A new two-step process was developed to prepare PVDF/reduced graphene oxide (PVDF/rGO) composite films: the synthesis of PVDF/GO composite films and immersion of such films in hydrobromic acids for reduction. This method avoided the agglomeration of rGO during reduction in PVDF/GO solutions and efficiently improved the dispersion effect of rGO in the PVDF matrix. Meanwhile, it simplified the preparation process due to no modification of GO being required, and opened a feasible way to scale up the production of PVDF/rGO composites. Experiments showed that PVDF with nearly all b phase was obtained when the content of rGO was 0.1 wt% (PrGO-0.1), and the dielectric constant increased from 10 for the neat PVDF to 41 for PrGO-0.1 at 1 kHz. The ferroelectric, piezoelectric, and dynamic mechanical properties of the PVDF/rGO composites were also comprehensively studied. As the content of the b phase was nearly 100%, the piezoelectric constant and remnant polarization of the PrGO-0.1 film increased by 78.6% and 69.3%, respectively, compared with those of the neat PVDF, and therefore became the highest among all composite films. The rGO also, to a great extent, helped to enhance the mechanical properties of the PVDF composites. As a result, the improved piezoelectric and ferroelectric properties made the PVDF/rGO composite films with 0.1 wt% rGO content much better piezoelectric energy transfer and ferroelectric storage materials than the neat PVDF.

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C/EBP homologous protein (CHOP) is an important mediator of endoplasmic reticulum (ER) stress-induced cell and organ injury. Here we show that lipopolysaccharide (LPS)-induced acute kidney injury (AKI) is associated with ER stress and elevated CHOP. We postulated that CHOP(-/-) mice would be protected against LPS-induced-AKI. Unexpectedly, while Toll-like receptor 4 (TLR4) expression levels were comparable in kidneys of CHOP(-/-) and wild-type (WT) mice, CHOP(-/-) mice developed more severe AKI after LPS injection. Furthermore, the severe kidney injury in CHOP(-/-) mice was associated with an exaggerated inflammatory response. Serum TNF-α levels were more elevated in LPS-treated CHOP(-/-) mice. There was a 3.5-fold higher amount of renal neutrophil infiltrates in LPS-treated CHOP(-/-) than in WT mice. Additionally, the kidneys of LPS-treated CHOP(-/-) mice had a more prominent increase in NF-κB activation and further upregulation of proinflammatory genes, i.e., c-x-c motif ligand 1 (CXCL-1), macrophage inflammatory protein-2 (MIP-2), and IL-6. Finally, proximal tubules, glomeruli, and podocytes isolated from CHOP(-/-) mice also had an exaggerated proinflammatory response to LPS. Since LPS directly increased CHOP in glomeruli and podocytes of WT mice, together these data suggest that the LPS-induced increase of CHOP in kidneys may inhibit inflammatory response in renal cells and provide protection against AKI.