Background: Postoperative abdominal adhesion is a prevalent complication following abdominal surgery, with the incidence of adhesion reaching up to 90%, which may precipitate a range of adverse outcomes. Although fibrous membranes loaded with various anti-inflammatory or other drugs have been proposed for anti-adhesion, most of them suffer from drug-induced adverse effects. Methods: In this study, a lecithin-based electrospun polylactic acid (PLA) nanofibrous membrane (L/P-NM) was developed for the prevention of postoperative abdominal adhesion, utilizing the hydration lubrication theory. The loaded zwitterionic lecithin allows the nanofiber surface to strongly bind water molecules to create a hydration lubrication interface. Results: As the TGA results show, the content of bound water in the nanofibers increased significantly with the increase in the lecithin content. Tribological test results show that L/P-NM reached a minimum coefficient of friction (COF) of about 0.112. Additionally, the developed nanofibrous membranes possess favorable tensile property and biocompatibility. Rat postoperative abdominal adhesion model evaluation results demonstrated that L/P-NM possesses significant anti-adhesive performance, with an adhesion score of only 1. Conclusions: Therefore, this study offers a promising strategy for efficiently preventing abdominal adhesion.

Long noncoding RNAs (lncRNAs) were dysregulated in many kinds of cancers, including hepatocellular carcinoma (HCC). AK021443, as a novel lncRNA, was found to be upregulated in HCC, while its potential value and function are still unknown. The pathological changes of liver tissues were observed by hematoxylin and eosin staining. The expression levels of AK021443 in HCC tissues and cell lines were examined by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation ability of AK021443 on HepG2 and Bel-7402 cells was assessed by CCK8 and EdU staining assays. The role of AK021443 in HepG2 and Bel-7402 cell invasion and migration was measured by Transwell and wound healing assays. Finally, the expression of epithelial–mesenchymal transition (EMT) markers, including E-cadherin, N-cadherin, vimentin, and snail, was investigated by qRT-PCR, Western blot, and immunofluorescence. The role of AK021443in vivo was also analyzed. Hepatoma cell nucleus increased in HCC tissues compared with normal liver tissues. AK021443 expression was increased in HCC tissues and cell lines. Knockdown of AK021443 significantly reduced HepG2 and Bel-7402 cell proliferation, invasion, and migration. Furthermore, inhibition of AK021443 in HepG2 and Bel-7402 cells significantly repressed EMT ability. Knockdown of AK021443in vivo also significantly inhibited tumor growth with decreased Ki-67 levels and EMT phenotype in tumor tissues. However, these functions could be reversed by overexpression of AK021443. AK021443 significantly controlled HepG2 and Bel-7402 cell proliferation, colony formation, invasion, and migration by repressing EMT, which might provide a potential therapeutic target for HCC diagnosis.