RESUMO
Photonic moiré-like lattices, a readily accessible platform for realizing the spatial localization of light, attract intensive attention due to their unique flatband characteristics. In this paper, a periodic moiré-like lattice with embedded defects is proposed theoretically, and the linear propagation of the probe beam in such a system is investigated intensively. The results show that the positions of defects in periodic moiré-like lattices depend on the sublattice rotation angle. Further studies show that the localization of light could be improved by adjusting the apodization function of defects. In addition, the experimental observation of the moiré-like lattice with apodized defects also confirms the theoretical analysis. Our study enriches the physical connotation of photonic moiré lattices and guides the design of novel photonic crystal fibers.
RESUMO
BACKGROUND/AIMS: Astragaloside (AGS) extracted from radix astragalin (Huangqi) has been considered to be beneficial to liver diseases. In this study, we examined the role played by AGS in alleviating hepatic fibrosis function via protease-activated receptor-2 (PAR2) mechanisms. We hypothesized that AGS affects PAR2 signaling pathway thereby improving hepatic function in rats with hepatic fibrosis induced by carbon tetrachloride (CCl4). We further hypothesized that AGS attenuates impaired hepatic function evoked by CCl4 to a greater degree in diabetic animals. METHODS: ELISA and Western Blot analysis were used to examine PAR2 signaling pathway in diabetic CCl4-rats and non-diabetic CCl4-rats. RESULTS: AGS inhibited the protein expression of PAR2 and its downstream pathway PKA and PKCÉ in CCl4-rats. Notably, the effects of AGS were greater in CCl4-rats with diabetes. AGS also significantly attenuated the CCl4-induced upregulations of pro-inflammatory cytokines, namely interleukin-1ß, interleukin-6 and tumor necrosis factor-α accompanied with decreases of collagenic parameters such as hexadecenoic acid, laminin and hydroxyproline. Additionally, AGS improved the CCl4-induced exaggerations of liver index and functions including alanine aminotransferase, aspartate aminotransferase. Moreover, TGF-ß1, a marker of hepatic fibrosis, was increased in CCl4-rats and AGS inhibited increases in TGF-ß1 induced by CCl4. CONCLUSIONS: AGS alleviates hepatic fibrosis by inhibiting PAR2 signaling expression and its effects are largely enhanced in diabetic animals. Targeting one or more of these signaling molecules may present new opportunities for treatment and management of hepatic fibrosis; and results of our study are likely to shed light on strategies for application of AGS because it has potentially greater therapeutic effectiveness for hepatic fibrosis in diabetes.
