The synthesis of a single‐layer covalent organic framework (COF) with spatially modulated internal potentials provides new opportunities for manipulating the electronic structure of molecularly defined materials. Here, the fabrication and electronic characterization of COF‐420: a single‐layer porphyrin‐based square‐lattice COF containing a periodic array of oriented, type II electronic heterojunctions is reported. In contrast to previous donor–acceptor COFs, COF‐420 is constructed from building blocks that yield identical cores upon reticulation, but that are bridged by electrically asymmetric linkers supporting oriented electronic dipoles. Scanning tunneling spectroscopy reveals staggered gap (type II) band alignment between adjacent molecular cores in COF‐420, in agreement with first‐principles calculations. Hirshfeld charge analysis indicates that dipole fields from oriented imine linkages within COF‐420 are the main cause of the staggered electronic structure in this square grid of atomically–precise heterojunctions.

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BackgroundPreviously, Huangqi decoction (HQD) has been found to have a potential therapeutic effect on DMN-induced liver cirrhosis. Here, the mechanisms of HQD action against liver fibrosis were investigated in relation to hepatocyte apoptosis and hepatic inflammation regulation.MethodsLiver fibrosis was induced by DMN administration for 2 or 4 weeks. Hepatocyte apoptosis and of Kupffer cells (KC) and hepatic stellate cells (HSC) interaction were investigated using confocal microscopy. The principle cytokines, fibrogenic proteins and apoptotic factors were investigated using western blot analysis.ResultsCompared with the DMN-water group, HQD showed decreased hepatocyte apoptosis and reduced expression of apoptotic effectors, cleaved-caspase-3, and fibrotic factors, such as smooth muscle α-actin (α-SMA), transforming growth factor beta-1 (TGF-β1). However, the KC marker CD68 increased significantly in DMN-HQD liver. Confocal microscopy demonstrated widespread adhesion of KCs to HSCs in DMN-water and DMN-HQD rats liver.ConclusionsHQD exhibited positive protective effects against liver fibrosis; its mechanism of action was associated with protection from hepatocyte apoptosis and the promotion of CD68 expression in the devolopment of liver fibrosis to cirrhosis development.