Nuclear Medicine Department of General Hospital of Northern Theater Command, Shenyang, 110016, China.
Emergency Department of General Hospital of Northern Theater Command, Shenyang, 110016, China.
Radiat Res. 2024 Nov 1;202(5):785-794. doi: 10.1667/RADE-23-00100.1.
In this work, we explored the role and mechanism of sea buckthorn oil in reducing radiation-induced skin damage. The radiation-induced rat skin injury model was established using strontium-90. Rats were treated with sea buckthorn oil twice a day postirradiation, and skin damage was observed at different times and evaluated using an injury score. Skin pathological changes were observed using hematoxylin and eosin (H&E) staining. Western blotting and immunohistochemistry were used to detect the expression of vascular growth and pathway proteins. ELISA was used to detect the secretion level of inflammatory factors. Immunohistochemistry was used to detect macrophage polarization marker proteins. We found that sea buckthorn oil can alleviate radiation-induced skin damage, accelerate skin vascular regeneration, and promote the up-regulation of vascular endothelial growth factor (VEGF) and its receptor (VEGFR). These results demonstrate the beneficial effects of sea buckthorn oil on radiation-induced skin damage. Furthermore, the levels of IL-1β and TNF-α in the sea buckthorn oil treatment group were significantly lower than those in the control group, while the levels of IL-4 and IL10 were significantly higher (P < 0.05). CD206 expression also increased in the sea buckthorn oil treatment group, while CD16 expression decreased compared to the control group (P < 0.05). Western blotting showed that PI3K, Akt and ERK expression increased in the sea buckthorn oil treatment group (P < 0.05). The beneficial effect of sea buckthorn oil in reducing the inflammatory response in irradiated rats was diminished when they were treated with PI3K inhibitor. We conclude that sea buckthorn oil may regulate macrophage M2 polarization by increasing the PI3K-Akt-ERK signaling pathway, thereby inhibiting the inflammatory response and promoting skin vascular regeneration to prevent and treat radiation-induced skin damage.
在这项工作中,我们探讨了沙棘油在减轻辐射诱导皮肤损伤中的作用和机制。使用锶-90 建立了辐射诱导的大鼠皮肤损伤模型。在照射后,每天两次用沙棘油处理大鼠,并在不同时间观察皮肤损伤,并使用损伤评分进行评估。用苏木精和伊红(H&E)染色观察皮肤病理变化。用 Western blot 和免疫组化检测血管生长和途径蛋白的表达。用 ELISA 检测炎症因子的分泌水平。用免疫组化检测巨噬细胞极化标记蛋白。我们发现沙棘油可以减轻辐射引起的皮肤损伤,加速皮肤血管再生,并促进血管内皮生长因子(VEGF)及其受体(VEGFR)的上调。这些结果表明沙棘油对辐射引起的皮肤损伤有益。此外,沙棘油治疗组的 IL-1β 和 TNF-α 水平明显低于对照组,而 IL-4 和 IL10 水平明显升高(P<0.05)。沙棘油治疗组 CD206 表达增加,而 CD16 表达与对照组相比降低(P<0.05)。Western blot 显示,沙棘油治疗组 PI3K、Akt 和 ERK 表达增加(P<0.05)。当用 PI3K 抑制剂处理时,沙棘油减轻照射大鼠炎症反应的有益作用减弱。我们得出结论,沙棘油可能通过增加 PI3K-Akt-ERK 信号通路来调节巨噬细胞 M2 极化,从而抑制炎症反应并促进皮肤血管再生,以预防和治疗辐射诱导的皮肤损伤。