摘要
目的观察肥大细胞、巨噬细胞在大鼠肺动脉高压(pulmonaryhypertension,PH)模型,及辛伐他汀干预肺组织中的变化。方法对大鼠行腹主动脉-下腔静脉分流术,术后第8d野百合碱腹腔注射制备PH模型,并应用辛伐他汀进行干预,35d后观察各组肺动脉压及心室重量变化。同时采用免疫组化方法半定量检测各组肺组织内肥大细胞及巨噬细胞数量的变化。结果平均肺动脉压(mPAP)模型组动物较对照组升高(P<0.05),干预组较模型组降低(P<0.05);右心室/(左心室+室间隔)(RV/LV+S)模型组较对照组增加(P<0.05),而干预组较模型组RV/LV+S降低(P<0.05)。模型组动物肺部肥大细胞及巨噬细胞数量较对照组均增高(P<0.05),干预组肥大细胞数量较模型组下降(P<0.05),巨噬细胞数量与模型组相比差异无统计学意义(P>0.05)。结论肥大细胞及巨噬细胞参与了肺动脉高压的形成或/和肺动脉高压造成的损伤促进了肥大细胞及巨噬细胞的聚集与活化。辛伐他汀对肺动脉高压有改善作用,减少肥大细胞的聚集与活化可能是其机制之一。
Objective To investigate the change of mast cells and maerophages in lung tissue of rats with pulmonary hypertension （PH） and the effect of simvastatin on it. Methods Pulmonary hypertension was established as follow, a shunt between abdominal aorta and inferior vena eava was created in rats, 8 days later, the rats were injected with monoerotaline （60 mg/kg）. Moreover, a subgroup of rats were given simvastatin 2 mg/ （kg· d）. The mean pulmonary artery pressure （mPAP） and right ventrieular weight were measured, and the ratio of right ventricle/left ventricle plus septum CRV/（LV＋S）] was calculated. The LSAB method was used to stain anti-tryptase and ED1 in the lung tissue of the rats. Results In eomparision with the control group, mPAP and RV/（LV ＋ S） of PH rats increased significantly （P 〈0. 05）. The RV[ （LV ＋ S） in simvastatin group was lower than that in PH rats （P〈0. 05）. The amount of mast cells and maerophages in PH rats were more than that in control group （P〈0. 05）. The amount of mast cells in simvastatin intervention group decreased in eomparision with the PH group while the maerophages showed no difference in simvastatin group （P〉0. 05）. Conclusion Mast cells and maerophages may be involved in the development of PH and/or the lesion caused by PH accelerate the accumulation and activation of mast cell and maerophages. Simvastatin has a preventive effect on rat PH, it inhibits mast cell proliferation may be one of mechanism.
出处
《四川大学学报（医学版）》
CAS
CSCD
北大核心
2006年第2期208-211,共4页
Journal of Sichuan University(Medical Sciences)
基金
四川省科技厅基金(03JY029-081-2)资助
