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Heavy metals pose a serious threat and damage to ecological health when released into the environment. n-HFP is usually used to remediate soils contaminated with heavy metals, but its ability to solidify heavy metals is limited. FA has good ability to trap heavy metals due to its abundant oxygen-containing functional groups. However, the solubility of FA in water limits its application in the field of heavy metal removal. In this paper, n-HFP@FA was prepared by co-precipitation method. Through FT-IR and BET analysis, the oxygen-containing functional groups and specific surface area of n-HFP@FA increased due to the addition of FA. The adsorption behaviour of n-HFP@FA on Pb, Cd, and Cu followed the pseudo-second-order and Langmuir isotherm models. In addition, the maximum adsorption capacities of n-HFP@FA for Pb, Cd, and Cu were 371.1, 190.5, and 129.75 mg/g, respectively. As shown by FT-IR and XPS analysis, the main mechanisms of Pb, Cd and Cu removal by n-HFP@FA are: complexation, electrostatic and precipitation. The n-HFP@FA showed high removal rates of Pb, Cd, and Cu in soil leachates of different pH. In the soil remediation experiments, the BCR method and Pearson correlation analysis showed that the acid-soluble, reducible and oxidizable fractions of Pb, Cd, and Cu in the soil were effectively converted into a more stable residual fraction. This study opens up a prospect for the application of n-HFP@FA composites in the remediation of contaminated soil. [ABSTRACT FROM AUTHOR]

Aristolochic acid nephropathy is a rapidly progressive tubulointerstitial disease induced by aristolochic acid (AA) and effective treatment is lacking. Nuclear factor erythroid 2-related factor 2 (Nrf2) has been proven to be protective in acute kidney injury and chronic kidney disease progression. But its role in AA-induced renal tubular epithelial cell injury has not been determined. This study aimed to investigate the role of Nrf2 in AA-induced renal tubular epithelial cell injury in vitro. NRK-52E cells were incubated with 5–50 μM AA to evaluate cell viability, reactive oxygen species (ROS) production, cell apoptosis/necrosis, and Nrf2 signaling pathway protein levels. We found that AA reduced cell viability and induced cell apoptosis in a time-dependent manner, accompanied by increased production of intracellular ROS. Meanwhile, the expression of Nrf2 signaling pathway proteins was significantly decreased. Downregulation of Nrf2 by Nrf2 siRNA decreased its downstream antioxidant proteins HO-1 and NQO1 and resulted in increased AA-induced ROS production and cell death. On the contrary, overexpression of Nrf2 increased HO-1 and NQO1 expression and resulted in decreased cell death. In conclusion, Nrf2 plays an important role in AA-induced injury. Enhanced Nrf2 signaling pathway could ameliorate AA-induced renal tubular epithelial cell injury, while downregulation of Nrf2 signaling exacerbated the injury. [ABSTRACT FROM AUTHOR]

Context: The proximal tubular epithelial cells (PTECs) are the primary target of aristolochic acids and especially vulnerable to mitochondrial injury from insults of toxic xenobiotics.Objectives: This study aimed to investigate the possible role of mitochondrial injury in CaulisAristolochia manshuriensis(CAM)-induced aristolochic acid nephropathy (AAN).Materials and methods: Male Sprague-Dawley rats were gavaged with CAM extract every other week for 1, 4, 8 and 12 weeks, respectively.Results: The rats in the model group showed chronic AAN as evidenced by worsening kidney function evaluated by blood urea nitrogen, creatinine and proteinuria levels, and severe tubulointerstitial injury marked by massive tubular atrophy and interstitial fibrosis in kidney tissues. Moreover, overt apoptosis and impaired regeneration of PTECs were observed in AAN rats. Furthermore, the study revealed that mitochondria in PTECs were fragmented into small, punctuate suborganelles in AAN rats. Two mitochondrial respiratory chain proteins, mitochondrial DNA (mtDNA)-encoded cytochrome c oxidase subunit І (COX-І) and nuclear DNA-encoded nicotinamide adenine dinucleotide dehydrogenase (ubiquinone)-1β subcomplex 8 (NDUFβ8), were both down-regulated after one week of CAM treatment. However, with AAN progression, NDUFβ8 level restored, while COX-І level maintained low. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α), master regulator of mitochondrial biogenesis, was significantly down-regulated at week 4 and week 8, but significantly up-regulated at week 12. In addition, mtDNA copy number reduced markedly along with AAN progression.Discussion and conclusion: A rat model of chronic AAN was successfully reproduced by gavage with CAM extract. Dynamic changes of mitochondrial injury induced by CAM might contribute to the AAN progression. [ABSTRACT FROM PUBLISHER]

Macrophage can be alternatively activated by TGF-β1, whether high-ambient glucose can enhance the sensitivity of TGF-β1 and the intracellular mechanisms involved in this process are not fully understood. We examined whether the mitogen-activated protein kinase is involved in the activation of macrophage induced by TGF-β1 and high-ambient glucose. The expression of arginase-1, CD206 and TGF-β1 was accessed by Western blot and immunofluorescence in RAW 264.7 cells stimulated with TGF-β1 and high-ambient glucose. The activation of MAPK pathways in the process was investigated by Western blot. The role of MAPK was assessed using biochemical inhibitors. The protein of arginase-1, CD206 and TGF-β1 was significantly overexpressed in RAW264.7 cells stimulated by TGF-β1 and high-ambient glucose. ERK and JNK phosphorylation occurred in 30 min and p38MAPK phosphorylation occurred in 30 min and 24 h after the stimulation. And the expression of arginase-1 and TGF-β1 was partially blocked by the pretreated ERK biochemical inhibitor (U0126) instead of the JNK inhibitor (SP600125) and p38MAPK inhibitor (SB203580). In conclusion, high-ambient glucose can enhance the sensitivity of TGF-β1 in RAW264.7 cells, which resulted in overexpression of TGF-β1 and arginase-1 in macrophages. ERK plays a role in this process. [ABSTRACT FROM PUBLISHER]