ABSTRACT
Aqueous zinc-bromine batteries (ZBBs) are highly promising because of the advantages of safety and cost. Compared with flow ZBBs, static ones without the assistance of pumping and tank components possess decreased cost and increased energy density and efficiency. Yet, the issues of Zn dendrites and shuttle effect of polybromide ions (Brn-) are more serious in nonflow ZBBs. Meanwhile, the hydrogen evolution reaction (HER) and the sluggish kinetics of the Br2/Br- couple are also in-negligible. Herein, a compressive approach, the cation-exchange membrane (CEM) coating on Zn anodes and N-defect decoration toward carbon felt cathodes, is developed. The CEM with cation-only function can inhibit the formation of Zn dendrites via tuning the Zn2+ flow at the interface, block the noncationic substances, and hence prevent the shuttle of Br2/Brn- and the water decomposition-concerned HER. The optimized nonflow ZBBs can deliver high Coulombic, voltage, and energy efficiencies of 94.1, 92.8, and 87.4%, respectively, which can be well remained in 1000 cycles. Meanwhile, the output voltage is as high as 1.7 V at 10 mA cm-2 with a high areal capacity of 2 mA h cm-2, and a LED with a rated voltage of 1.6 V can be powered successfully, exhibiting high application value.
ABSTRACT
Recent clinical studies highlight the neuroprotective effects of esketamine, but its benefits following traumatic brain injury (TBI) have not been defined. Here, we investigated the effects of esketamine following TBI and its associated neuroprotection mechanisms. In our study, controlled cortical impact injury on mice was utilized to induce the TBI model in vivo. TBI mice were randomized to receive vehicle or esketamine at 2 h post-injury for 7 consecutive days. Neurological deficits and brain water content in mice were detected, respectively. Cortical tissues surrounding focal trauma were obtained for Nissl staining, immunofluorescence, immunohistochemistry, and ELISA assay. In vitro, esketamine were added in culture medium after cortical neuronal cells induced by H2O2 (100µM). After exposed for 12h, neuronal cells were obtained for western blotting, immunofluorescence, ELISA and CO-IP assay. Following administration of 2-8 mg/kg esketamine, we observed that 8 mg/kg esketamine produced no additional recovery of neurological function and ability to alleviate brain edema in TBI mice model, so 4 mg/kg esketamine was selected for subsequent experiments. Additionally, esketamine can effectively reduce TBI-induced oxidative stress, the number of damaged neurons, and the number of TUNEL-positive cells in the cortex of TBI models. Meanwhile, the levels of Beclin 1, LC3 II, and the number of LC3-positive cells in injured cortex were also increased following esketamine exposure. Western blotting and immunofluorescence assays showed that esketamine accelerated the nuclear translocation of TFEB, increased the p-AMPKα level and decreased the p-mTOR level. Similar results including nuclear translocation of TFEB, the increases of autophagy-related markers, and influences of AMPK/mTOR pathway were observed in H2O2-induced cortical neuronal cells; however, BML-275 (AMPK inhibitor) can reverse these effects of esketamine. Furthermore, TFEB silencing not only decreased the Nrf2 level in H2O2-induced cortical neuronal cells, but also alleviated the oxidative stress. Importantly, CO-IP confirmed the interaction between TFEB and Nrf2 in cortical neuronal cells. These findings suggested that esketamine exerts the neuroprotective effects of esketamine in TBI mice model via enhancing autophagy and alleviating oxidative stress; its mechanism involves AMPK/mTOR-dependent TFEB nuclear translocation-induced autophagy and TFEB/Nrf2-induced antioxidant system.
