Cell junctions are protein structures located at specific cell membrane domains that determine key processes in multicellular development. Here we report spatially selective imaging of cell junctions by electrochemiluminescence (ECL) microscopy. By regulating the concentrations of luminophore and/or co-reactant, the thickness of ECL layer can be controlled to match with the spatial location of different cell junctions. At a low concentration of luminophore, ECL generation is confined to the electrode surface, thus revealing only cell-matrix adhesions at the bottom of cells. While at a high concentration of luminophore, the ECL layer can be remarkably extended by decreasing the co-reactant concentration, thus allowing the sequential imaging of cell-matrix and cell-cell junctions at the bottom and near the apical surface of cells, respectively. This strategy not only provides new insights into the ECL mechanisms but also promises wide applications of ECL microscopy in bioimaging.Cell junctions are specific domains on the cell membrane that tether cells to the extracellular matrix or connect the lateral surfaces of adjacent cells. [1] The junctions located at the bottom of basal cell membrane are called cell-matrix adhesions, while those near the apical surface of cell are termed as cell-cell junctions. [2] They are not only responsible for the physical integration of individual cells to threedimensional tissues, [3] but also regulate a variety of biological processes in multicellular organisms, such as neuronal pathfinding, embryonic development, cancer invasion and metastasis. [4] Although cell junctions have distinct structures and functions, they are all involved in a continuous crosstalk. [5] Knowing precisely how cell-matrix and cell-cell junctions are distributed in the cellular structure is critical for understanding their functions and associated biological events. Surfacesensitive methods such as interference reflection, [6] total internal reflection fluorescence [7] and surface plasmon resonance microscopies [8] have been used in mapping cell-matrix adhesions, while electron microscopy and fluorescence microscopy (in particular confocal laser scanning microscopy, CLSM) are the most frequently used methods for imaging cell-cell junctions, [9] which however often require expensive facilities or specific immunofluorescent labelling.

Electrochemiluminescence (ECL) is a powerful transduction technique in biosensing and diagnostics, while mechanistic studies are still scarce. Herein we report the combined use of microtube electrode (MTE) and microscopy to measure the thickness of ECL layer (TEL) to decipher reaction mechanisms. For the classical system involving tris(2,2'-bipyridyl)ruthenium and tri-n-propylamine, the ECL pattern generated at the MTE tends to change from ring to spot upon increasing the luminophore concentration, with the TEL varying from ca. 3.1 mm to > 4.5 mm. This variation is rationalized to arise from the contribution of the so-called catalytic route. While using 2-(dibutylamino)ethanol as the coreactant, the ECL pattern remains ring-shaped and independent on the luminophore concentration. The TEL in this case is ca. 2.1 mm, implying that ECL generation is always surfaceconfined. MTEs can thus act as optical rulers for measuring the TEL and providing insightful mechanistic information.

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Luteoin is one of the main flavones and the crucial effective component of peanut hull extract (PHE). The present paper aims to elucidate the absorption mechanism of luteolin and clarify whether its absorption occurs primarily at a specific site of the intestine by an in situ single-pass intestinal perfusion (SPIP) model. Moreover, the paper investigates the difference in absorption of luteolin when it is administered in PHE form and as pure luteolin by the SPIP model and in vivo pharmacokinetics studies. Results showed that the effective permeability ( P eff) and absorption rate constant ( k a) of pure luteolin(5.0 microg/mL) in duodenum and jejunum were not significantly different, but markedly higher than that in the colon and ileum. The P eff and k a of luteolin in jejunum were concentration-independent, and the ATP inhibitor (DNP) did not influence P eff and k a of pure luteolin. However, the P eff and k a of luteolin in PHE were significantly greater than that of pure luteolin. The pharmacokinetics study showed that following oral administration of a single dose of pure luteolin (14.3 mg/kg) or PHE (= 14.3 mg/kg of luteolin) in rats, the peak concentration of luteolin in plasma ( C max) and the area under the concentration curve (AUC) for pure luteolin were 1.97 +/- 0.15 microg/mL and 10.7 +/- 2.2 microg/mL.h, respectively. These parameters were significantly lower than those of the PHE group ( P < 0.05), C max = 8.34 +/- 0.98 microg/mL and AUC = 20.3 +/- 1.3 microg/mL.h, respectively. It can be concluded that luteolin is absorbed passively in the intestine of rats and that its absorption is more efficient in the jejunum and duodenum than in the colon and ileum. The bioavailability of luteolin in PHE form is significantly greater than that of pure luteolin.

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