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Objective To establish a simple animal model of cough variant asthma(CVA)through sensitizing Brown-Norway(BN)rats with ovalbumin(OVA). Methods A total of 36 BN rats were randomly divided into three groups, including the normal control group,the model control group and the montelukast group. BN rats in the model group and the montelukast group were intraperitoneally administered with 2.0 mg of OVA and 100 mg of Al(OH)3,and the same volume of sterile saline was given to the normal group by intraperitoneal injection. Boosting was carried out by intraperitoneal administration with 0.01 mg of OVA and 100 mg of Al(OH)33 weeks later,and the rats in the normal group were injected with the same dose of physiological saline. Three weeks later,the actively sensitized BN rats were challenged with aerosolized OVA for 7 times on alternative days,and the rats in the normal group were treated with sterile saline instead of OVA. At the same time, the montelukast group was given 1.3 mg/kg of montelukast 30 minutes before atomization by intragastric administration once a day for 2 weeks,and the normal group and the model group were given the same volume of water. The tests of cough sensitivity to capsaicin and bronchial responsiveness were performed 24 h after the last administration. Results Compared with the normal group, the times of coughing(P< 0.01)and the lung resistance(RL)(P< 0.05)in the model group were significantly increased,while the lung compliance(Cdyn)was significantly decreased(P< 0.05). There was a significant difference(P < 0.05)in the times of coughing caused by capsaicin between the model group and the montelukast group. Compared with the model group,RLin the montelukast group was decreased significantly(P< 0.05), and Cdynwas increased significantly(P< 0.05). Conclusions This rat model of CVA is similar to a variety of clinical features of CVA and is easy to operate. Thus it can be used as an effective animal model of CVA.
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Objective To explore the effects and mechanisms of prenatal hypoxia on vasomotor functions of fetal rats.Methods Sixteen pregnant Sprague-Dawley rats were randomly divided into two groups:control and hypoxia groups (eight in each group).Rats in the hypoxia group were provided with 10.5％ of oxygen from gestation day 5 to 21,while those in the control group were exposed to normoxic condition.Fetuses were removed from the pregnant rats by cesarean section on gestational day 21.Fetal body weight,blood gas and electrolyte levels were measured.Thoracic aorta rings were separated from fetal rats and used in different vascular function tests.Effects of hypoxia during pregnancy on angiotensin Ⅱ (Ang Ⅱ)-mediated vasoconstrictions and acetylcholine (Ach)-mediated vasodilatations in fetal thoracic aortas were measured.Changes in vasomotor functions were observed after both endothelial nitric oxide synthase (eNOS) inhibitor NG-nitro-L-arginine methyl ester (L-Name) and L-type calcium channel (LTCC) inhibitor nifedipine were administered.T-test and two-way analysis of variance were used for statistical analysis.Results (1) Compared with the control group,fetal body weight [(4.40±0.23) vs (3.33±0.42) g,t=2.871],blood partial pressure of oxygen [(50.64±2.17) vs (42.50-±-2.32) mmHg (1 mmHg=0.133 kPa),t=-2.618] and blood oxygen saturation [(58.95±1.97)％ vs (47.73±2.24)％,t=3.564] in the hypoxia group were significantly reduced (all P＜0.05).(2) Compared with the control group,Ang Ⅱ-mediated vasoconstrictions increased,but Ach-mediated vasodilatations in fetal thoracic aortas decreased in the hypoxia group (both P＜0.05).L Name induced stronger Ang Ⅱ-mediated contractions in thoracic aortas in the control group than that in the hypoxia group (P＜0.05).However,nifedipine decreased Ang Ⅱ-induced contractions,especially in the hypoxia group (P＜0.05).Conclusions Maternal hypoxia during pregnancy not only affects the growth and development of fetuses but also changes their blood vessel functions,which may be related to the change of LTCC and the impairment of eNOS.
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Objective: To research the anti-inflammatory and anti-allergic effects of Qifangbimin particle.Methods: The anti-inflammatory effects were observed by the methods of xylene-induced ear-swelling in mice and cotton-ball induced granuloma in rats.The anti-allergic effects were evaluated by the method of passive skin allergy model in rats and ear-heterogeneous passive skin allergy model in mice.Results: In the treatment groups with Qifangbimin particle, the swelling degree of ear edema induced by dimethylbenzene in mice was significantly suppressed when compared with that in the control groups (P<0.01 or 0.05) , however, the particle had no significantly inhibitory effect on granulation tissue hyperplasia induced by cotton-ball in rats.The Qifangbimin particle groups obviously decreased the absorbance value of locus coeruleus on rats' back (P<0.01 or 0.05), and Qifangbimin particle at high dose significantly reduced the absorbance value of locus coeruleus of auricle in mice (P<0.01 or 0.05).Conclusion: Qifangbimin particle has significant anti-inflammatory and anti-allergic effects.
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Objective To determine the effects of β-estradiol on vasoconstriction in human umbilical artery and vein and its potential mechanisms.Methods Human umbilical cord samples were obtained from 96 term neonates of healthy singleton pregnant women born in the First Hospital of Soochow University between December 2013 and June 2015 (multiple pregnancy,pregnancy complications,cesarean delivery and low birth weight were excluded).Human umbilical arteries and veins were isolated and suspended in 37 2 organ baths containing 5 ml Krebs solution and exposed to β-estradiol followed by phenylephrine (PE) for vasoconstriction test.The subjects were divided into β-estradiol group and control group according to the presence or absence of β-estradiol incubation.To determine the effects and the possible underlying mechanisms of β-estradiol on PE-induced vasoconstriction,human umbilical artery and vein rings were pretreated with N ω-nitro-L-arginine (L-NMMA,nitric oxide synthesis inhibitor),fulvestrant (ICI182780,estradiol receptor antagonist),indomethacin (prostaglandin synthesis blocker),and removal of endothelium,then incubated with β-estradiol for 60 min followed by PE,and the concentration-response curves to PE were recorded.The concentrationresponse curves to phorbol 12,13-dibutyrate (PDBU,protein kinase C agonist) in Krebs solution in the presence or absence of β-estradiol were also obtained.Nonlinear regression and fitting curve were performed,and the two-sample ANOVA was used for analysis.Results (1) β-estradiol suppressed PE-induced vasoconstriction of human umbilical vein and artery.In human umbilical vein and artery of the control group,the maximum contraction intensity induced by PE was (59.17± 5.98)％ and (43.35± 5.02)％ of that induced by potassium chloride,respectively.The maximum contraction induced by PE in β-estradiol group was (5.87± 1.32)％and (4.52±1.22)％ of that induced by potassium chloride.(2) In both groups,incubation with L-NMMA or endothelium removal enhanced the vasoconstriction of human umbilical artery and vein,indicating that the inhibitory effect of β-estradiol was not influenced by the endothelium.(3) The suppression of β-estradiol on PE-induced vasoconstriction in human umbilical artery and vein was not significantly decreased by estrogen receptor antagonist.(4) β-estradiol did not affect human umbilical artery and vein vasoconstriction induced by PDBU.(5) In the control group,incubation with indomethacin did not affect human umbilical artery and vein vasoconstriction induced by PE.In the β-estradiol group,indomethacin significantly enhanced the contraction response induced by PE,suggesting that prostacycline synthesis was partly involved in β-estradiol-suppressed contractility in human umbilical artery and vein.The contractile response induced by phenylephrine was still lower in the β-estradiol group than in the control group,which was induced by indomethacin.Conclusions (1) β-estradiol can suppress vasoconstriction in human umbilical artery and vein,which is not dependent on endothelium and estrogen receptors,or protein kinase C activity,(2) Prostacycline synthesis is partly involved in β-estradiol-suppressed vasoconstriction in human umbilical artery and vein.