Elements doping has been used to improve the electrochemical performances of O3-type layered transition metal oxide cathodes for sodium-ion batteries. However, their roles and the improvement mechanism have not been clearly understood. Herein, the effects of Mg substitution for Mn on the structure and electrochemical performances of NaMnNiFeMgO have been comprehensively investigated and some new insights into the roles of Mg in improving the rate capability and cycling stability have been presented. (1) The substitution of Mg for Mn enlarges the interlayer spacing, which not only enhances Na diffusion and the rate capability but also alleviates the lattice strains induced by Na intercalation/deintercalation. (2) The substitution of Mg by Mn also shrinks TM-O bond and TMO slabs, which enhances the layered structure stability. (3) The Mg substitution also mitigates the structure distortion or volume change of the crystal lattices and suppresses the irreversible phase transitions. (4) The substitution of low-valence Mg for Mn reduces Mn and minimizes Jahn-Teller effect, which also further alleviates the irreversible phase transformations and improves the layered structure stability. This study not only unveils the roles of Mg but also presents some insights into designing the cathode materials with both high rate capability and high cycling stability through the lattice structure regulation.
Podocytes are terminally differentiated epithelial cells lacking the ability to proliferate. The loss of podocytes is a hallmark of progressive kidney diseases, including diabetic nephropathy (DN). Endoplasmic reticulum stress (ERS)-induced apoptosis is involved in a number of pathological conditions, including DN. The aim of the present study was to investigate whether a high glucose environment induces the apoptosis of podocytes through ERS. Differentiated mouse podocytes were divided into three groups: the normal glucose group (NG, 1 g/l D-glucose), the high glucose group (HG, 4.5 g/l D-glucose) and the mannitol group (M, 1 g/l D-glucose plus 24.4 mM mannitol). The cells were harvested following stimulation with the indicated treatments for 12, 24, 48 and 72 h. Podocyte apoptosis was determined using TUNEL assay and flow cytometry (propidium iodide staining). Glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP/GADD153) and caspase-12 expression was analyzed by RT-PCR, western blot analysis and immunocytochemistry. The apoptotic rate increased significantly in the HG group compared with the NG and M groups at 48 and 72 h (all P<0.01). GRP78 expression, an indicator of ERS, was increased from 12 h, indicating that ERS was activated. Subsequently, two ER-associated death (ERAD) pathways, the CHOP/GADD153- and caspase-12-dependent pathways, were detected. CHOP/GADD153 expression reached its peak at 48 h, and caspase-12 expression gradually increased with time. Spearman’s correlation analysis revealed that caspase-12 and CHOP/GADD153 positively correlated with the apoptotic rate (r=0.915, P<0.01 and r=0.639, P<0.01). Our results demonstrated that hyperglycemia (high glucose) induced apoptosis partly through ERS in the differentiated mouse podocytes, which possibly contributes to the pathogenesis of DN.
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