Synthesis and Characterization of g-C3N4/Ag3PO4/TiO2/PVDF Membrane with Remarkable Self-Cleaning Properties for Rhodamine B Removal.

g-C3N4/Ag3PO4/TiO2 nanocomposite materials were loaded onto a polyvinylidene fluoride (PVDF) membrane using a phase inversion method to obtain a photocatalytic flat membrane for dye removal. The morphology, structure, and photocatalytic activity of the g-C3N4/Ag3PO4/TiO2 nanoparticles and composite membrane were evaluated. The g-C3N4/Ag3PO4/TiO2/PVDF membrane exhibited superior morphology, hydrophilic properties, and antifouling performance compared with the raw PVDF membrane. Four-stage filtration was performed to evaluate the self-cleaning and antifouling capacity of the g-C3N4/Ag3PO4/TiO2/PVDF membrane. Upon irradiating the composite membrane with visible light for 30 min, its irreversible fouling resistance (Rir) was low (9%), and its flux recovery rate (FRR) was high (71.0%) after five filtration cycles. The removal rate of rhodamine B (RhB) from the composite membrane under visible light irradiation reached 98.1% owing to the high photocatalytic activity of the membrane, which was superior to that of raw PVDF membrane (42.5%). A mechanism of photocatalytic composite membranes for RhB degradation was proposed. Therefore, this study is expected to broaden prospects in the field of membrane filtration technology.

Emodin ameliorates LPS-induced acute lung injury, involving the inactivation of NF-κB in mice.

Acute lung injury (ALI) and its severe manifestation of acute respiratory distress syndrome (ARDS) are well-known illnesses. Uncontrolled and self-amplified pulmonary inflammation lies at the center of the pathology of this disease. Emodin, the bio-active coxund of herb Radix rhizoma Rhei, shows potent anti-inflammatory properties through inactivation of nuclear factor-κB (NF-κB). The aim of this study was to evaluate the effect of emodin on lipopolysaccharide (LPS)-induced ALI in mice, and its potential bio-mechanism. In our study, BALB/c mice were stimulated with LPS to induce ALI. After 72 h of LPS stimulation, pulmonary pathological changes, lung injury scores, pulmonary edema, myeloperoxidase (MPO) activity, total cells, neutrophils, macrophages, TNF-α, IL-6 and IL-1ß in bronchoalveolar lavage fluid (BALF), and MCP-1 and E-selectin expression were notably attenuated by emodin in mice. Meanwhile, our data also revealed that emodin significantly inhibited the LPS-enhanced the phosphorylation of NF-κB p65 and NF-κB p65 DNA binding activity in lung. Our data indicates that emodin potently inhibits LPS-induced pulmonary inflammation, pulmonary edema and MCP-1 and E-selectin expression, and that these effects were very likely mediated by inactivation of NF-κB in mice. These results suggest a therapeutic potential of emodin as an anti-inflammatory agent for ALI/ARDS treatment.