Pericardial barrier destruction, inflammatory cell infiltration, and fibrous tissue hyperplasia, trigger adhesions after cardiac surgery. There are few anti-adhesion materials that are both functional and sutureable for pericardial reconstruction. Besides, a few studies have reported on the mechanism of preventing pericardial adhesion. Herein, a functional barrier membrane with sutureability was developed via a modified electrospinning method. It was composed of poly(l-lactide-co-caprolactone) (PLCL) nanofibers, poly(vinyl alcohol) (PVA) aerogel, and melatonin, named PPMT. The PPMT had a special microstructure manifested as a staggered arrangement of nanofibers on the surface and a layered macroporous aerogel structure in a cross-section. Besides providing the porosity and hydrophilicity obtained from PVA, the structure also had suitable mechanical properties for stitching due to the addition of PLCL nanofibers. Furthermore, it inhibited the proliferation of fibroblasts by suppressing the activation of Fas and P53, and achieved anti-inflammatory effects by affecting the activity of inflammatory cells and reducing the release of pro-inflammatory factors, such as interleukin 8 (IL-8) and tumor necrosis factor α (TNF-α). Finally, in vivo transplantation showed that it up-regulated the expression of matrix metalloproteinase-1 (MMP1) and tissue inhibitor of metalloproteinase-1 (TIMP1), and down-regulated the expression of Vinculin and transforming growth factor β (TGF-β) in the myocardium, thereby reducing the formation of adhesions. Collectively, these results demonstrate a great potential of PPMT membrane for practical application to anti-adhesion.

心包屏障破坏、炎性细胞浸润和纤维组织增生，会在心脏手术后引发粘连。很少有抗粘连材料既可用于心包重建又可缝合。此外，一些研究报道了防止心包粘连的机制。在此，通过改进的静电纺丝方法开发了一种具有可缝合性的功能性屏障膜。它是由聚（升-lactide-合作-己内酯) (PLCL) 纳米纤维、聚乙烯醇 (PVA) 气凝胶和褪黑激素，命名为 PPMT。PPMT 具有特殊的微观结构，表现为表面纳米纤维交错排列，横截面呈层状大孔气凝胶结构。除了提供从 PVA 获得的孔隙率和亲水性外，由于添加了 PLCL 纳米纤维，该结构还具有适合缝合的机械性能。此外，它通过抑制Fas和P53的激活来抑制成纤维细胞的增殖，并通过影响炎症细胞的活性和减少促炎因子的释放来达到抗炎作用，如白细胞介素 8 (IL-8) 和肿瘤坏死因子α（TNF-α）。最后，在体内移植显示其上调基质金属蛋白酶-1（MMP1）和金属蛋白酶-1组织抑制剂（TIMP1）的表达，下调心肌中Vinculin和转化生长因子β（TGF-β）的表达，从而减少粘连的形成。总的来说，这些结果证明了 PPMT 膜在抗粘连的实际应用中的巨大潜力。