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Heteroatom-doped hard carbon is a popular method to optimize the electrochemical performance of anode electrodes for sodium-ion batteries. Herein, phosphorus-doped hollow carbon nanorods (P-HCNs) are obtained by a one-step synthesis with a high phosphorus content of 7.5 atom %. By controlling the P configuration, the P-HCNs03 exhibits reversible capacity as high as 260 mA h g–1at the current density of 1.0 A g–1after 500 cycles with an initial Coulombic efficiency (ICE) of 73%. When the amount of phosphorus in the as-prepared materials is changed, the different structures of the P-doped carbon lattices are analyzed by X-ray diffraction, Raman spectroscopy, and X-ray photoelectron spectroscopy. Based on the first-principles calculation, although the P–O bond has the most configurations, the excellent reversible capacity of the electrode is attributed to the strong Na-absorption ability of P═O and P–C bonds. The sodium-based dual-ion batteries (NDIBs) assembled with P-HCNs03 as an anode and expanded graphite as a cathode (P-HCNs03//EG) exhibited a high energy density of 138 W h kg–1at a power density of 159 W kg–1. The results provide an important angle to optimize the performance of hard carbons with other functionalized heteroatoms.

Objective: Gastric cancer (GC) remains a prevailing threat to life. Baicalein exhibits anti-cancer properties. This study estimated the mechanism of baicalein in GC cell apoptosis by mediating endoplasmic reticulum stress (ERS) through the PI3K/AKT pathway. Methods: After treatment with different concentrations of baicalein, GC cell (HGC-27 and AGS) viability was detected by MTT assay. AGS cells more sensitive to baicalein treatment were selected as study subjects. The IC50 of baicalein on AGS cells was determined. Colony formation, cell cycle, and apoptosis were detected using crystal violet staining and flow cytometry. Levels of ERS-related and BTG3/PI3K/AKT pathway-related proteins were determined by Western blot. Intracellular Ca2+level was measured using Fluo-3 AM fluorescence working solution. GC mouse models were established by subcutaneously injecting AGS cells into the right rib and were intragastrically administrated with baicalein. Tumor volume and weight were recorded. Expression of Ki67 in tumor tissues and positive expression of apoptotic cells were detected by immunohistochemistry and TUNEL staining. Results: Baicalein inhibited cell proliferation and induced G0/G1 arrest and apoptosis by regulating the cell cycle, and triggered ERS in GC cells. Baicalein impeded the PI3K/AKT pathway by activating BTG3, thereby triggering ERS and inducing apoptosis. BTG3 inhibition reversed baicalein-induced apoptosis and ERS. Baicalein regulated GC cells in a concentration-dependent manner. Moreover, in xenograft mice, baicalein prevented tumor growth, decreased Ki67-positive cells, activated BTG3, and inhibited the PI3K/AKT pathway, thus activating ERS and increasing apoptotic cells. Conclusion: Baicalein facilitates GC cell apoptosis by triggering ERS via repression of the PI3K/AKT pathway.