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BACKGROUND: Scavenger receptor class B (SRB) is a multifunctional protein in animals that participates in physiological processes, including recognition of a wide range of ligands. Astaxanthin is a major carotenoid found in shrimp. However, the molecular mechanism of astaxanthin and SRB protein binding has not been reported. RESULTS: In the present study, a member of the SRB subfamily, named PmSRB, was identified from the transcriptome of black tiger shrimp (Penaeus monodon). The open reading frame of PmSRB was 1557 bp in length and encoded 518 amino acids. The structure of PmSRB included a putative transmembrane structure at the N-terminal region and a CD36 domain. Multiple sequence alignment indicated that the CD36 domain were conserved. Phylogenetic analysis showed four separate branches (SRA, SRB, SRC, and croquemort) in the phylogenetic tree and that PmSRB was clustered with SRB of Eriocheir sinensis. Quantitative real-time polymerase chain reaction showed that the PmSRB gene was widely expressed in all tissues tested, with the highest expression level observed in the lymphoid organ and brain. Subcellular localization analysis revealed that PmSRB-GFP (green fluorescent protein) fusion proteins were predominantly localized in the cell membrane. The recombinant proteins of PmSRB showed binding activities against astaxanthin in vitro. CONCLUSIONS: PmSRB was identified and characterized in this study. It is firstly reported that PmSRB may take as an important mediator of astaxanthin uptake in shrimp.
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Animals , Penaeidae , Receptors, Scavenger/metabolism , In Vitro Techniques , Blotting, Western , Chromatography, High Pressure Liquid , Sequence Alignment , Xanthophylls , Receptors, Scavenger/isolation & purification , Receptors, Scavenger/genetics , Real-Time Polymerase Chain Reaction/methods , TranscriptomeABSTRACT
Drusen is one of the early hallmark changes of AMD. The oxidative stress and inflammatory reaction caused by oxidative phospholipids (OxPLs) in drusen can lead to retinal pigment epithelium (RPE) cell death (apoptosis, pyroptosis, etc.) and the formation of choroidal neovascularization, which is the pathogenesis of AMD. Pyroptosis, also known as inflammatory necrosis, is one of the main forms of OxPLs induced cell death. Proinflammatory factors released by pyroptic cells can in turn aggravate the inflammatory reaction, leading to further damage. In order to prevent AMD, inflammatory response and cell death may be reduced by regulating lipid metabolism, reducing OxPLs endocytosis and increasing cholesterol efflux. In-depth understanding effects of OxPLs, inflammation and RPE pyrosis in the pathogenesis of AMD in elucidate the pathogenesis of AMD and to seek new treatment measures has important clinical significance.
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DNA-nanotechnology-based nano-architecture scaffolds based on circular strands were designed in the form of DNA-nanowires(DNA-NWs)as a polymer of DNA-triangles.Circularizing a scaffold strand(84-NT)was the critical step followed by annealing with various staple strands to make stiff DNA-triangles.Atomic force microcopy(AFM),native polyacrylamide gel electrophoresis(PAGE),UV-analysis,MTT-assay,flow cytometry,and confocal imaging were performed to assess the formulated DNA-NWs and cisplatin(CPT)loading.The AFM and confocal microscopy images revealed a uniform shape and size distribution of the DNA-NWs,with lengths ranging from 2 to 4 μm and diameters ranging from 150 to 300 nm.One sharp band at the top of the lane(500 bp level)with the loss of electrophoretic mobility during the PAGE(native)gel analysis revealed the successful fabrication of DNA-NWs.The loading efficiency of CPT ranged from 66.85％to 97.35％.MTT and flow cytometry results showed biocompatibility of the blank DNA-NWs even at 95％concentration compared with the CPT-loaded DNA-NWs.The CPT-loaded DNA-NWs exhibited enhanced apoptosis(22％)compared to the apoptosis(7％)induced by the blank DNA-NWs.The release of CPT from the DNA-NWs was sustained at＜75％for 6 h in the presence of serum,demonstrating suitability for systemic applications.The IC50 of CPT@DNA-NWs was reduced to 12.8 nM CPT,as compared with the free CPT solution exhibiting an IC50 of 51.2 nM.Confocal imaging revealed the targetability,surface binding,and slow internalization of the DNA-NWs in the scavenger-receptor-rich cancer cell line(HepG2)compared with the control cell line.
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The study aimed to achieve enhanced targeted cytotoxicity and cell-internalization of cisplatin-loaded deoxyribonucleic acid-nanothread (CPT-DNA-NT),mediated by scavenger receptors into HeLa cells.DNA-NT was developed with stiff-topology utilizing circular-scaffold to encapsulate CPT.Atomic force microscopy (AFM) characterization of the DNA-NT showed uniformity in the structure with a diameter of 50-150 nm and length of 300-600 nm.The successful fabrication of the DNA-NT was confirmed through native-polyacrylamide gel electrophoresis analysis,as large the molecular-weight (polymeric) DNA-NT did not split into constituting strands under applied current and voltage.The results of cell viability confirmed that blank DNA-NT had the least cytotoxicity at the highest concentration (512 nM) with a viability of 92％ as evidence of its biocompatibility for drug delivery.MTT assay showed superior cyto-toxicity of CPT-DNA-NT than that of the free CPT due to the depot release of CPT after DNA-NT inter-nalization.The DNA-NT exhibited targeted cell internalizations with the controlled intracellular release of CPT (from DNA-NT),as illustrated in confocal images.Therefore,in vitro cytotoxicity assessment through flow cytometry showed enhanced apoptosis (72.7％) with CPT-DNA-NT (compared to free CPT;64.4％).CPT-DNA-NT,being poly-anionic,showed enhanced endocytosis via scavenger receptors.
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Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a member of C-type lectin-like receptor family.It can recognize many ligands and is the main receptor of oxidized low-density lipoprotein for inducing vascular endothelial dysfunction.Early studies focused on the role of LOX-1 in atherosclerosis and diabetes mellitus.Recent studies have shown that LOX-1 is closely associated with ischemic stroke.This article reviews the biological characteristics of LOX-1 and its association with ischemic stroke.
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Objective To evaluate the effect of over-expression of phosphatase and tensin homolog does on chromosome ten (PTEN) in podocytes on kidney under high fat diet (HFD) in vivo and clarify the mechanism how PTEN regulates scavenger receptor A (SR-A) expression exposed to oxidized low density lipoprotein (ox-LDL) in podocytes in vitro.Methods The podocyte-specific PTEN knockin (PPKI) mice were fed with HFD to establish mouse model of lipid-induced renal injury.Mice were divided into four groups:ND+Ctrl group,ND+PPKI group,HFD+Ctrl group and HFD+PPKI group.After 24 weeks of dietary intervention,all mice were tested for clinical and biochemical parameters,including serum creatinine (Scr) as well as urine albumin excretion rate (UAER);renal lipid content was measured by oil red O staining and cholesterol quantitative analysis;the pathological changes of glomeruli were observed by PAS staining and electron microscope.Podocyte injury was induced by ox-LDL in vitro.Western blotting was used to detect the changes of SR-A expression induced by ox-LDL after YAP-siRNA interfering (si-YAP),as well as YAP phosphorylation induced by ox-LDL after interfering by PTEN-siRNA (si-PTEN) and PTEN phosphatase inhibitor (Bpv-PTEN),and overexpressing by recombinant adenovirus (ad-PTEN).Results Compared with ND+Ctrl group,HFD+ Ctrl group significantly aggravated the levels of Scr and UAER,the expression of SR-A in podocytes,renal lipid content,mesangial matrix expansion,effacement of podocyte foot processes,and incrassation of glomerular basement membrane (all P ＜ 0.05).Conversely,compared with HFD+Ctrl group,HFD+ PPKI group obviously alleviated the above lipid-induced renal damage (all P ＜ 0.05).In vitro,the expression of SR-A in podocytes was up-regulated when stimulated with ox-LDL (P ＜ 0.05),and the knockout of YAP significantly down-regulated the expression of SR-A induced by ox-LDL (P ＜ 0.05).Exposed to ox-LDL,the expression of p-YAP increased in podocytes (P ＜ 0.05);over-expression of PTEN inhibited p-YAP up-regulation induced by ox-LDL (P ＜ 0.05),while either knockdown of PTEN or inhibition of PTEN phosphatase activity displayed opposite effect (all P ＜ 0.05).Conclusions Over-expression of PTEN in podocytes protected the kidney against damage from HFD in vivo and PTEN might suppress SR-A mediated lipid uptake via dephosphorylating p-YAP to prevent podocyte injury from ox-LDL.
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Objective To discuss the diagnostic value of soluble scavenger receptor(sCD163)for the patients of malignant tumor associated with fever in early infection .Methods Collect 102 cases of patients confirmed with malignant tumor in this hospi-tal since January to December 2014 ,all the patients were examined with blood culture .102 patients were divided into two groups ac-cording to the results of blood culture :infection group (60 cases) and uninfected group (42 cases) .ELISA ,electrochemical lumines-cence and immune transmission turbidimetric methods were used to detect the levels of sCD163 ,PCT and CRP in serum ,to compare the differences in the above indicators between two groups .The receiver-operating characteristic curve (ROC curve) was applied to evaluate the application value of sCD163 in diagnosing of malignant tumor associated with fever in early infection .Results The lev-el of sCD163 ,PCT and CRP had statistically difference in two groups(P< 0 .05) ;the critical values of sCD163 、PCT and CRP were 110 .80 ng/mL ,0 .45 ng/mL ,15 .60 mg/L respectively which can suggest the patients with malignant tumor complicated with fever in early infection .The area under the curve were 0 .894 ,0 .835 ,0 .743 respectively ,among that sCD163 area was the largest ;The corresponding sensitivity were 88 .9% ,77 .9% and 88 .0% ;specificity were 77 .0% ,74 .0% and 50 .0% respectively .Conclusion Compared with PCT ,CRP ,sCD163 has more value for diagnosing the patients of malignant tumor associated with fever in early in-fection .
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Objective To develop a duplex fluorescence RT-PCR assay for detection of scavenger receptor class B, typeⅠ(SRBⅠ) knockout mice. Methods Primers and probes were designed according to knockout region of SRBⅠgene and related substituted sequence. DNA samples were extracted from tails of mice and performed amplification using real-time PCR. SRBⅠgenotypes of mice were analyzed according to amplification curves of FAM and CY5 channels. Finally, the sensitivity of the method was detected and the accuracy was verified by the direct sequencing. Results The homozygous SRBⅠwild genotype showed an amplification curve only in FAM channel. When the homozygous SRBⅠknockout genotype was present, the typical S amplification curve appeared only in the CY5 channel. Heterozygous genotype showed two typical S amplification curves in both FAM and CY5 channels, respectively. The results showed that the sensitivity reached 4×101 copies/μL, and there was complete concordance between this method and direct DNA sequencing. Conclusion The new method is simple, rapid and accurate, which is suitable for genotyping SRBⅠknockout mice.
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Objective To explore the association of lectin-like oxidized low-density lipoprotein (oxLDL) receptor-1 (LOX-1),CX3C chemokine receptor 1 (CX3CR1) with coronary artery stenosis disease and its outcomes.Methods A case-control study was conducted.A total of 176 cases of coronary artery stenosis which were confirmed coronary artery stenosis ≥ 50％ by coronary angiography(CAG) were served as case group from department of cardiology of TEDA International Cardiovascular Hospital of Tianjin from May 2011 to April 2013.A total of 129 patients without coronary artery lesion by CAG from this hospital in the same period were served as control group,which has no history of heart disease,liver and kidney dysfuction,brain disease,hematological disease,other disorders that could bring out atherosclerosis and thrombosis.General information and laboratory parameters,LOX-1,CX3CR1,uric acid (UA) and creatinine (CREA) were measured in 2 groups.These parameters of each group were compared,the levels of LOX-1 and CX3CR1 in one-vessel stenosis were compared than that in multi-vessels stenosis in case group,the correlations between LOX-1,CX3CR1 and Gensini score and other variables were analyzed.Comparison of the levels of LOX-1 and CX3CR1 between major adverse cardiovascular events (MACEs) group and nonmajor adverse cardiovascular event (MACE) group was made during follow up 1.5 years.MACEs in patients with different levels of LOX-1 and CX3CR1 were compared during 1.5-year follow up.All of the data were analyzed by SPSS 16.0 software.The independent-samples T test,Mann-Whitney U test,Chi-square test,Spearman correlation,Binary Logistic Regression and Kaplan-Meier probability were adopted for data analysis.Results Comparison between case group and control group,LOX-1:3.72 (1.44,8.15) μg/L vs 0.75(0.50,1.19) μg/L,z =11.072,P ＜0.001 ;CX3CR1:(2.82 ± 1.85) μg/L vs (2.32 ±0.79) μg/L,t =2.021,P ＜ 0.05 ; UA:(351.34 ± 94.82) μmol/L vs (326.74 ± 79.51) μmol/L,t =2.094,P ＜ 0.05 ;CREA:(70.86 ± 20.94) μmol/L vs (65.55 ± 12.96) μmol/L,t =2.077,P ＜ 0.05.CX3CR1 level was significantly higher in patients with multi-vessels stenosis (2.84 ± 1.78) μg/L than that in one-vessel stenosis(2.48 ± 1.64) μg/L,there was significance in difference (t =2.207,P ＜ 0.05).There were no statistically significant correlation between LOX-1,CX3CR1 and Gensini score (R was 0.032,0.079 respectively,P＞ 0.05).LOX-1 was negatively related to left ventricular ejection fraction(LVEF) (R =-0.272,P ＜ 0.01),but positively related to left ventricular end-diastolic diameter (LVDD)(R =0.190,P＜0.05),positively related to UA (R =0.121,P ＜ 0.05).Comparison between MACE group and nonMACE group,LOX-1:7.38(4.97,11.88)μg/L vs 3.52(1.45,7.75) μg/L,z =2.762,P ＜0.01;CX3CRl:(4.02 ±2.90) μg/L vs (2.67 ± 1.48) μg/L,t =3.086,P ＜0.01.LOX-1 and TG were independent risk effects of coronary artery stenosis disease.MACEs were increased in patients with high levels of LOX-1 after PCI during following up 1.5 years (comparison between high-LOX-1 group and lowLOX-1 group,the probability of non-MACE was 87.1％ (115/132) vs 97.7％ (43/44),Log-ranK test,x2 =6.957,P ＜ 0.01).Conclusions LOX-1 and CX3CR1 may be involved in the process of coronary artery stenosis,and a high level of LOX-1 may be associated with left ventricular systolic dysfunction in patients with coronary artery stenosis.Elevated LOX-1 level are closely related to afterwards MACE incidence after PCI in patients with coronary artery stenosis.
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Objective To express and preliminary identify scavenger receptor B2 (SCARB2)protein.Methods SCARB2 cDNA was amplified by reverse transcription-polymerase chain reaction (RT-PCR)from mRNA extracted from RD cells,and cloned into pMD19-T vector.Expression vector pET28a(+)/SCARB2 was constructed,and SCARB2 protein was expressed in prokaryotic ex-pression system.Obtained recombinant proteins were identified by detection of Western blot using His labeled monoclonal antibody.Results Recombinant SCARB2 proteins,expressed by induction of isopropy-β-D-thiogalactoside (IPTG),were success-fully purified and specifically recognized by His labeled monoclonal antibody.Conclusion SCARB2 proteins could be expressed and identified successfully,which could provide reference for researching mechanism of enterovirus type 71 (EV71)and scavenger re-ceptor protein,and for preparation of SCARB2 monoclonal antibodies.
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Obesity is consistently increasing in prevalence and can trigger insulin resistance and type 2 diabetes. Many lines of evidence have shown that macrophages play a major role in inflammation associated with obesity. This study was conducted to determine metformin, a widely prescribed drug for type 2 diabetes, would regulate inflammation through down-regulation of scavenger receptors in macrophages from obesity-induced type 2 diabetes. RAW 264.7 cells and peritoneal macrophages were stimulated with LPS to induce inflammation, and C57BL/6N mice were fed a high-fat diet to generate obesity-induced type 2 diabetes mice. Metformin reduced the production of NO, PGE2 and pro-inflammatory cytokines (IL-1beta, IL-6 and TNF-alpha) through down-regulation of NF-kappaB translocation in macrophages in a dose-dependent manner. On the other hand, the protein expressions of anti-inflammatory cytokines, IL-4 and IL-10, were enhanced or maintained by metformin. Also, metformin suppressed secretion of TNF-alpha and reduced the protein and mRNA expression of TNF-alpha in obese mice as well as in macrophages. The expression of scavenger receptors, CD36 and SR-A, were attenuated by metformin in macrophages and obese mice. These results suggest that metformin may attenuate inflammatory responses by suppressing the production of TNF-alpha and the expressions of scavenger receptors.
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Animals , Mice , Cytokines , Diet, High-Fat , Dinoprostone , Down-Regulation , Hand , Inflammation , Insulin Resistance , Interleukin-10 , Interleukin-4 , Interleukin-6 , Macrophages , Macrophages, Peritoneal , Metformin , Mice, Obese , NF-kappa B , Obesity , Prevalence , Receptors, Scavenger , RNA, Messenger , Tumor Necrosis Factor-alphaABSTRACT
Objective To explore the effect of ACE-inhibitor perindopril on the expression of scavenger receptor A (SR-A) gene in the kidney of diabetic rats.Methods Diabetes were induced in male Sprague-Dawley rats by peritoneal injection with streptozotocin (60mg/kg).The rats were then random di vided into normal control group, diabetes group and ACEI treatment group [4mg/(kg·d) for 24 weeks].Blood glucose concentration and 24h urinary albumin excretion were determined.The renal morphological change was observed.Immunohistochemistry was used to analyze CD68 positive macrophages,and the Mrna of SR-A in renal tissue was detected by quantitative real-time PCR.Results Compared with normal control group,blood glucose concentration,24h urinary albumin excretion and the number of CD68 positive macrophages were significantly increased [(5.3 ± 0.6) mmol/L vs (26.7 ± 3.3) mmol/L;(2.7 ± 1.3) mg/24h vs (26.7 ± 1.8)mg/24h;(0.77 ±0.24)/gcs vs (2.55 ±0.46)/gcs;(6.13 ±0.50)/HPF vs (11.9 ±2.12)/HPF;P ＜0.05],and the expression of SR-A Mrna were significantly up-regulated in diabetes group [ (5.6 ± 1.2 vs 1.5 ±0.2),P ＜0.05].After intervention with ACE-inhibitor,the up-regulations of the above mentioned parameters,except blood glucose concentration,were all significantly inhibited [ (3.6 ±1.4)mg/24h;(1.03±0.37)/gcs;(8.28±1.19)/HPF;3.4±0.7;P ＜0.05].Conclusion ACE-inhibitor might have renoprotective effects of diabetic nephropathy,it probably was associated with inhibiting the expression of SR-A gene.
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Objective: To investigate whether atorvastatin can prevent renal injury in mice independent of the lipid-lowering effects. Methods: CD36-/- SR-A-/- ApoE-/- mice were randomly assigned to a high fat diet (high fat group) and high fat diet plus atorvastatin (atorvastatin) group; male C57BL mice with a chow diet served as controls. Terminal blood samples were taken for plasma cholesterol assay 14 weeks later. Renal sections were used for histological and immunohistochemistry assessments. The lipid accumulation in the kidney was evaluated by Oil Red O (ORO) staining. The mRNA expression of transforming growth factor-β (TGF-β), collagen I and IV, fibronectin, and α-smooth muscle actin (α-SMA) were analyzed by real-time PCR. Results: Blood total cholesterol levels (LDL-cholesterol and HDL-cholesterol) were not nd high fat group. Meanwhile, ORO staining showed that atorvastatin significantly different between atorvastatin group a decreased lipid accumulation in the kidney; Masson and H-E staining demonstrated that atorvastatin therapy attenuated massive structural changes, including mesangial proliferation, interstitial matrix deposition, accumulation of extracellular matrix proteins, tubular-interstitial inflammatory cell infiltration, and renal deformations with glomerulosclerosis/tubulointerstitial fibrosis in the high fat group. Moreover, atorvastatin therapy not only decreased TGF-β expression at mRNA and protein levels, but also decreased the expression of factors related to fibrosis. Conclusion: Atorvastatin can protect the kidney independent of the lipid-lowering effects and SR-A, CD36 receptor pathways, and it might be related to decrease of TGF-beta expression.
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Objective To investigate the role of oxidized low-density lipoprotein (oxLDL) and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-I) in pre-ecalmpsia. Methods From June 2007 to January 2008,73 women with pre-eelampsia who delivered in the Department of Obstetrics, Affiliated Hospital of Qingdao University Medical College,were recruited, including 35 women with mild pre-eclampsia (MPE group) and 38 women with severe pre-eclampsia(SPE group). And 45 healthy pregnant women were taken as control group. Enzyme-linked immunosorbent assay (ELISA) was used to measure the plasma concentrations of oxLDL in these women. Semiquantitative RT-PCR and Western blot were used to investigate the expression of LOX-1 mRNA and protein in placenta. The expression of caspase-3 mRNA in placenta was determined using Semiquantitative RT-PCR. Results (1) The plasma concentrations of oxLDL in MPE group ( 0.42 ± 0.11 ) mg/L, SPE group ( 0.68 ± 0.12 ) mg/L, were significantly higher compared with control group (0.35 ± 0.14 )mg/L( P < 0.01 ) and the concentrations of oxLDL in MPE group were significantly higher compared with SPE group (P<0.01 ). (2) The expression of LOX-1 mRNA in placenta of MPE group(0.70 ±0.10) and SPE group(0.84 ±0.08) were significantly higher than that in control group(0.58 ± 0.11 ) ( P<0.01 ) and the expression of LOX-1 mRNA in MPE group was significantly higher than that of SPE group (P<0.01 ). (3) The expression of LOX-1 protein in placenta of MPE group (0.79±0.15 )and SPE group(0.90±0.12) were significantly higher compared with control group(0.68 ±0.11)( P<0.01 ), while the expression of LOX-1 protein of MPE group was significantly higher compared with SPE group (P <0.01 ). (4) The expression of caspase-3 mRNA in placenta of MPE group(3.82± 0.18) and SPE group(5.39±0.14) were significantly higher than that in control group(2.19±0.20) (P <0.01 ), and the expression of caspase-3 mRNA in MPE group was significantly higher than that of SPE group (P<0.01 ). (5) In pre-eclampsia groups, the levels of LOX-1 mRNA in placenta were positively correlated with the plasma concentrations of ox LDL ( r=0.93, P<0.05 ), and caspase-3 mRNA expression were positively correlated with the expression of LOX-1 mRNA in placenta( r=0.84, P<0.05). Conclusion Increased levels of oxLDL in plasma may induce excess expression of LOX-1 in placenta, which may be involved in the pathophysiological processes of pre-eclampsia.
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Objective To explore the expressions of lectin-like oxidized low-density lipoprotein receptor-1(LOX-1)and apoptosis related genes caspase-3,Bax and bcl-2 in placenta,and their associations with the pathogenesis of preeclampsia.Methods Thirty preeclampsia patients(preeclampsia group),hospitalized in Department of Obstetrics,Shengiing Hospital of China Medical University from June 2005 to December 2006,were selected as the subject group,and 40 normal pregnant women as control group.The expressions of LOX-1 and apoptosis related genes caspase-3.Bax and bel-2 in different gestational weeks'placenta tissues were examined using immunohistochemistry.RT-PCR and western-blot.Results (1)Immunohistochemical detection in preeclampsia group:at 20 w+1-24 w,24 w+1-28 w,28 w+1-32 w.32w+1-36 w+1-36 w+1-40 w,respectively,the results of LOX-1 were 20.1±1.8,25.6±1.3,32.8±1.6,34.3 ±1.5,39.9±1.2;in the control group they respectively were 11.2±0.6,18.5±1.6,26.1±1.8,28.3 4-1.6,32.3±1.6;the difierence was significant(P<0.05).In preeclampsia group,the results of easpase-3 were 12.3±0.9,16.3±0.9,24.4 4-0.8,28.3±0.5,36.3±1.1.and in the control group they respectively were 8.5±1.0,12.3±1.1,17.4±1.2,20.4±stronger than those in normal pregnant women at different gestational weeks(P<0.05).However,the expression tendency of bcl-2 mRNA and proten was converse to the expression tendency of Bax.Conclusion The expressions of LOX-1,caspase-3,and Bax are upregulated in placentas of preeclampsia patients,while bcl-2 iS downregulated,both of which are associated with the pathogenesis of preeclampsia.
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Objective To investigate the influence of transforming growth factor-?1(TGF-?1) on macrophage scavenger receptor (ScR) class A and B(ScR-B,CD36) in order to provide theoretical foundation for expounding the formation and therapy of atherosclerosis(AS).Methods THP-1 derived macrophages were divided into control group and experimental group,the cells in experimental group were treated with 3.0 mg?L-1Anti TGF-?1 Ab,the cells in control group were treated with 3.0 mg?L-1 IgG. The 125I-acetylated low density lipoprotein (125I-Ac-LDL for ScR-A) and 125I-oxidized low density lipoprotein (125I-Ox-LDL for CD36) uptaking (including 4℃ binding,37℃ association and degradation) were measured respectively.Influence of anti TGF-?1 antibody (Anti TGF-?1 Ab) on the ScR-A and CD36 mRNA expressions in THP-1 derived macrophages was measured meanwhile,respectively.Results Compared with control group ( binding: 8.23 ?g?g-1 ?1.24 ?g?g-1 protein,association:45.69 ?g?g-1 ?6.92 ?g?g-1 protein,and degradation: 112.18 ?g?g-1 ?20.15 ?g?g-1 protein),Anti TGF-?1 Ab increased 125I-Ac-LDL binding(48.67 ?g?g-1 ?6.52 ?g?g-1 protein),association (412.30 ?g?g-1?12.21 ?g?g-1 protein),and degradation (896.48 ?g?g-1 ?32.74 ?g?g-1 protein) significantly (P
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Objective To investigated the expression of scavenger receptor A(SR-A) and lipopolysaccharide(LPS) receptor CD14 in endotoxin-induced acute liver injury.Methods Ninety Wistar rats were randomly divided into endotoxaemia group(LPS group) and normal saline group(NS group).The model of endotoxaemia and acute endotoxin-induced liver injury was established by injection of endotoxin(5mg/kg) via tail veins in LPS group,while the rats in NS group received injection of 0.2ml normal saline as control.At 0,1.5,3,6,12h after injection,the levels of endotoxin,TNF-?,IL-1,alanine transaminase(ALT) and total bilirubin(TB) in plasma,SR-A and CD14 expressions in liver tissues were determined,pathological changes of liver tissues and ultrastructural changes of Kupffer cells(KCs) were observed by light and electron microscopy respectively,while the phagocytosis of KCs was determined too.Results Compared with NS group,KCs were activated on morphology and functions(proliferated diffusely,enlarged in size and increased in phagocytosis function),levels of TNF-? and IL-1 increased markedly,the pathological changes of cell degeneration and necrosis and the liver function were gradually aggravated,while SR-A expression decreased and CD14 expression increased obviously(P