A prerequisite for exploiting most proposed applications for MoS2 is the availability of water-dispersible functionalized MoS2 nanosheets in large quantities. Here we report one-step synthesis and surface functionalization of MoS2 nanosheets by a facile ionic liquid assisted grinding method in the presence of chitosan. The selected ionic liquid with suitable surface energy could efficiently overcome the van der Waals force between the MoS2 layers. Meanwhile, chitosan molecules bind to the plane of MoS2 sheets non-covalently, which prevents the reassembling of exfoliated MoS2 sheets and facilitates the exfoliation progress. The obtained chitosan functionalized MoS2 nanosheets possess favorable stability and biocompatibility, which renders them as promising and biocompatible near-infrared agents for photothermal ablation of cancer. This contribution provides a facile way for the green, one-step and large-scale synthesis of advanced functional MoS2 materials.

Metformin is a well-known AMP-activated protein kinase (AMPK) activator, and it has been shown to inhibit organ fibrosis. Whether AMPKα2 mediates metformin protection against renal fibrosis remains unknown. Here, we aimed to investigate the role of the AMPKα2 isoform in mediating the inhibitory effect of metformin on renal fibrosis. Unilateral ureteral obstruction (UUO) was used to induce renal fibrosis in wild-type (WT) and AMPKα2 knockout (AMPKα2 ) mice. Metformin treatment was initiated 3 days before UUO and was continued until 7 days after UUO. In WT mice, metformin significantly inhibited UUO-induced renal fibrosis. In AMPKα2 mice, metformin also tended to inhibit UUO-induced renal fibrosis. Specifically, metformin significantly reduced UUO-induced transforming growth factor β1 (TGFβ1) mRNA and protein expression in WT mice but not in AMPKα2 mice. In contrast, metformin reduced UUO-induced TGFβ1 downstream Smad3 phosphorylation in both WT and AMPKα2 mice, suggesting that this regulation occurs in an AMPKα2-independent manner. In conclusion, the underlying mechanisms for the protective effects of metformin against renal fibrosis include AMPKα2-dependent targeting of TGFβ1 production and AMPKα2-independent targeting of TGFβ1 downstream signalling. In this regard, metformin has an advantage over other AMPK activators for the treatment of renal fibrosis.

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