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1.
Artigo em Chinês | WPRIM | ID: wpr-1036479

RESUMO

Objective@#To investigate whether GIV , a coiled helix structural domain protein containing 88A , has an effect on the neuroinflammatory response in a model of cerebral ischemia⁃reperfusion injury.@*Methods@# A middle cerebral artery embolization⁃reperfusion model (MACO/R) and an oxygen glucose deprivation/reoxygenation model ( OGD 6 h + R 24 h) of BV2 microglia were constructed in C57BL/6 mice , and the area of cerebral infarction was detected by TTC staining; the Longa neurobiological score was used to evaluate the degree of neurological deficit in mice ; ELISA was used to detect the release of IL⁃6 and TNF⁃α in the supernatant of peripheral blood and cell cultures , and Western blot was used to detect the protein expression of GIV , TREM2 and TLR4 in the cortical area around the infarct foci in mice ; different concentrations of lipopolysaccharide (LPS , 1 , 5 , 10 μg/ml) were used to stimulate BV2 cells for 24 h to establish a neuroinflammation model , qRT⁃PCR was performed to detect the mRNA levels of IL⁃6 , TNF⁃α and IL⁃1β , and Western blot was used to detect the expression of GIV ; OGD/R culture treatment was performed after knocking down the expression of GIV gene using siRNA interference technique ;ELISA was performed to detect the release concentration of IL⁃6 and TNF⁃α in cell culture medium supernatant;protein immunoblotting was performed to detect the knockdown efficiency of GIV.@*Results @#Both the successfully constructed MCAO/R and OGD/R models activated the neuroinflammatory response and induced a decrease in protein expression of GIV ; MCAO/R induced increased concentrations of IL⁃6 and TNF⁃α release in peripheral blood of mice and promoted the protein expression of TREM2 and TLR4 ; LPS activated IL⁃6 , IL⁃1β and TNF⁃α expression in BV2 cells , but did not affect GIV expression ; siRNA interference with GIV gene expression further in creased the expression of inflammatory factors IL⁃6 and TNF⁃α .@*Conclusion@#The GIV gene may be characteristically involved in regulating the neuroinflammatory response induced by cerebral ischemia⁃reperfusion injury , and it may be a potential therapeutic target for cerebral ischemia⁃reperfusion injury.

2.
Artigo em Chinês | WPRIM | ID: wpr-1038387

RESUMO

Objective @#To explore the regulatory mechanism of ginsenoside Rb1 on focal cerebral ischemia-reperfusion injury ( CIRI) .@*Methods @# A total of 60 C57 / BL mice were randomly divided into 6 groups (n = 10) : shamoperated group ,CIRI model group ,ginsenoside Rb1 low -,medium -,and high-dose group and nimodipine (positive control) group.The surgical method was used to construct the focal CIRI mouse model.The neurological function scores and behavioral tests were performed,and Nissl staining was utilized to detect the number of nissl bodies in the hippocampus.The effect of ginsenoside Rb1 on the molecule expression of the Wnt signaling pathway in the hippocampus was detected by qPCR , Western blot and immunohistochemistry assays.The regulatory mechanism of ginsenoside Rb1 was investigated through molecular docking and co-precipitation assays. @*Results @#Compared with the CIRI model group,the addition of ginsenoside Rb1 reduced the neurological function scores of mice (P<0. 05) ,shortened the time passing the balance beam (P<0. 05) ,but increased the time entering the correct arm (P<0. 05) and the swinging time and climbing time of mice (P <0. 05 ) ,indicating that ginsenoside Rb1 could effectively resume the function of the nervous system in mice and improve the behavioral ability of model mice.After ginsenoside Rb1 treatment,axis inhibition protein 2 (Axin2) and glycogen synthase kinase-3 β ( GSK- 3 β) in the hippocampus decreased,whereas the expression of Wnt3a,Wnt1 and β-catenin increased.@*Conclusion@#The ginsenoside Rb1 can improve neurological function of the CIRI mouse model and increase the number of Nissl bodies in the hippocampus,which is correlated with the activation of the Wnt signaling pathway,and it may be neuroprotective against focal CIRI during stroke treatment.

3.
Artigo em Inglês | WPRIM | ID: wpr-880664

RESUMO

OBJECTIVES@#To analyze the expressions and distributions of hypoxia-inducible factor-1α (HIF-1α), CD147, and glucose transporter 1 (GLUT1) in epidermis from psoriasis vulgaris and normal people, and to explore the associations among these proteins and their roles in hypoxic HaCaT cell line.@*METHODS@#The expression levels of HIF-1α, CD147, and GLUT1 were determined by immunohistochemistry staining in skin biopsies from 48 psoriasis vularis patients and 33 healthy subjects. Cobalt chloride (CoCl@*RESULTS@#HIF-1α, CD147, and GLUT1 were highly expressed and the glycolytic capacity was increased in lesions of psoriasis vulgaris; HIF-1α upregulated the expression of CD147 and GLUT1, increased the lactate production and decreased the ATP level in CoCl@*CONCLUSIONS@#Glycolytic capacity increases in the injured keratinocytes of psoriasis vulgaris, suggesting that HIF-1α, CD147, and GLUT1 are associated with glycolysis, which can be considered as the promising targets for psoriasis therapy.


Assuntos
Humanos , Basigina , Transportador de Glucose Tipo 1 , Glicólise , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Psoríase/genética , Ativação Transcricional , Regulação para Cima
4.
Artigo em Chinês | WPRIM | ID: wpr-697627

RESUMO

Objective To investigate the clinical diagnostic value of serum procalcitonin(PCT),D-dimer (DD),C-reactive protein(CRP)in acute-on-chronic liver failure(ACLF). Methods 124 ACLF patients, 63 chronic hepatitis B patients,32 chronic hepatitis C patients,24 chronic hepatitis E patients and 60 healthy controls from the second affiliated hospital of Nanchang University were enrolled in this study.PCT was detected by a sandwish immunodetection method. D-dimer was detected by Latex Turbidimetry. CRP was detected by rate nephenometry. The detection results were used for analyzing the clinical diagnostic value of ACLF with infection. Results(1)The level of PCT,DD and CRP in ACLF group were significantly higher than non-ACLF group and healthy controls(P<0.05).The levels of PCT,DD and CRP in the infection group were significantly higher than non-infection group(P<0.05).(2)The positive rates of PCT,DD and CRP in the infection group were 93.24%, 78.38%,89.19%,which were significantly higher than the non-infection group and healthy controls respectively (P < 0.05).(3)The sensitivity(93.24%)and specificity(90.00%)of PCT were the highest among all indexes. (4)The area under the ROC curve of PCT,DD,CRP were 0.892,0.715,0.755,respectively.PCT had the highest diagnostic value. Conclusion The levels of serum PCT,DD and CRP have a significant clinical value for the early diagnosis of ACLF with infection.

5.
Chinese Journal of Immunology ; (12): 849-853,858, 2017.
Artigo em Chinês | WPRIM | ID: wpr-617557

RESUMO

Objective:To investigate the effects of Acanthopanax Senticosus polysaccharides (ASPS) on TLR4 signaling pathway in Lewis tumor-bearing mice,and to explore the immunomodulatory mechanism of ASPS.Methods:Lewis lung carcinoma cells and C57BL/6 mice were used to establish the animal model for solid tumor.The tumor-bearing mice were divided into five groups:normal saline (NS) group,Adriamycin (ADM) group,ASPS low-dose group,ASPS middle-dose group and ASPS high-dose group.Mter 25 d treatment,the weight of tumor,tumor inhibition rate and immune organ index were measured.ELISA were applied to detected the cytokines in peripheral blood of tumor-bearing mice.Quantitative real-time PCR (Q-PCR) and Western blot were selectively used to detect the gene and protein expression of TLR4 signaling pathway in splenocytes.Results:The tumor inhibition rate,immune organ index and the secretion of TNF-α,IL-1β and IL-6 were increased by ASPS,compared with NS group (P<0.05).The gene and protein expression of TLR4,MyD88,TRAF6,NF-κB p65 and AP-1 were also induced by ASPS (P<0.05).Meanwhile,ASPS had no obvious effects on the secretion of IL-12p70 and the expression of TRAM (P>0.05).Conclusion:TLR4 signaling pathway may be involved in the immunomodulatory effects of ASPS on Lewis tumor-bearing mice.

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