Construction of a Reversible Solid-state Fluorescence Switching Via Photochromic Diarylethene and Si-ZnO Quantum Dots.

Developing fluorescence switching as functional system is highly desirable for potential applications in the fields of light-responsive materials or devices. Attempt to construct fluorescence switching system tend to focus on the high fluorescence modulation efficiency, especially in solid state. Herein, a photo-controlled fluorescence switching system was constructed with photochromic diarylethene and trimethoxysilane modified zinc oxide quantum dots (Si-ZnO QDs) successfully. It was verified by the measurement of modulation efficiency, fatigue resistance as well as theoretical calculation. Upon irradiation with UV/Vis lights, the system exhibited excellent photochromic property and photo-controlled fluorescence switching performance. Furthermore, the excellent fluorescence switching characters could also be realized in solid state and the fluorescence modulation efficiency was determined to be 87.4%. The results will provide new strategies to the construction of reversible solid-state photo-controlled fluorescence switching for the application in the fields of optical data storage and security labels.

A photo-controlled fluorescent switching based on carbon dots and photochromic diarylethene for bioimaging.

Carbon dots (CDs) as luminescent zero-dimensional carbon nanomaterials have good aqueous dissolution, photostability, high quantum yield, and tunability of emission color. It has great application potential in many fields, including bioimaging, labeling of biological species, drug delivery, and sensing in biomedical. However, controlling the fluorescence emission of carbon dots remains a formidable challenge. Herein, we designed and exploited a photo-controlled fluorescent switching based on photochromic diarylethene (DT) and CDs for bioimaging. It could be modulated reversibly between "ON" and "OFF" under UV/vis light exposure. The fluorescent modulation efficiency was as high as 95.3%. The fluorescent switching could be used to the bioimaging in HeLa cells with low cell toxicity. Therefore, this fluorescent switching could be a promising candidate in many potential application areas, especially in bioimaging.

Effect of tangnaikang on TGF-beta1-induced transdifferentiation of human renal tubular epithelial HK-2 cells.

OBJECTIVE: To explore the function of Tangnaikang (TNK) in the prevention and treatment of renal interstitial fibrosis through transdifferentiation of the human renal tubular epithelial cell line HK-2 induced by transforming growth factor-beta1 (TGF-beta1). METHODS: HK-2 cells cultured in dulbecco's modified eagle medium/F12 (1 : 1) with 10% fetal calf serum were divided into six groups: blank control group, TGF-beta1 group (TGF-beta1 10 ng/mL), serum control group (TGF-beta1 10 ng/mL + 10% serum), treatment group 1 (TGF-beta1 10 ng/mL + 5% TNK serum), treatment group 2 (TGF-beta1 10 ng/mL + 10% TNK serum), and treatment group 3 (TGF-beta1 10 ng/mL + 20% TNK serum). Cell proliferation was detected by 4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Expression of alpha-smooth muscle actin (alpha-SMA) and E-cadherin were observed by immunohistochemical assay. The contents of collagen I (Col I), collagen III (Col III), and fibronectin (FN) in the culture medium supernatant were detected by ELISA. RESULTS: E-cadherin was expressed and alpha-SMA was not expressed in normal HK-2 cells. In HK-2 cells cultured with TGF-beta1, alpha-SMA expression significantly increased, HK-2 cells significantly proliferated, and secretion of Col I, Col III, and FN significantly increased compared with the blank control group (all P < 0.05). In the HK-2 cells cultured with TGF-beta1 and TNK serum, the expression of alpha-SMA significantly decreased, the expression of E-cadherin significantly increased, and the cell proliferation and the secretion of Col I, Col III and FN were significantly inhibited compared with the TGF-beta1 group (all P < 0.05). CONCLUSION: TNK can inhibit cell proliferation and reduce secretion of Col I, Col III, and FN. This indicates that TNK can inhibit transdifferentiation of human renal tubular epithelial cells induced by TGF-beta1, with the effect of preventing and treating renal interstitial fibrosis.