蕲艾挥发油通过PI3K/Akt信号通路促进感染性皮肤创口愈合的机制研究

Study on the Effect of Qiai Essential Oil Promotes the Healing of Infectious Skin Wounds by Activating the PI3K/Akt Signaling Pathway

    摘要
  • 摘要:
    目的 观察蕲艾(Artemisia argyi Levl.et Van.var.argyi cv.Qiai)挥发油对感染性皮肤创口愈合的作用并探索其机制。
    方法 将30只雄性昆明小鼠随机分为5组: 空白对照组、膜剂基质组、阳性对照组(3 mL·kg-1莫匹罗星软膏)、低剂量膜剂组(每贴含7.3 mg蕲艾挥发油)和高剂量膜剂组(每贴含57.6 mg蕲艾挥发油)。小鼠麻醉后在背部剪一直径10 mm的全层皮肤圆形伤口, 止血后在创口处涂抹100 μL金黄色葡萄球菌菌液(1.5×108 CFU·mL-1), 各组采取前述方式处理伤口, 每日换药并观察皮肤创面愈合情况。术后12 d处死小鼠取创面皮肤做HE和Masson染色, 观察病理学特征; 利用qPCR和Western blot检测创口皮肤组织愈合相关因子Col1a1、Col3a1、Fn1、VEGFA及炎症因子IL-1β、IL-6、TNF-α mRNA和PI3K/Akt信号通路蛋白的表达。在小鼠胚胎成纤维细胞NIH-3T3利用PI3K抑制剂PI-103探究蕲艾挥发油对PI3K/Akt信号通路活性的潜在影响。
    结果 动物实验表明, 与空白对照组相比, 低剂量和高剂量膜剂组的相对创口面积显著降低; 创口组织的炎性细胞浸润减少, 胶原纤维表达增加; qPCR显示, 与空白对照组相比, 低剂量和高剂量膜剂组的VEGFA、Col3a1和Col1a1 mRNA的表达显著上升, 炎症因子IL-1β和TNF-α mRNA表达降低; Western blot结果表明, 与空白对照组相比, 低剂量和高剂量给药组的p-PI3K/PI3K及p-Akt/Akt比值均显著上升并呈现剂量依赖性。细胞实验结果也证实, 蕲艾挥发油对NIH-3T3细胞的PI3K/Akt信号通路存在调控作用。
    结论 蕲艾挥发油可促进创口愈合, 其机制可能与激活PI3K/Akt信号通路, 抑制炎症因子表达及促进胶原表达有关。

     

    Abstract:
    OBJECTIVE To observe the effect of Qiai (Artemisia argyi Levl.et Van.var.argyi cv.Qiai) essential oil on the healing of infected skin wounds and explore its mechanism.
    METHODS 30 Kunming mice were randomly divided into five equal groups: blank control group, substrate group, positive control group (3 mL·kg-1 Mupirocin ointment), low-dose group (each patch containing 7.3 mg of Qiai essential oil), and high-dose group (each patch containing 57.6 mg of Qiai essential oil).After anesthesia, a 10 mm full-thickness circular skin wound was created on the back of each mouse.Following hemostasis, 100 μL of Staphylococcus aureus bacterial solution (1.5×108 CFU·mL-1) was applied to the wound.The wounds in each group were treated in the aforementioned manner, the dressing was changed daily, and the healing of the skin wound was observed.On the 12th day post-surgery, the mice were euthanized and the skin around the wounds was collected for HE and Masson staining to observe pathological features; qPCR and Western blotting were used to detect the expression of genes related to wound healing (Col1a1, Col3a1, Fn1, VEGFA), inflammatory factors (IL-1β, IL-6, TNF-α), and the PI3K/Akt signaling pathway in the wound skin tissue.Further, in NIH-3T3 mouse embryonic fibroblasts, the potential impact of Artemisia argyi volatile oil on PI3K/Akt signaling pathway activity was investigated using the PI3K inhibitor PI-103.
    RESULTS Animal experiments have shown that compared to the blank control group, the relative wound area in both the low-dose and high-dose groups significantly decreased; the infiltration of inflammatory cells in the wound tissues reduced, while the expression of collagen fibers increased; qPCR showed that, compared to the blank control group, the expression of VEGFA, Col3a1, and Col1a1 in the low-dose and high-dose groups significantly increased, while the expression of inflammatory factors IL-1β and TNF-α decreased; further Western blotting revealed that compared to the blank control group, both the phosphorylated PI3K/total PI3K ratio and the phosphorylated Akt/total Akt ratio in the low-dose and high-dose groups significantly increased in a dose-dependent manner.Cellular experimental results also confirmed that the volatile oil from Artemisia argyi exerts a regulatory effect on the PI3K/Akt signaling pathway in NIH-3T3 cells.
    CONCLUSION The essential oil of Qiai can promote wound healing, with its mechanism possibly involving the activation of the PI3K/Akt signaling pathway, suppression of inflammatory factor expression, and promotion of collagen expression.

     

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