Molybdenum disulfide (MoS 2 ) nanosheets are promising candidates as earth-abundant and lowcost catalyst for hydrogen evolution reaction (HER). Nevertheless, compared with the benchmark Pt/C catalyst, the application of MoS 2 nanosheets is limited to its relatively low catalytic activity, especially in alkaline environments. Here, we developed a dual-cation doping strategy to improve the alkaline HER performance of MoS 2 nanosheets. The designed Ni, Co codoped MoS 2 nanosheets can promote the tandem HER steps simultaneously, thus leading to a much enhanced catalytic activity in alkaline solution. Density functional theory calculations revealed the individual roles of Ni and Co dopants in the catalytic process. The doped Ni is uncovered to be the active site for the initial water-cleaving step, while the Co dopant is conducive to the H desorbing by regulating the electronic structure of neighboring edge-S in MoS 2 . The synergistic effect resulted by the dual-cation doping thus facilitates the tandem HER steps, providing an effective route to raise the catalytic performance of MoS 2 materials in alkaline solution.

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Background: As a pentacyclic triterpenoid, OA (oleanolic acid) has exhibited anti-inflammatory, immunomodulatory and antitumor effects. VEGFR-2 (vascular endothelial cells receptor-2) tyrosine kinase activity could be inhibited by apatinib, a small-molecule anti-angiogenic agent. Thus, this study sought to investigate the mechanism underlying the synergistic anti-tumor activity of combined OA and apatinib. Materials and Methods: Through CCK8 (Cell counting kit 8 assay), flow cytometric and western blotting techniques, we conducted in vitro studies on apatinib and OA effects on cell proliferation and apoptosis in H22 cell line. H22 tumor-burdened mice model was established in vivo, while the related signaling pathways were studied via pathological examination, western blotting and qPCR (quantitative polymerase chain reaction). Results: Growth of H22 cells in vitro and in vivo could be inhibited effectively by apatinib and OA. Thus, OA repaired liver function and inhibited oxidative stress induced by apatinib. Conclusion: OA can treat apatinib induced liver injury in H22 Tumor-burdened mice by enhancing the suppresssive effect of apatinib on the growth of tumor.

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