Benign prostatic hyperplasia (BPH) patients experience complications after surgery. We studied oxidative stress scavenging by porous Se@SiO₂ nanospheres in prostatic urethra wound healing after transurethral resection of the prostate (TURP). Beagle dogs were randomly distributed into two groups after establishing TURP models. Wound recovery and oxidative stress levels were evaluated. Re-epithelialization and the macrophage distribution at the wound site were assessed by histology. The mechanism by which porous Se@SiO₂ nanospheres regulated macrophage polarization was investigated by qRT-PCR, western blotting, flow cytometry, immunofluorescence and dual luciferase reporter gene assays. Our results demonstrated that Porous Se@SiO₂ nanosphere-coated catheters advance re-epithelization of the prostatic urethra, accelerating wound healing in beagle dogs after TURP, and improve the antioxidant capacity to inhibit oxidative stress and induced an M2 phenotype transition of macrophages at the wound. By restraining the function of reactive oxygen species (ROS), porous Se@SiO₂ nanospheres downregulated Ikk, IκB and p65 phosphorylation to block the downstream NF-κB pathway in macrophages in vitro. Since activation of NF-κB signaling cascades drives macrophage polarization, porous Se@SiO₂ nanospheres promoted macrophage phenotype conversion from M1 to M2. Our findings suggest that porous Se@SiO₂ nanosphere-coated catheters promote postoperative wound recovery in the prostatic urethra by promoting macrophage polarization toward the M2 phenotype through suppression of the ROS-NF-κB pathway, attenuating the inflammatory response.

Statement of Significance

The inability to effectively control post-operative inflammatory responses after surgical treatment of benign prostatic hyperplasia (BPH) remains a challenge to researchers and surgeons, as it can lead to indirect cell death and ultimately delay wound healing. Macrophages at the wound site work as pivotal regulators of local inflammatory response. Here, we designed and produced a new type of catheter with a coating of porous Se@SiO₂ nanosphere and demonstrated its role in promoting prostatic urethra wound repair by shifting macrophage polarization toward the anti-inflammatory M2 phenotype via suppressing ROS-NF-κB pathway. These results indicate that the use of porous Se@SiO₂ nanosphere-coated catheter may provide a therapeutic strategy for postoperative complications during prostatic urethra wound healing to improve patient quality of life.

中文翻译：

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多孔Se @ SiO2纳米球涂层导管通过活性氧-NF-κB通路抑制调节巨噬细胞极化，从而加速前列腺尿道伤口愈合

良性前列腺增生（BPH）患者在手术后会出现并发症。我们研究了多孔Se @ SiO ₂纳米球清除经尿道前列腺电切术（TURP）后前列腺尿道伤口愈合中的氧化应激。建立TURP模型后，将比格犬随机分为两组。评估伤口恢复和氧化应激水平。通过组织学评估再上皮化和伤口部位的巨噬细胞分布。通过qRT-PCR，蛋白质印迹，流式细胞仪，免疫荧光和双重荧光素酶报告基因分析研究了多孔Se @ SiO ₂纳米球调节巨噬细胞极化的机制。我们的结果表明，多孔Se @ SiO ₂纳米球涂层的导管可促进前列腺尿道的再上皮化，加速TURP后比格犬的伤口愈合，并提高抗氧化能力以抑制氧化应激并在伤口处诱导巨噬细胞的M2表型转变。通过限制活性氧（ROS）的功能，多孔Se @ SiO ₂纳米球在体外下调了Ikk，IκB和p65磷酸化，从而阻断了巨噬细胞的下游NF-κB途径。由于NF-κB信号级联反应的激活驱动巨噬细胞极化，所以多孔Se @ SiO ₂纳米球促进了巨噬细胞表型从M1到M2的转化。我们的发现表明，多孔Se @ SiO ₂ 纳米球涂层的导管通过抑制ROS-NF-κB通路促进巨噬细胞向M2表型的极化，从而促进前列腺尿道术后伤口的恢复，从而减轻了炎症反应。

重要声明

良性前列腺增生症（BPH）手术治疗后无法有效控制术后炎症反应仍然是研究人员和外科医生的挑战，因为它可能导致间接细胞死亡并最终延迟伤口愈合。伤口部位的巨噬细胞是局部炎症反应的关键调节剂。在这里，我们设计并生产了一种新型的带有多孔Se @ SiO ₂纳米球涂层的导管，并展示了其通过抑制ROS-NF-κB通路使巨噬细胞极化朝着抗炎M2表型转移，从而促进前列腺尿道伤口修复的作用。 。这些结果表明使用多孔Se @ SiO ₂ 纳米球涂层导管可为前列腺尿道伤口愈合期间的术后并发症提供治疗策略，以改善患者的生活质量。