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The design of advanced supercapacitors requires electrode materials that combine high surface area with a developed hierarchical porous structure to facilitate ion transport and electrolyte permeability.

Icariside II (ICAII) is a bioflavonoid compound which has demonstrated anti-oxidative, anti-inflammatory and anti-apoptotic biological activities. However, to the best of our knowledge, whether ICAII can alleviate myocardial ischemia and reperfusion injury (MIRI) remains unknown. The aim of the present study was to determine whether ICAII exerted a protective effect on MIRI and to investigate the potential underlying mechanism of action. A rat MIRI model was established by ligation of the left anterior descending coronary artery for 30 min, followed by a 24 h reperfusion. Pretreatment with ICAII with or without a PI3K/AKT inhibitor was administered at the beginning of reperfusion. Morphological and histological analyses were detected using hematoxylin and eosin staining; the infarct size was measured using Evans blue and 2,3,5-triphenyltetrazolium chloride staining; and plasma levels of lactate dehydrogenase (LDH) and creatine kinase-myocardial band (CK-MB) were analyzed using commercialized assay kits. In addition, the cardiac function was evaluated by echocardiography and the levels of cardiomyocyte apoptosis were determined using a TUNEL staining. The protein expression levels of Bax, Bcl-2, cleaved caspase-3, interleukin-6, tumor necrosis factor-α, PI3K, phosphorylated (p)-PI3K, AKT and p-AKT were analyzed using western blotting analysis. ICAII significantly reduced the infarct size, decreased the release of LDH and CK-MB and improved the cardiac function induced by IR injury. Moreover, ICAII pretreatment significantly inhibited myocardial apoptosis and the inflammatory response. ICAII also upregulated the expression levels of p-PI3K and p-AKT. However, the protective effects of ICAII were abolished by an inhibitor (LY294002) of the PI3K/AKT signaling pathway. In conclusion, the findings of the present study suggested that ICAII may mitigate MIRI by activating the PI3K/AKT signaling pathway.

Background: As an important nutrient, soybean protein-derived peptides (SPP) affect the immune function of animals. Objective: This study describes the effects of nutrient supplementation with SPP on the negative nitrogen balance in the burn injury-induced inflammatory response of aged rats. Design: Soybean protein isolate (SPI) was hydrolyzed to obtain SPP. A negative nitrogen-balance aged rat model and a major full-thickness 30% total body surface area (TBSA) burn-injury rat model were utilized. Results: The results show that SPP can increase the speed and ability of inflammatory stress by adjusting white blood cell counts. Soybean protein-derived peptides significantly increased serum immunoglobulin M (IgM), immunoglobulin G (IgG) and immunoglobulin A (IgA) levels; significantly decreased serum interleukin-1 beta (IL-β), tumor necrosis factor-alpha (TNF-α) and regulated upon activation normal T-cell expressed and secreted (RANTES) levels. These results give conclusive evidence that SPP has a significantly positive effect in improving the immune function on the condition of negative nitrogen balance with burn-injury, and reducing excessive inflammation. Conclusions: Nutrient supplementation of SPP can, therefore, be used as an adjuvant treatment to inhibit the development and severity of inflammatory reactions caused by burns, providing a novel therapy for the treatment and positive prognosis of burn patients.