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• W2359930470 abstract "Objective To observe the activation of local renin-angiotensin system in pulmonary tissues of asthmatic rats,and to explore the possible roles of the Angiotensin Ⅱ (Ang Ⅱ) in asthmatic airway remodeling.Methods Thirty Wistar rats were evenly divided into 3 groups according to random number table:control group (group C),asthmatic model group (group A),and Irbesartan group (group Ⅰ).Both group A and group Ⅰ were immunized by intraperiton-eal injection of ovalbumin(OVA) and aerosolized OVA in order to get the asthmatic rats.The following examinations were performed on all rats.The pulmonary function were tested;the levels of Ang Ⅱ in serum and in bronchoalveolar lavage fluid (BALF) were detected by enzyme-linked-immunosorbent assay (ELISA);semi-quantitative assessment was used to analyze the thickness of airway wall(total wall area/basement membrane perimeter,WAt/Pbm) and airway smooth muscle(smooth muscle area/basement membrane perimeter,WAm/Pbm);the expression of transforming growth factor-β_1 (TGF-β_1) and the expression of collagen Ⅰ (Col Ⅰ) and collagenⅢ (Col Ⅲ) in the airway wall were observed by means of immunohistochemical staining and picrosirius staining-polarization method, respectively;semi-quantitative assessm-ent was used to analyze the levels of three above factors.Results ① The level of Ang Ⅱ:The level of Ang Ⅱ in serum was significantly higher in group Ⅰ than those in groupA ( P0.05) and group C (P0.05).The difference was not statistically signifycant between group A and group C(P 0.05).The level of AngⅡ in BALF in group A was higher than that of group C(P0.05). The difference between Group Ⅰ and group A was significant (P0.05).②The test of the pulmonary function:The inspiratory resistance(Ri) of asthmatic rats was higher than that of normal rats (P0.05). Ri of group Ⅰ had no difference with those of group A and group C(P0.05).The expiratory resistance (Re) of asthmatic rats was significantly higher than that of control rats (P0.05).Re of group Ⅰ significantly decreased compared with that of group A(P0.05),and had no difference with that of group C(P0.05).Compliance of lung(C_L) of asthmatic rats was significantly lower than that of control group ( P0.05).C_L of group Ⅰ significantly ameliorated compared with that of group A (P0.05),but it was still lower than normal ratsCL(P0.05).③The thickness of airway wall:The thickness of airway wall in group A was (53.30±12.30) μm~2/μm,which is significantly increased compared with that of group C (P 0.05).Although the thickness of airway wall in group I significantly decreased compared with the thickness in group A (P0.05),it was still much higher than that of group C (P0.05).Both the thickness of ASM in group A and group Ⅰ were statistically higher than group C (P0.05).The thickness of ASM in group I was significantly thinner than that of group A(P0.05).④TGF-β_1 expression:The TGF-β_1 was significantly smaller in group I than that of group A(P0.05).However,it was still greater than that of group C(P0.05).⑤Angiotensin expression:The difference among the Col Ⅰ in group C、 group A and group Ⅰ was not significant (P 0.05).The Col Ⅲ in group A is much higher than those of group Ⅰ and group C(P0.05).The expression of Col Ⅲ in group Ⅰ was still significantly higher tban that of group C (P0.05).⑥ The analysis of correlations:The concentration of Ang Ⅱ in BALF was significantly correlated with TGF-β_1 (r =0.876,P0.01),and also correlated with Col Ⅲ and WAm/Pbm (r =0.744,P0.05;r =0.718,P0.05).TGF-β_1 also significantly associated with ColⅢ and WAm/ Pbm(r =0.915,P0.01;r =-0.832,P0.01).When the effect of TGF-β_1 was controlled,the partial correlation analysis showed that the association between Ang Ⅱ and Col Ⅲ or WAm/Pbm disappeared. However,after adjusting for Ang Ⅱ,the association between TGF-β_1 and Col Ⅲ or WAm/Pbm was still signify-cant though the partial correlation coefficients were decreased lightly(r = 0.733,P0.05;r = 0.816,P0.01).Conclusions The activation of local RAS was observed in asthmatic rats,which produced more AngⅡ in the lungs.AngⅡ promotes ASM proliferation and hypertrophy and accelerates the deposition of airway collagen maybe through up the expression of TGF-β_1.All of these aspects may contribute to the asthmatic airway remodeling.Irbesartan can alleviate the extent of airway remodeling and have some effects on improving the pulmonary functior." @default.
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• W2359930470 date "2007-01-01" @default.
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• W2359930470 title "Effect of angiotensin II On airway remodeling in asthmatic rats" @default.
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