Search

[Display omitted] • A method using nanoslit-grating structures was proposed to measure the propagation length of SPPs. • A model for performing quantitative measurements was established. • The standard deviation of the proposed method can be as small as 2.33% of its mean value. • The measurement error of the proposed method in measuring the intensity ratio can be smaller than 2% of its theoretical value. The propagation attenuation of surface plasmon polaritons (SPPs) has an important impact on the performance of plasmonic devices, so measuring their propagation length is important for designing plasmonic devices. Here we propose a method using a single nanoslit surrounded on both sides by surface gratings to measure the propagation length of SPPs. In this method, the propagation length of SPPs is obtained by using a narrow-area statistical averaging method to process the data of the intensity ratio of two diffracted light waves, which are converted from two SPPs that have the same initial intensity but travel different distances in opposite directions in a narrow area of a surface of a metal film. We demonstrate experimentally that at the illumination wavelength of 632.8 nm, the mean value of the propagation length of SPPs propagating at the interface between the air and a gold film with a thickness of about 360 nm measured using the proposed method is 9.88 μm, with a standard deviation of 0.23 μm (i.e., 2.33 % of the mean value). In addition, we demonstrate experimentally that the measurement error of the proposed method in measuring the intensity ratio of the two diffracted light waves, which is the dominant error of the proposed method in measuring the propagation length of SPPs, can be smaller than 2 % of its theoretical value. [ABSTRACT FROM AUTHOR]

Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases with limited treatment options. Moreover, its prevalence is doubled in type 2 diabetes mellitus (T2DM). Kaempferol (KAP) is a flavonoid compound that has been suggested to have beneficial effects on NAFLD, but studies on the mechanism are lacking, especially in the diabetic state. Herein, we investigated the effect of KAP on NAFLD associated with T2DM and its underlying mechanism in vitro and in vivo. The results of in vitro studies indicated that KAP treatment (10−8–10−6 M) significantly reduced lipid accumulation in oleic acid-induced HepG2 cells. Moreover, in the T2DM animal model of db/db mice, we confirmed that KAP (50 mg/kg) significantly reduced lipid accumulation and improved liver injury. Mechanistic studies in vitro and in vivo showed that Sirtuin 1 (Sirt1)/AMP-activated protein kinase (AMPK) signal was involved in KAP regulation of hepatic lipid accumulation. KAP treatment activated Sirt1 and AMPK, upregulated the levels of fatty acid oxidation-related protein proliferator activated receptor gamma coactivator 1α (PGC1α); and downregulated lipid synthesis-related proteins, including acetyl-coA carboxylase (ACC), fatty acid synthase (FASN), and sterol regulatory element-binding protein 1 (SREBP1). Furthermore, the curative effect of KAP on lipid accumulation was abolished by siRNA-mediated knockdown of either Sirt1 or AMPK. Collectively, these findings suggest that KAP may be a potential therapeutic agent for NAFLD associated with T2DM by regulating hepatic lipid accumulation through activation of Sirt1/AMPK signaling. [Display omitted] • Kaempferol attenuates hepatic steatosis in type 2 diabetic mice. • Kaempferol improves metabolic disorder and reduces adipose tissue mass in type 2 diabetic mice. • Kaempferol mitigates lipid accumulation in OA-induced HepG2 cells. • Kaempferol alleviates NAFLD through activation of Sirt1/AMPK signaling pathway. [ABSTRACT FROM AUTHOR]

• Puerarin ameliorates muscle wasting in type 1 diabetic rats. • Puerarin improves skeletal muscle weight and strength in type 1 diabetic rats. • Puerarin promotes transformation of muscle fiber types from slow-twitch to fast-twitch in type 1 diabetic rats. • Puerarin activates Akt/mTOR while inhibites autophagy in skeletal muscle. Puerarin is an isoflavonoid extracted from Pueraria lobate with extensive pharmacological effects in traditional Chinese medicine. The evidence implicates that puerarin mitigates hyperglycemia and various relevant complications. Here, the effect of puerarin on skeletal muscle wasting induced by type 1 diabetes (T1D) was explored. Streptozotocin (STZ)-induced T1D male Sprague Dawley (SD) rats were used in this study. Muscle strength, weight and size were measured. L6 rat skeletal muscle cells were applied for in vitro study. Our results showed that eight-week oral puerarin administration (100 mg/kg) increased muscle strengths and weights accompanied by enhanced skeletal muscle cross-sectional areas in diabetic rats. Simultaneously, puerarin also reduced expressions of several muscle wasting marker genes including F-box only protein 32 (Atrogin-1) and muscle-specific RING-finger 1 (Murf-1) in diabetic group both in vitro and in vivo. Transformation from type I fibers (slow muscle) to type II fibers (fast muscle) were also observed under puerarin administration in diabetic rats. Puerarin promoted Akt/mTOR while inhibited LC3/p62 signaling pathway in skeletal muscle cells. In conclusion, our study showed that puerarin mitigated skeletal muscle wasting in T1D rats and closely related with Akt/mTOR activation and autophagy inhibition. Whether this effect in murine applies to humans remains to be determined. [ABSTRACT FROM AUTHOR]