Self-supported nanotube arrays of sulfur-doped TiO2 on metal substrates are fabricated using electrochemical anodization and subsequent sulfidation. The nanotube arrays can serve as an efficient anode for sodium storage, enabling ultrastable cycling (retaining 91% of the 2nd capacity up to 4400 cycles) and robust rate capability (167 mA h g(-1) at 3350 mA g(-1)), remarkably outperforming any other reported TiO2 -based electrodes.

Sodium‐ion batteries have attracted extraordinary attention owing to their low cost and raw materials in abundance. A major challenge of practical implementation is the lack of accessible and affordable anodes that can reversibly store a substantial amount of Na ions in a fast and stable manner. It is reported that surface engineered sodium titanate (Na2Ti3O7) nanotube arrays directly grown on Ti substrates can serve as efficient anodes to meet those stringent requirements. The fabrication of the nanotube arrays involves hydrothermal growing of Na2Ti3O7 nanotubes, surface deposition of a thin layer of TiO2, and subsequent sulfidation. The resulting nanoarrays exhibit a high electrochemical Na‐storage activity that outperforms other Na2Ti3O7 based materials. They deliver high reversible capacities of 221 mAh g−1 and exhibit a superior cycling efficiency and rate capability, retaining 78 mAh g−1 at 10 C (1770 mA g−1) over 10 000 continuous cycles. In addition, the full cell consisting of Na2Ti3O7 nanotube anode and Na2/3(Ni1/3Mn2/3)O2 cathode is capable of delivering a specific energy of ≈110 Wh kg−1 (based on the mass of both electrodes). The surface engineering can provide useful tools in the development of high performance anode materials with robust power and cyclability.

We present a general and rational approach to fabricate highly accessible and affordable sodium-ion battery anodes by engineering three-dimensional hydrogenated Na2Ti3O7 nanoarrays supported on flexible Ti substrates. The hydrogenated Na2Ti3O7 nanoarrays exhibit desirable properties for sodium storage, such as high surface area, high electrical conductivity, and Na(+) diffusivity. The as-obtained nanoarrays demonstrate remarkably stable and robust Na-storage performance when tested as binder-free anodes for sodium-ion battery. They can afford a high reversible (desodiation) capacity of 227 mAh g(-1) and retain a capacity of 65 mAh g(-1) over 10,000 continuous cycles at a high rate of 35 C. Therefore, through this synergy of array architecture and hydrogenation, it is possible to engineer numerous anodes that can reversibly store Na(+) ions in a fast and stable manner.

Sodium-ion batteries (SIBs) offer a promise of a scalable, low-cost, and environmentally benign means of renewable energy storage. However, the low capacity and poor rate capability of anode materials present an unavoidable challenge. In this work, it is demonstrated that surface phosphorylated TiO nanotube arrays grown on Ti substrate can be efficient anode materials for SIBs. Fabrication of the phosphorylated nanoarray film is based on the electrochemical anodization of Ti metal in NH F solution and subsequent phosphorylation using sodium hypophosphite. The phosphorylated TiO nanotube arrays afford a reversible capacity of 334 mA h g at 67 mA g , a superior rate capability of 147 mA h g at 3350 mA g , and a stable cycle performance up to 1000 cycles. In situ X-ray diffraction and transmission electron microscopy reveal the near-zero strain response and robust mechanical behavior of the TiO host upon (de)sodiation, suggesting its excellent structural stability in the Na storage application.

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Objectives Investigating the antipulmonary fibrosis effect of mangiferin from Mangifera indica and the possible molecular mechanism. Methods In vivo, bleomycin (BLM)‐induced pulmonary fibrosis experimental model was used for evaluating antipulmonary fibrosis effect of mangiferin. Histopathologic examination and collagen deposition were investigated by HE and Masson staining as well as detecting the content of hydroxyproline. The expression of transforming growth factor‐β1 (TGF‐β1), α‐smooth muscle actin (α‐SMA), TLR4 and p‐P65 in lung tissue was analysed through immunofluorescence. Leucocytes and inflammatory cytokines including IL‐1β, IL‐6, TNF‐α and MCP‐1 in bronchoalveolar lavage fluid were detected by cell counting and enzyme‐linked immunosorbent assay. In vitro, TGF‐β1‐induced A549 epithelial–mesenchymal transition (EMT) cell model was used for investigating the possible molecular mechanism. Reactive oxygen species (ROS) generation was detected by DCFH‐DA assay. Expression of all proteins was examined by Western blot. Key findings Oral administration of mangiferin could attenuate the severity of BLM‐induced pulmonary fibrosis through increasing the survival rate, improving histopathological lesion and body weight loss as well as decreasing pulmonary index visibly. Pulmonary hydroxyproline content, TGF‐β1, and α‐SMA levels were reduced significantly. The molecular mechanism of mangiferin for inhibiting pulmonary fibrosis is that it could obviously inhibit the occurrence of inflammation and the secretion of inflammatory cytokine through inhibiting activation of TLR4 and phosphorylation of p65. Meanwhile, EMT process was suppressed obviously by mangiferin through blocking the phosphorylation of Smad2/3 and reducing MMP‐9 expression. Besides, mangiferin could significantly inhibit the process of oxidant stress through downregulating the intracellular ROS generation. Conclusions Mangiferin attenuates BLM‐induced pulmonary fibrosis in mice through inhibiting TLR4/p65 and TGF‐β1/Smad2/3 pathway.

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