Enhanced inhibition of talc flotation using acidified sodium silicate and sodium carboxymethyl cellulose as the combined inhibitor

The flotation separation of chalcopyrite and talc is challenging due to their similar natural floatability characteristics.Besides,it is usually difficult to effectively inhibit talc by adding sodium carboxymethyl cellulose(CMC)alone during chalcopyrite flotation.Here,a combined inhibitor comprising acidified sodium silicate(ASS)and CMC was employed to realize effective flotation separation of chalcopyrite and talc,and the combined inhibition mechanism was further investigated.Microflotation results showed that adding ASS strengthened the inhibitory effect of CMC on talc and improved the separation of chalcopyrite and talc.The zeta potential,Fourier transform infrared,and X-ray photoelectron spectroscopy analysis indicated that CMC was mainly adsorbed on the talc surface via hydroxyl and carboxyl groups.Moreover,the addition of ASS improved the adsorption of carboxyl groups.Furthermore,the adsorption experiments and apparent viscosity measurements revealed that adding ASS dispersed the pulp well,which reduced the apparent viscosity,improved the adsorption amount of CMC on the talc surface,and enhanced the inhibition of talc in chalcopyrite flotation.

Bioinformatic Analysis and Experimental Verification of QJHGD on Caerulein-induced Inflammatory Response in SAP Model Rats Based on TLR4/NF-κB/My D88 Pathway

[Objectives]To conduct bioinformatic analysis and experimental verification of Qingjie Huagong Decoction(QJHGD)on caerulein-induced inflammatory response in severe acute pancreatitis(SAP)model rats based on TLR4/NF-κB/MyD88 pathway.[Methods]The effective component groups and potential targets of QJHGD were collected by the network pharmacology method.A drug-component-target network was constructed.The GO and KEGG of targets were enriched and analyzed with the aid of Metascape database,and the target pathway related to SAP inflammation was screened.The SAP rat model was established by caerulein combined with lipopolysaccharide,and QJHGD was intragastrically administered.Pancreatic tissue was observed by HE staining.In addition,enzyme-linked immunosorbent assay and immunohistochemistry were used to verify the anti-inflammatory effect of QJHGD on SAP rats and its regulatory effect on TLR4/NF-κB/MyD88 target pathway.[Results]A total of 105 active components of QJHGD and 148 key targets of SAP were predicted and screened;KEGG was enriched in 320 different pathways including toll-like receptor and NF-κB classical pathways.Animal experiment verified that QJHGD reduced serum amylase,serum lipase activity,IL-6,TNF-αlevels in SAP rats;HE staining showed the effect of QJHGD on the pathological changes of pancreas,and QJHGD inhibited the positive expression of key proteins of TLR4,NF-κB and MyD88 in the inflammatory transduction pathway.[Conclusions]The mechanism of QJHGD improving pancreatic injury in SAP rats may be related to down-regulating the expression of key proteins in the TLR4/NF-κB/MyD88 pathway.