ABSTRACT
Phosphate removal from water by lanthanum-modified tobermorite synthesized from fly ash (LTFA) with different lanthanum concentrations was studied. LTFA samples were characterized by X-ray diffraction, Fourier transform infrared spectroscopy, scanning electron microscopy, and BrunauerâEmmettâTeller specific surface area analysis. The results showed that the LTFA samples were mainly composed of mesoporous tobermorite-11 Å, and LTFA1 with a lanthanum concentration of 0.15 M had a high specific surface area (83.82 m2/g) and pore volume (0.6778 cm3/g). The phosphate adsorption capacities of LTFA samples were highest at pH 3 and gradually decreased with increasing pH. The phosphate adsorption kinetics data on LTFA samples were most accurately described by the Elovich model. The adsorption isotherms were in the strongest agreement with the Temkin model, and LTFA1 showed the highest phosphate adsorption capacity (282.51 mg P/g), which was higher than that of most other lanthanum-modified adsorbents. LTFA1 presented highly selective adsorption of phosphate with other coexisting ions (HCO3-, Cl-, SO42-, and NO3-). In addition, phosphate was adsorbed onto LTFA samples by forming inner-sphere phosphate complexes and amorphous lanthanum phosphate. This study provides technical support for development of efficient fly ash-based phosphate adsorbents.
Subject(s)
Coal Ash , Lanthanum , Phosphates , Lanthanum/chemistry , Coal Ash/chemistry , Phosphates/chemistry , Adsorption , Kinetics , X-Ray Diffraction , Spectroscopy, Fourier Transform Infrared , Water Pollutants, Chemical/chemistryABSTRACT
BACKGROUND: Hepatic stellate cell (HSC) activation plays a pivotal role in hepatic inflammation and liver fibrosis. TLR4 pathway activation has been reported to be involved in mice liver fibrosis induced by hepatitis virus infection, alcohol abuse, biliary ligation, carbon tetrachloride 4 treatment, and Schistosoma japonicum (Sj) infection. The effect and mechanisms of the cyclooxygenase 2 (COX2)/prostanoid E2 (PGE2) axis on liver fibrosis induced by Sj are still unclear. METHODS: Mice liver fibrosis were induced by cutaneous infection of Sj cercariae. COX-2 inhibitor, NS398 were injected from week 5 to week 7, while TLR4 inhibitor TAK242 were injected from week 4 to week 8 post Sj infection. Human HSCs line, LX-2 cells were cultured and exposed to LPS or synthetic PGE2, or pretreated by TAK242, TLR4-siRNA or NS398. Liver tissue and serum or in vitro cultured cell lysaste were collected at indicated time courses for exploring the relationship between TLR4 and COX2-PGE2 axis through qPCR, western blot, immunohistochemical assay, ect. One-way analysis of variance among multiple groups followed by Uncorrected Fisher's LSD-t test or paired comparisons through t test were performed to tell the statistical differences. RESULTS: This study investigated the link between the COX2/PGE2 axis and TLR4 signaling in the induction of liver fibrogenesis in mice during Sj infection and in vitro culture of HSC strain-LX-2. The COX2/PGE2 axis was positively associated with Sj-induced liver fibrosis. TLR4 pathway activation stimulated the COX2/PGE2 axis in Sj-infected mice and in lipopolysaccharide (LPS)-exposed cultured HSCs. Synthetic PGE2 activated cultured HSCs through upregulation of alpha smooth muscle actin (α-SMA) expression. In LPS-triggered HSCs, NS398, a COX2 inhibitor, led to suppression of PGE2 synthesis and reduced expression of α-SMA and type I collagen (COL I). CONCLUSIONS: These results indicate firstly the positive association of the COX2/PGE2 axis with liver fibrosis induced by Sj infection. TLR4 signaling may at least partially control the COX2/PGE2 axis in Sj-infected mice liver and in vitro cultured HSCs. The COX2/PGE2-EP2/EP4 axis might be a good drug target against liver fibrosis induced by Sj infection.
Subject(s)
Cyclooxygenase 2/genetics , Dinoprostone/genetics , Liver Cirrhosis/metabolism , Liver Cirrhosis/parasitology , Schistosomiasis japonica/metabolism , Signal Transduction , Toll-Like Receptor 4/metabolism , Animals , Cells, Cultured , Cyclooxygenase 2/metabolism , Dinoprostone/metabolism , Female , Hepatic Stellate Cells/metabolism , Mice , Mice, Inbred C57BL , Schistosomiasis japonica/immunology , Toll-Like Receptor 4/geneticsABSTRACT
Liver fibrosis induced by Schistosoma japonicum (Sj) infection is characterized by the accumulation of extracellular matrix (ECM). The activated and differentiated hepatic stellate cells (HSCs) are the predominant ECM-producing cell type in the liver. Toll-like receptor (TLR) 4 pathway activation plays a key role in mice liver fibrosis models induced by alcohol, biliary ligation, and carbon tetrachloride 4. In this work, we found that TLR4 pathway activation correlated with the severity of liver fibrosis post Sj infection. The TLR4 receptor inhibitor TAK242 reduced the extent of liver fibrosis. The increased expression of TLR4, α-smooth muscle actin (α-SMA), and cytoglobin was observed in the HSCs of mouse liver after Sj infection. In response to stimulation with either lipopolysaccharide or Sj's soluble egg antigen (SEA), high levels of TLR4 and α-SMA were induced in HSCs and were inhibited by TAK242 treatment. In previous work, we had reported that a high level of transglutaminase 2 (TGM2) is crucial for liver fibrosis post Sj infection. Herein, we found that TLR4 signaling also controlled Tgm2 expression. Inhibition of TGM2 activity by cystamine (CTM) in Sj-infected mice or in HSCs induced with all-trans-retinoic acid (ATRA) stimulation led to a lowered activation of TLR4 signaling and a reduced α-SMA expression. These results were confirmed by downregulating the Tgm2 gene by specific siRNA. These observations implied the presence of a positive feedback regulation between TGM2 and TLR4 signaling in HSCs that correlated with liver fibrosis post Sj infection. This novel connection between TGM2 and TLR4 pathway activation in liver fibrosis induced by Sj infection enhances our understanding of liver diseases.
