RESUMEN
Graphene has attracted tremendous attention as a potential building block of modern high performance coating systems. Herein, we demonstrate a green method for making reduced oxide graphene (rGO) using the natural product rutin as the reducing agent. The rGO, with residual rutin on the surface to provide surface affinity, is used in the one-step fabrication of a nanocomposite of rGO and silica nanoparticles (SN) with a corrosion inhibitor, benzotriazole (BTA), loaded in situ. The ternary nanocomposite, BTA@SN-rGO, can be easily dispersed in water. It not only has a high inhibitor loading capacity (85.1 µg mg-1) but also can release the inhibitor in a controlled manner triggered by pH. Combining both the extraordinarily good barrier properties and smart nanocontainer features, BTA@SN-rGO was further incorporated into an epoxy latex to assemble an intelligent anticorrosion coating. The effective duration of the coating protection for steel was remarkably prolonged in different media, especially in acidic media. In addition to the barrier capability, smart self-healing of artificial damage to the modified coating films is also shown. Electrochemical impedance spectroscopy (EIS) was applied to monitor the failure process of different kinds of coatings. All the results confirm the synergy of the passive and active functions of the BTA@SN-rGO coating.
RESUMEN
BACKGROUND: Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease (ILD) with unknown etiology, characterized by sustained damage repair of epithelial cells and abnormal activation of fibroblasts, the underlying mechanism of the disease remains elusive. METHODS: To evaluate the role of Tuftelin1 (TUFT1) in IPF and elucidate its molecular mechanism. We investigated the level of TUFT1 in the IPF and bleomycin-induced mouse models and explored the influence of TUFT1 deficiency on pulmonary fibrosis. Additionally, we explored the effect of TUFT1 on the cytoskeleton and illustrated the relationship between stress fiber and pulmonary fibrosis. RESULTS: Our results demonstrated a significant upregulation of TUFT1 in IPF and the bleomycin (BLM)-induced fibrosis model. Disruption of TUFT1 exerted inhibitory effects on pulmonary fibrosis in both in vivo and in vitro. TUFT1 facilitated the assembly of microfilaments in A549 and MRC-5 cells, with a pronounced association between TUFT1 and Neuronal Wiskott-Aldrich syndrome protein (N-WASP) observed during microfilament formation. TUFT1 can promote the phosphorylation of tyrosine residue 256 (Y256) of the N-WASP (pY256N-WASP). Furthermore, TUFT1 promoted transforming growth factor-ß1 (TGF-ß1) induced fibroblast activation by increasing nuclear translocation of pY256N-WASP in fibroblasts, while wiskostatin (Wis), an N-WASP inhibitor, suppressed these processes. CONCLUSIONS: Our findings suggested that TUFT1 plays a critical role in pulmonary fibrosis via its influence on stress fiber, and blockade of TUFT1 effectively reduces pro-fibrotic phenotypes. Pharmacological targeting of the TUFT1-N-WASP axis may represent a promising therapeutic approach for pulmonary fibrosis.