Fig 2: Effects of ZJP on PI3K, AKT Expressions Levels Assessment of aortic expression of PI3K and AKT in rats by Western blot. *, P < 0.05 vs. Control group. #, P < 0.05 vs Model group, n = 3.

Fig 3: Validation of key proteins in signaling pathways. (a) Immunofluorescence results of a2ß1. The expression level of Group G was significantly higher than that of group N. (b) Western blot analysis of integrin a2ß1. a2ß1 was significantly increased in Group G. (c) Western blot analysis of the PI3K/AKT signaling pathway. The TNC, TNMD, and phosphorylated PI3K/AKT (p-PI3K, p-AKT308, and p-AKT473) were significantly increased in Group G. After adding PI3K/AKT pathway inhibitors, the expression of TNC and TNMD was inhibited simultaneously with phosphorylated PI3K and AKT. (d) Schematic diagram of the signaling pathway of micropattern SF films regulating TSPCs.

Fig 4: Bioinformatic analyses of DEGs induced by NAC. The gene expression bioinformatics analysis was performed using data obtained from RNA-seq of 2 group different cells after 7 days culturing. A GO analysis revealed that the DEGs centered on the main BP of ECM rganization and collagen fiber organization; the main MF of ECM structural constituent, integrin binding and collagen binding; the main CC of ECM and basement membrane. B The heatmap of the DEGs. C KEGG enrichment analysis indicated that DEGs focused on the PI3K/AKT signaling [30–32]. D A signaling network illustrated the DEGs concentrated in the integrin-related PI3K/AKT pathway

Fig 5: NAC upregulates integrin a5ß1 protein expression and PI3K/AKT phosphorylation in TSPCs. TSPCs were treated in triplicate with, or without, NAC in the presence or absence of Ly294002 for 1 or 2 weeks, and the relative levels of integrin a5ß1 protein expression and PI3K/AKT phosphorylation in TSPCs were determined by immunofluorescence and Western blotting. Data are representative images or expressed as the mean ± SD of each group from three separate experiments. * P < 0.05; **P < 0.01