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目的探讨血管紧张素Ⅱ(AngⅡ)-血管紧张素Ⅱ1型受体(ATR1)途径在介导大鼠肺部炎症反应和急性肺损伤中的作用。方法清洁级SD大鼠24只,随机分为对照组、AngⅡ组、AngⅡ+氯沙坦组和氯沙坦组。光镜观察肺组织病理改变并测定肺湿/干重比(W/D)。凝胶迁移率改变电泳(EMSA)测定肺组织核因子-κB(NF-κB)活性,逆转录-聚合酶链反应(RT-PCR)检测肿瘤坏死因子-α(TNF-α)mRNA表达水平,酶联免疫吸附法(ELISA)测定血浆血管性血友病因子(vWT)的含量,比色法测定髓过氧化物酶(MPO)和丙二醛(MDA)含量。结果AngⅡ可致肺泡间隔增宽、出血及大量炎性细胞浸润等急性肺损伤病理改变,氯沙坦可缓解由AngⅡ所致的肺组织病理损伤。AngⅡ组肺W/D、NF-κB活性、TNF-αmRNA表达、MPO、MDA及vWF含量均明显高于其余3组(P<0.05),对照组与AngⅡ+氯沙坦组和氯沙坦组的肺W/D、NF-κB活性、TNF-αmRNA表达、MPO、MDA及vWF含量差异无统计学意义(P>0.05)。结论AngⅡ可激活肺部炎症反应并导致急性肺损伤,AngⅡ在肺部的促炎作用主要是通过其1型受体介导的。
Objective To investigate the role of Angiotensin Ⅱ-angiotensin Ⅱ type 1 receptor (ATR1) pathway in mediating lung inflammation and acute lung injury in rats. Methods Twenty - four SD rats were randomly divided into control group, Ang Ⅱ group, Ang Ⅱ + losartan group and losartan group. Lung pathological changes were observed under light microscope and lung wet / dry weight ratio (W / D) was measured. The activity of nuclear factor-κB (NF-κB) was measured by EMSA and the expression of tumor necrosis factor-α (TNF-α) mRNA was detected by reverse transcriptase-polymerase chain reaction (RT- The content of vWT in plasma was determined by enzyme-linked immunosorbent assay (ELISA), and the content of MPO and MDA was measured by colorimetry. Results Ang Ⅱ could induce the pathological changes of acute lung injury such as widening of alveolar septum, hemorrhage and a large number of inflammatory cell infiltration. Losartan could alleviate the pathological damage of lung tissue induced by AngⅡ. The levels of lung W / D, NF-κB, TNF-αmRNA, MPO, MDA and vWF in AngⅡgroup were significantly higher than those in other three groups (P <0.05) The lung W / D, NF-κB activity, TNF-αmRNA expression, MPO, MDA and vWF content had no significant difference (P> 0.05). Conclusions Ang Ⅱ can activate pulmonary inflammatory response and cause acute lung injury. The proinflammatory effect of AngⅡ in the lungs is mainly mediated by its type 1 receptor.