水平升高（P<0.05）。与H-SHI组相比，H-SHI+Verteporfin组表皮结构异常，炎性浸润增加，结痂未脱落完全；血清IL-6、IL-1β、TNF-α水平升高；创面愈合率、CD31阳性率、p-MST1/MST1、p-LATS1/LATS1、p-YAP/YAP、CTGF、CYR61、VEGF蛋白水平及MST1、LATS1、YAP、CTGF、CYR61、VEGF mRNA水平降低（P<0.05）。结论 SHI可通过激活Hippo-YAP通路，促进血管新生并减少炎症反应，从而加速大鼠烧伤创面愈合。

Objective To investigate whether shikonin (SHI) can promote burn wound healing in rats by regulating the Hippo-Yes-associated protein（YAP）signaling pathway. Methods Burn models were established in SD rats and randomly assigned into groups: the model (Mod) group, L-SHI group, H-SHI group (with SHI applied to the burn wound at doses of 4 mg/cm2 or 8 mg/cm2), and the H-SHI + verteporfin group (with 8 mg/cm2 SHI applied to the burn wound followed by intraperitoneal injection of 100 mg/kg verteporfin, an inhibitor of the Hippo-YAP signaling pathway), with 10 rats in each group. Another 10 rats were included as the control (Ctrl) group, and both the Ctrl and Mod groups received an equivalent volume of saline externally. Wound healing rates were calculated on days 3, 7, and 14. HE staining was performed to evaluate epidermal repair and tissue structure. Immunohistochemistry was used to detect CD31-positive cells. Serum levels of interleukin(IL)-6, tumor necrosis factor α(TNF-α), and IL-1β were measured by ELISA. Western blotting was conducted to detect the protein expression levels of macrophage stimulating 1(MST1), p-MST1, large tumor suppressor kinase 1(LATS1), p-LATS1, YAP, p-YAP, connective tissue growth factor(CTGF), cysteine-rich angiogenic inducer 61(CYR61), and vascular endothelial growth factor(VEGF). Real-time PCR was performed to detect the expression changes of related genes. Results Compared with the Ctrl group, the Mod group showed reduced epidermal thickness, degeneration and necrosis of dermal fibrous tissue, aggravated inflammatory infiltration, more scab residue on the wound, elevated serum levels of IL-6, IL-1β, and TNF-α, and decreased CD31-positive rate, protein levels of p-MST1/MST1, p-LATS1/LATS1, p-YAP/YAP, CTGF, CYR61, and VEGF, as well as mRNA levels of MST1, LATS1, YAP, CTGF, CYR61, and VEGF (P<0.05). Compared with the Mod group, the L-SHI and H-SHI groups exhibited new epidermal layer formation, connective tissue and angiogenesis, complete scab shedding, reduced levels of IL-6, IL-1β, and TNF-α, and increased wound healing rate, CD31-positive rate, protein levels of p-MST1/MST1, p-LATS1/LATS1, p-YAP/YAP, CTGF, CYR61, and VEGF, as well as mRNA levels of MST1, LATS1, YAP, CTGF, CYR61, and VEGF (P<0.05). Compared with the H-SHI group, the H-SHI+Verteporfin group showed abnormal epidermal structure, increased inflammatory infiltration, incomplete scab shedding, elevated serum levels of IL-6, IL-1β, and TNF-α, and decreased wound healing rate, CD31-positive rate, protein levels of p-MST1/MST1, p-LATS1/LATS1, p-YAP/YAP, CTGF, CYR61, and VEGF, as well as mRNA levels of MST1, LATS1, YAP, CTGF, CYR61, and VEGF (P < 0.05). Conclusion SHI has the potential to promote angiogenesis and reduce inflammatory responses by activating the Hippo-YAP signaling pathway, thus accelerating wound healing in burned rats.