由于受损伤愈合能力的下降，发达国家已记录数百万例急性和慢性伤口病例，患病率不断上升。这主要原因归因于创面处的无法控制的炎症反应，使得愈合长期无法实现。近年来，红细胞（RBC）幽灵或红细胞膜在不同的诊断治疗应用中因其生物相容性和类生物模仿性质引起了极大的关注。我们的研究基于这一概念，通过使用RBC幽灵包裹的肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）改性的AuNPs（金纳米颗粒），提出了一种改进和控制炎症反应的新方法，以加速早期伤后（约48小时）的伤口愈合。结果表明，所研制的GTNFα-IL6@AuNPs能够产生受控的、时间依赖的TNF-α反应，并在约12小时内增加了活性氧的产生。此外，观察到巨噬细胞在不同时间间隔内正确地进行M1/M2功能转换。表达结果表明，在较晚阶段，伤口愈合生物标志物如转化生长因子-β（增加了1.8倍）和胶原蛋白（增加了2.4倍）的水平升高，而基质金属蛋白酶的水平下降（3-8倍），这可能提高了NP处理细胞的迁移速度，达到约90%。因此，我们在此通过在早期伤后阶段创造一个受控炎症反应，从而减少了伤口愈合的炎症阶段的时间线，并进一步帮助细胞重新获得进行伤口重塑和修复的能力。我们希望这种新方法在体外和体内条件下能够改善当前的伤口治疗和皮肤修复策略。

Due to impaired wound healing, millions of acute and chronic wound cases with increased morbidity have been recorded in the developed countries. The primary reason has been attributed to uncontrolled inflammation at the wound site, which makes healing impossible for years. The use of red blood cell (RBC) ghosts or erythrocyte membranes for different theranostic applications has gained significant attention in recent years due to their biocompatibility and biomimicking properties. Our study builds upon this concept by presenting a new approach for creating an improved and controlled inflammatory response by employing RBC ghost encapsulated tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) modified AuNPs (gold nanoparticles) for accelerating the wound healing at early postinjury stage (∼48 h). The results suggested that the developed GTNFα-IL6@AuNPs created a controlled and time dependent TNF-α response and showed increased reactive oxygen species generation at ∼12 h. Further, proper M1/M2 functional transition of macrophages was observed in macrophages at different time intervals. The expression results suggested that the levels of wound healing biomarkers like transforming growth factor-β (1.8-fold) and collagen (2.4-fold) increased while matrix metalloproteinase (3-8-fold) levels declined at later stages, which possibly increased the cell migration rate of NP treated cells to ∼90%. Hence, we are here reducing the timeline of the inflammatory phase of wound healing by actually creating a controlled inflammatory response at an early postinjury stage and further assisting in regaining the ability of cells for wound remodelation and repair. We intend that this new approach has the potential to improve the current treatment strategies for wound healing and skin repair under both in vitro and in vivo conditions.