ABSTRACT
NaHCO3-activated buckwheat biochar was studied, and an optimal biochar of 0.25N-BC [m(NaHCO3):m(buckwheat bark)=0.25:1]was selected. SEM, BET, XRD, Raman, FTIR, and XPS methods were applied to analyze the effects of NaHCO3 on the physicochemical properties of buckwheat biochar. The adsorption properties and mechanism of NaHCO3-activated buckwheat biochar for iopamidol(IPM), a nonionic iodol X-ray contrast agent, were also investigated. The results showed that compared with buckwheat skin biochar(BC), NaHCO3-activated biochar had higher structural defects(surface area and pore volume increased, respectively, from 480.40 m2·g-1 and 0.29 cm3·g-1 to 572.83 m2·g-1 and 0.40 cm3·g-1, with ID/IG being 1.22 times that of BC), the carbon and oxygen functional groups on the BC surface changed significantly, and the polarity increased [(N+O)/C from 0.15 to 0.24]. The maximum adsorption capacity of 0.25N-BC for IPM was 74.94 mg·g-1, which was 9.51 times that of BC(7.88 mg·g-1). The pseudo-second-order adsorption kinetics and Langmuir and Freundlich isotherm models could well fit the adsorption of 0.25N-BC for IPM. The adsorption processes were mainly chemical, monolayer, and heterogeneous multilayer adsorption. Pore filling, hydrogen bonding, π-π, and n-π interactions were the main mechanisms of 0.25N-BC adsorption for IPM. Comparing the activated buckwheat biochar by different bases [KOH, Na2CO3, NaHCO3, KHCO3, and Ca(HCO3)2], 0.25N-BC exhibited high adsorption capability and short equilibrium time and could effectively remove the IPM residue in the actual water(secondary sedimentation tank effluent and lake). The removal rate of IPM remained at 74.91% after three adsorption-desorption cycles. The results showed that NaHCO3-activated buckwheat biochar was a green, effective, and sustainable adsorbent for the removal of iodine-containing organic matter.
Subject(s)
Fagopyrum , Water Pollutants, Chemical , Iopamidol , Adsorption , Water Pollutants, Chemical/analysis , Charcoal/chemistry , KineticsABSTRACT
Microglia plays an important role in mediating neuroinflammation in Alzheimer's disease (AD). Intervention in microglia activation may exert a neuroprotective effect. In the present study, we reported that oligomeric Abeta1-42 dramatically increased the level of tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta compared to monomeric and fibrillar Abeta1-42 in rat microglial cultures. Pretreatment of the cultures with triptolide, an anti-inflammatory reagent, alleviated the elevation of TNF-alpha and IL-1beta level induced by oligomeric Abeta1-42. Our results showed that oligomeric Abeta played an important role in mediating neuroinflammation and triptolide was able to suppress the production of pro-inflammatory cytokines from microglia.
Subject(s)
Amyloid beta-Peptides/pharmacology , Diterpenes/pharmacology , Immunosuppressive Agents/pharmacology , Interleukin-1beta/metabolism , Microglia/drug effects , Peptide Fragments/pharmacology , Phenanthrenes/pharmacology , Tumor Necrosis Factor-alpha/metabolism , Analysis of Variance , Animals , Animals, Newborn , Brain/cytology , Cells, Cultured , Dose-Response Relationship, Drug , Enzyme-Linked Immunosorbent Assay/methods , Epoxy Compounds/pharmacology , Rats , Rats, Sprague-Dawley , Time FactorsABSTRACT
Activated microglia participate in neuroinflammation which contributes to neuronal damage in neurodegenerative diseases. Inhibition of microglial activation may have potential anti-inflammatory effects. Our laboratory has previously reported that triptolide, a natural biologically active compound extracted from Tripterygium wilfordii, could protect dopaminergic neurons from inflammation-mediated damage. However, the mechanism by which triptolide inhibits inflammation remains unknown. We reported here that inhibition of prostaglandin E(2) (PGE(2)) production could be a potential mechanism of triptolide to suppress inflammation. Triptolide suppressed c-jun NH2-terminal kinase (JNK) phosphorylation, cyclooxygenase 2 (COX-2) expression and PGE(2) production in microglial cultures treated with lipopolysaccharide (LPS). Triptolide also greatly inhibited the transcriptional activity, but not the DNA-binding activity of nuclear factor-kappaB (NF-kappaB) in microglia following LPS stimulation. These results indicate that triptolide might suppress NF-kappaB activity to down-regulate COX-2 expression. The LPS-stimulated transcriptional activity of NF-kappaB was suppressed by inhibition of p38MAPK, but not by that of JNK and extracellular signal-regulated kinase. Furthermore, the LPS-induced PGE(2) production was reduced by inhibiting these kinases. Taken together, these results suggest that triptolide may suppress neuroinflammation via a mechanism that involves inactivation of two parallel signaling pathways: p38-NF-kappaB-COX-2-PGE(2) and JNK-PGE(2).
Subject(s)
Cyclooxygenase 2/drug effects , Dinoprostone/metabolism , Diterpenes/pharmacology , Immunosuppressive Agents/pharmacology , Microglia/drug effects , Phenanthrenes/pharmacology , Signal Transduction/drug effects , Animals , Blotting, Western , Cells, Cultured , Cyclooxygenase 2/biosynthesis , Electrophoretic Mobility Shift Assay , Epoxy Compounds/pharmacology , Inflammation/chemically induced , Inflammation/prevention & control , Lipopolysaccharides/toxicity , MAP Kinase Kinase 4/drug effects , MAP Kinase Kinase 4/metabolism , Microglia/metabolism , NF-kappa B/drug effects , NF-kappa B/metabolism , Rats , Rats, Sprague-Dawley , Signal Transduction/physiology , TransfectionABSTRACT
Thirty-eight individuals with normal glucose regulation and thirty-nine newly diagnosed type 2 diabetic patients were observed by continuous glucose monitoring system(CGMS)for three days.The mean blood glucose,mean amplitude of glycemic excursions(MAGE),and absolute means of daily differences(MODD)were calculated in each subject.The results suggested that the amplitude of glyeemic excursions revealed by CGMS could be used to evaluate the quality of glycemic control in type 2 diabetic patients.
