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目的研究百草枯致大鼠肺纤维化微血管变化情况,探索百草枯中毒致肺纤维化的机制。方法 60只雄性SD大鼠随机分为百草枯组(PQ组)和生理盐水对照组(NS组),每组30只行肺组织病理组织学检查,观察肺纤维化程度;检测百草枯组和生理盐水组VEGF的表达及MVD计数。结果 30例百草枯组大鼠肺组织中VEGF分3.13±0.98;生理盐水组肺组织VEGF分1.88±1.01,两组间比较差异有统计学意义(P<0.05)。百草枯组MVD计数为29.67±5.03;而生理盐水组MVD为11.03±3.06,组间比较差异有统计学意义(P<0.05);且VEGF、MVD与肺纤维化呈明显正相关性(P<0.001)。结论百草枯导致大鼠肺组织纤维化,百草枯致大鼠新生血管形成,微血管变化是促进肺纤维化机制之一。
Objective To study the changes of pulmonary fibrosis induced by paraquat in rats and to explore the mechanism of paraquat poisoning induced pulmonary fibrosis. Methods 60 male Sprague-Dawley rats were randomly divided into paraquat group (PQ group) and saline control group (NS group). Pathological examination of lung tissue was performed in 30 rats in each group to observe the degree of pulmonary fibrosis. The expression of VEGF and MVD in normal saline group. Results The lung tissue of 30 rats in paraquat group had a VEGF score of 3.13 ± 0.98, and the lung tissue of normal saline group had a score of 1.88 ± 1.01. There was significant difference between the two groups (P <0.05). The MVD count in paraquat group was 29.67 ± 5.03, while the MVD in normal saline group was 11.03 ± 3.06 (P <0.05). There was a positive correlation between VEGF and MVD and pulmonary fibrosis (P < 0.001). Conclusion Paraquat causes lung fibrosis in rats and paraquat-induced neovascularization in rats. Microvascular changes are one of the mechanisms of pulmonary fibrosis.