Objective To observe the effect of Kaixin Powder on neuroinflammation in APP/PS1 mice by regulating WDFY1/TLR4/NF-κB signaling pathway;To explore its mechanism of intervening in Alzheimer disease(AD).Methods APP/PS1 transgenic mice were randomly divided into model group,donepezil hydrochloride group(0.66 mg/kg),and Kaixin Powder low-,medium-and high-dosage groups(1.625,3.25,6.5 g/kg),C57BL/6J mice were set as blank control group,with 8 mice in each group,and corresponding drug intervention was given to medicaction group for 24 weeks.Morris water maze,Y maze and novel object recognition experiments were conducted to assess the cognitive function and learning and memory abilities of mice,immunohistochemical staining was used to detect the deposition of β-amyloid protein(Aβ)in hippocampus,the morphology and Nissl bodies of hippocampal CA1 neurons were observed using HE staining and Nissl staining,ELISA was used to detect the serum contents of interleukin(IL)-6,IL-17,IL-1β and tumor necrosis factor-α(TNF-α),Western blot was used to detect the protein expression of calcium-binding adapter molecule 1(Iba1),glial fibrillary acidic protein(GFAP),WDFY1,Toll like receptor 4(TLR4),Toll like receptor associated molecule(TRAM),TIR domain adapter protein(TRIF),NF-κB p65 and p-NF-κB p65 in hippocampal tissue,RT-qPCR was used to detect the mRNA expression of WDFY1,TLR4,TRAM,TRIF and NF-κB p65 in hippocampal tissue.Results Compared with the blank control group,the model group had significantly prolonged escape latency,reduced platform crossings,decreased autonomous reaction alternation rate and relative recognition index(P<0.05,P<0.01),with increased deposition of Aβ in hippocampal tissue(P<0.01),damaged morphological structure of neurons,reduced number of neurons and Nissl bodies,the serum contents of IL-6,IL-17,IL-1β and TNF-α significantly increased,the expression of Iba1,GFAP,WDFY1,TLR4,TRAM,TRIF,p-NF-κB p65 protein and WDFY1,TLR4,TRAM,TRIF mRNA in hippocampal tissue significantly increased(P<0.01).Compared with the model group,Kaixin Powder groups and donepezil hydrochloride group had significantly shortened escape latency and increased platform crossings,autonomous reaction alternation rate and relative recognition index(P<0.05,P<0.01),hippocampal Aβ deposition reduced in Kaixin Powder medium-,high-dosage groups and donepezil hydrochloride group,the morphological structure of neurons recovered,the number of neurons and Nissl bodies increased,the serum contents of IL-6,IL-17,IL-1β and TNF-α significantly decreased(P<0.05,P<0.01),and the protein expression of Iba1,GFAP,WDFY1,TLR4,TRAM,TRIF,p-NF-κB p65 and the mRNA expressions of WDFY1,TLR4,TRAM and TRIF in hippocampal tissue significantly decreased(P<0.05,P<0.01).Conclusion Kaixin Powder can improve cognitive function and learning and memory abilities in AD model mice,alleviate hippocampal neuron damage and Aβ deposition,inhibit the activation of microglia and astrocytes,and thereby reduce serum inflammatory cytokine release.Its mechanism may be related to regulating the WDFY1/TLR4/NF-κB signaling pathway to inhibit neuroinflammation.

Objective To observe the effect of Kaixin Powder on neuroinflammation in APP/PS1 mice by regulating WDFY1/TLR4/NF-κB signaling pathway;To explore its mechanism of intervening in Alzheimer disease(AD).Methods APP/PS1 transgenic mice were randomly divided into model group,donepezil hydrochloride group(0.66 mg/kg),and Kaixin Powder low-,medium-and high-dosage groups(1.625,3.25,6.5 g/kg),C57BL/6J mice were set as blank control group,with 8 mice in each group,and corresponding drug intervention was given to medicaction group for 24 weeks.Morris water maze,Y maze and novel object recognition experiments were conducted to assess the cognitive function and learning and memory abilities of mice,immunohistochemical staining was used to detect the deposition of β-amyloid protein(Aβ)in hippocampus,the morphology and Nissl bodies of hippocampal CA1 neurons were observed using HE staining and Nissl staining,ELISA was used to detect the serum contents of interleukin(IL)-6,IL-17,IL-1β and tumor necrosis factor-α(TNF-α),Western blot was used to detect the protein expression of calcium-binding adapter molecule 1(Iba1),glial fibrillary acidic protein(GFAP),WDFY1,Toll like receptor 4(TLR4),Toll like receptor associated molecule(TRAM),TIR domain adapter protein(TRIF),NF-κB p65 and p-NF-κB p65 in hippocampal tissue,RT-qPCR was used to detect the mRNA expression of WDFY1,TLR4,TRAM,TRIF and NF-κB p65 in hippocampal tissue.Results Compared with the blank control group,the model group had significantly prolonged escape latency,reduced platform crossings,decreased autonomous reaction alternation rate and relative recognition index(P<0.05,P<0.01),with increased deposition of Aβ in hippocampal tissue(P<0.01),damaged morphological structure of neurons,reduced number of neurons and Nissl bodies,the serum contents of IL-6,IL-17,IL-1β and TNF-α significantly increased,the expression of Iba1,GFAP,WDFY1,TLR4,TRAM,TRIF,p-NF-κB p65 protein and WDFY1,TLR4,TRAM,TRIF mRNA in hippocampal tissue significantly increased(P<0.01).Compared with the model group,Kaixin Powder groups and donepezil hydrochloride group had significantly shortened escape latency and increased platform crossings,autonomous reaction alternation rate and relative recognition index(P<0.05,P<0.01),hippocampal Aβ deposition reduced in Kaixin Powder medium-,high-dosage groups and donepezil hydrochloride group,the morphological structure of neurons recovered,the number of neurons and Nissl bodies increased,the serum contents of IL-6,IL-17,IL-1β and TNF-α significantly decreased(P<0.05,P<0.01),and the protein expression of Iba1,GFAP,WDFY1,TLR4,TRAM,TRIF,p-NF-κB p65 and the mRNA expressions of WDFY1,TLR4,TRAM and TRIF in hippocampal tissue significantly decreased(P<0.05,P<0.01).Conclusion Kaixin Powder can improve cognitive function and learning and memory abilities in AD model mice,alleviate hippocampal neuron damage and Aβ deposition,inhibit the activation of microglia and astrocytes,and thereby reduce serum inflammatory cytokine release.Its mechanism may be related to regulating the WDFY1/TLR4/NF-κB signaling pathway to inhibit neuroinflammation.

Objective To investigate the periprocedural effects of atorvastatin plus ezetimibe and atorvastatin monotherapy on lipopro-tein-associated phospholipase A2(Lp-PLA2)levels in patients with non-ST-segment elevation acute coronary syndrome(NSTE-ACS)after percutaneous coronary intervention(PCI).Methods In total,193 patients with NSTE-ACS who underwent PCI were divided into four groups:20 mg atorvastatin(A20 group),40 mg atorvastatin(A40 group),20 mg atorvastatin combined with 10 mg ezetimibe(A20+E10 group),and 40 mg atorvastatin combined with 10 mg ezetimibe(A40+E10 group).Changes in plasma Lp-PLA2 and low-density lipopro-tein cholesterol(LDL-C)levels during the perioperative period were observed,and major adverse cardiovascular events(MACE)and sta-tin-related adverse reactions were monitored for 30 d.Results Factorial analysis revealed no interaction between intensive atorvastatin and ezetimibe.Intensive atorvastatin and atorvastatin combined with ezetimibe significantly reduced the postoperative plasma Lp-PLA2 levels(P<0.05).Plasma Lp-PLA2 levels were similar between the four groups before PCI and decreased significantly after PCI(P<0.05).The changes in Lp-PLA2 during the perioperative period were compared between the four groups,and it was significantly higher in the A40 group than in the A20 group,in the A20+E10 group than in the A20 group,in the A40+E10 group than in the A20 group,and in the A40+E10 group than in the A40 group(P<0.05).No significant difference in LDL-C levels and no significant correlation between the changes in LDL-C and Lp-PLA2 levels were observed between the four groups(P>0.05).In addition,no significant differences in the incidence of major adverse cardiovascular event or statin-related adverse reactions were observed(P>0.05).Conclusion Compared with atorvastatin(20 mg)monotherapy,both intensive atorvastatin(40 mg)and atorvastatin plus ezetimibe can further reduce postoperative Lp-PLA2 levels,independent of the changes in LDL-C in patients with NSTE-ACS undergoing PCI.

Objective To study the gene expression profile in mice kidney with acute paraquat (PQ) poisoning and identify key genes related to renal injury.Methods A total of 20 mice (C57BL/6) were randomly (random number) divided into four groups, namely control group (group A, n =5) and poisoned groups (groups B, C, D, n =5/group).In group A, mice were administrated with distilled water (0.01 mL/g weight) while in groups B, C, D were administered with equivalent volume of PQ solution (diluted from 20％ to 0.05％ with distilled water) dissolved in distilled water via a gastric tube.Mice of group A were sacrificed immediately and mice of groups B and C at 6 h and 24 h after administration of PQ.The gene expression profile changes of kidney tissue were measured by cDNA Arraychip technology.Mice of group D were observed for mortality rate 48 h later.Results The body weights of mice decreased significantly after administration of PQ.The mortality in group D at 48 h after PQ poisoning was 100％.Compared with the control group, totally 1 792 genes with differential expression variations were identified in 6 h group and 24 h group.There were 8 key genes selected through bioinformatics analysis and they were arranged in real-time PCR: Nlrc5 , Serpinb9 , Cd40 , Rnf135 , Dhx58 , Spl 10 , Fcgrl , and Arhgef12.And then, Nlrc5 , Serpinb9 and Rnf135 were under Western blot investigation.The results of PCR and Western blot showed no significant difference to those from bioinformatics genetic analysis.Conclusions The investigation based on genome wide chip in researching related genes of PQ kidney has offered a novel idea in studying pathogenesis of acute PQ intoxication.

Objective To analyze the constituent of the 32 kD protein band and its expression in schizophrenia se?rum. Methods Sixty schizophrenia patients and 58 health controls were recruited. The serum samples were collected and precipitated with 7%PEG. The sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) was used to ob?tain the abnormal 32 kD proteins band in patients. This protein band was cut and then analyzed using mass spectrometric technique. Results The 32 kD protein band was present in 38 schizophrenia patients but not in control and positive rate was 63.33%. The mass spectrometric analysis showed that 32 kD protein band contained 14 proteins ranging from 30 kD to 35 kD, including 6 high-frequency proteins (cDNA coded protein 1 and 2, Apolin protein A-1, Isoform 2 of ficolin-2, Complement factor H and clusterin) and 8 low-frequency proteins (IgG H chain, zinc-alphg-2-glycoprotein, fermitin,family apolin protein L-1, isoform 10 of collectin-1, purine nucleoside, anne xin and cDNA coded protein 3). Three cD?NA coded unknown proteins were highly similar to complement C4-B, β2-glycoprotein and erythrocyte band 7 integral membrane protein. Conclusion There is a unknown specific 32 kD protein that is consisted mainly of fourteen proteins in serum of schizophrenia.