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Graphite is an attractive cathode material for energy storage because it allows reversible intercalation/deintercalation of many compound anions at high potentials. However, because the sizes of the compound anions are greatly larger than the lamellar spacing of graphite, common graphite used as cathode may suffer from slow kinetics and large volume expansion. Here, it is demonstrated that graphite with high crystallinity and nanosheet-bricked porous structure can be an excellent cathode for aluminum-ion batteries. This porous graphite is derived from carbon black via a simple electrochemical graphitization in molten CaCl, and the high crystallinity and thin layer characters facilitate the high capacity and high rate storage of aluminum tetrachloride ions. Moreover, the bricked porous structure endows the fabricated cathode with a providential porosity to perfectly match the huge volume expansion of graphite (650% against a charging capacity of 100 mA h g), thus this electrochemical graphite exhibits integrated high gravimetric and volumetric capacities as well as high structural stability during cycling.

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Background Diabetic nephropathy (DN) is a disease characterized by oxidative stress and apoptosis of renal tubular epithelial cells driven by hyperglycemia. Apigenin is a flavonoid compound that possesses potent anti-apoptotic properties. The present study aimed to explore the protective effects and underlying mechanisms of apigenin on renal tubular epithelial cells exposed to hyperglycemia. Material/Methods Human renal epithelial cell HK-2 were incubated to D-glucose to establish in vitro DN model. The cell viability, lactate dehydrogenase (LDH) release, apoptosis and oxidative stress were evaluated. qRT-PCR was performed to determine the mRNA levels of NF-E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). Western blot analysis was performed to measure the protein expressions of Nrf2. Results In HK-2 cells, high glucose reduced cell viability in a concentration- and time-dependent manner. Apigenin suppressed the decrease in cell viability and increase in supernatant LDH release at 100 and 200 μM after 48-h treatment. Apigenin reduced apoptotic rate and pro-inflammatory cytokines production. Apigenin suppressed oxidative stress and increased mRNA expressions of Nrf2 and HO-1. Inhibition of Nrf2 using small interfering RNA (siRNA), or cotreatment with LY294002, an inhibitor of PI3K/Akt, abolished the protective effect on high glucose-induced injury, oxidative stress, and pro-inflammatory cytokines production by apigenin. LY294002 also attenuated the increase in Nrf2 protein by apigenin in high glucose-treated HK-2 cells. Conclusions Apigenin protects renal tubular epithelial cells against high glucose-induced injury through suppression of oxidative stress and inflammation via activation of the Nrf2 pathway.