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Objective To investigate the effects of urotensin Ⅱ/urotensin Ⅱreceptor ( UⅡ/UT) system on the expression of inflammatory signal molecules p 38 mitogen-activated protein kinase ( p38 MAPK) and nuclear factor-κB ( NF-κB ) in lipopolysaccharide ( LPS )-stimulated Kupffer cells ( KCs ) . Methods Rat KCs were isolated and purified by means of in situ perfusion and density gradient centrifuga-tion.The isolated cells were randomly divided into six treatment groups including group 1:UⅡ(-) urantide (-)LPS(-), group 2:UⅡ(+)urantide(-)LPS(-), group 3: UⅡ(-)urantide(+)LPS(-), group 4:UⅡ(-)urantide(-)LPS(+), group 5:UⅡ(+) urantide(-) LPS(+) and group 6:UⅡ(-)urantide(+) LPS(+) .Western blot assay was performed to detect p 38 MAPK/p-p38 MAPK protein and NF-κB p65 sub-unit.The DNA-binding activity of NF-κB was tested by electrophoretic mobility shift assay (EMSA).Re-sults There was no significant difference with the expression of p 38 MAPK protein in KCs among the six groups (P>0.05).The expression of p65 protein and p-p38 MAPK and the DNA-binding activity of NF-κB were significantly enhanced in LPS-stimulated KCs from groups 4, 5 and 6 in comparison with those in group 1 (P0.05), but that were decreased in group 6 than those in group 4 (all P<0.01).Conclusion UⅡ/UT system participated in the activation of p38 MAPK and NF-κB signaling pathways in LPS-stimulated primary Kupffer cells .
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Objective To investigate the alteration of urotensin Ⅱ in plasma of acute lung injury(ALI)rats,which affected by the urotensin Ⅱ receptor antagonist(URA),and to study the function of URA to ALI.Methods Forty-two Sprague Dawley(SD)rats were divided into two groups randomly,with each containing 21 rats.All rats were injected with oleic acid for ALI models.G1 as ALI model group,the other group was injected with URA as experiment group(G2).2 ml blood was drawn in 3,12,24 hours after injection,with each time blood being drawn in seven rats of each group.Plasma was separated from the blood.Keep plasma in-80℃ to be detected.Results The concentration of UⅡ of G1 in 3,12,24hours was(105.57?9.52)pg/ml,(119.30?8.30)pg/ml,(133.33?9.65)pg/ml,respectively;and(133.65?8.89)pg/ml,(131.99?9.80)pg/ml,(114.03?9.12)pg/ml in the same time of G2.With the time going on,the plasma concentration of UⅡwas significantly increased(P
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Objective To investigate the effects of urotensinⅡ(UⅡ)receptor antagonist(URA)on UⅡ in plasma and bronchoalveolar lavage fluid(BALF)in rats with acute lung injury(ALI).Methods Twenty eight Sprague Dawley(SD)rats were randomly divided into four groups:saline control group(group A),the other three groups(group B,group C,group D).Rats were injected with oleic acid and URA to produce ALI models.Three hours after injection,arterial blood was drawn for blood gas analysis in all rats.Immediately after this,blood of heart was collected in group A and group B.Then blood of heart were collected after 12 hours in group C and after 24 hours in group D.Rats were killed when blood of heart was drawn.Bronchoalveolar lavage(BAL)with saline was performed in the right lung.BALF was centrifugated and the upper fluid was put to the EP tube.Plasma was separated from the blood of heart.Both plasma and BALF were kept at -80 ℃ to be determined.Results Compared with group A,arterial pressure of oxygen was significantly decreased in the group B,group C,group D(P
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Urotensin Ⅱ,a cycle peptide originally found from the fish,is the most potent vasoconstrictor.Urotensin Ⅱand its receptor have been found in central nerve system,cardiovascular system and other organs and tissues.It has been suggested that urotensin Ⅱplays important roles in the physiological and pathological procedures.Based on the evidences obtained from experiments,urotensin Ⅱmay become a new target for treating many diseases,particularly for cardiovascular diseases.