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目的 观察光气致肺水肿小鼠肺Ⅱ型细胞发生凋亡情况和血清、肺脏的血管内皮生长因子 (VEGF)、VEGF受体 (Flt1)的变化及肺脏VEGFmRNA的表达。方法 2 6只二级BALB C小鼠 ,雄性 ,随机分为 2组 :对照组和染毒组 (各 13只 )。对照组小鼠以空气为对照 ,染毒组小鼠给予 11.9mg L剂量的光气 ,时间均为 5min ,染毒后 4h ,分离小鼠原代肺Ⅱ型细胞 ,电镜观察两组小鼠肺Ⅱ型细胞凋亡情况 ,酶联免疫法测定血清和肺脏的VEGF、Flt1的含量及反转录PCR法测定肺脏VEGFmRNA的表达。结果 电镜显示光气染毒肺水肿小鼠原代肺Ⅱ型细胞出现凋亡小体 ;染毒小鼠血清VEGF和肺脏的VEGF、Flt1含量 [(134.0 7± 12 0 .2 6 )、(4 77.76± 98.0 6 )、(12 818.4 8± 2 30 4 .15 )pg ml]明显低于对照组 [(4 4 5 .5 7± 173.30 )、(10 2 6 .87± 4 74 .5 6 )、(2 1976 .5 1± 74 2 1.0 1)pg ml],差异有显著性 (P <0 .0 5 ) ;染毒小鼠血清Flt1含量 [(2 36 9.5 6± 381.70 )pg ml]明显高于对照组 [(1898.0 0± 4 5 3.6 9)pg ml],差异有显著性 (P <0 .0 5 ) ;染毒小鼠肺脏VEGFmRNA表达降低。结论 光气经呼吸道染毒可引起肺水肿小鼠原代肺Ⅱ型细胞发生凋亡 ,使血清VEGF和肺脏VEGF、Flt1降低及肺脏VEGFmRNA表达降低。
Objective To observe the apoptosis of pulmonary type Ⅱ cells induced by phosgene induced pulmonary edema and the changes of serum and lung vascular endothelial growth factor (VEGF) and VEGF receptor (Flt1) and the expression of VEGFmRNA in lung tissue. Methods Twenty-six secondary BALB C mice, male, were randomly divided into two groups: control group and exposure group (13 rats each). The control group of mice with air as control, the mice were exposed to a dose of 11.9mg L dose of phosgene, both for 5min, 4h after exposure to isolated mouse primary lung type Ⅱ cells were observed by electron microscopy of two lungs The apoptosis of type Ⅱ cells was detected by enzyme-linked immunosorbent assay (ELISA). The contents of VEGF and Flt1 in serum and lung were detected by enzyme-linked immunosorbent assay (ELISA). Results Electron microscopy showed apoptotic bodies of type II cells in primary lung of mice with phosgene-induced pulmonary edema. Serum levels of VEGF and Flt1 in the lung of mice exposed to phosgene-induced pulmonary edema [(134.0 7 ± 12.0.26), (4 77.76 ± 98.0 6), (12 818.4 8 ± 2 30 4 .15) pg ml] was significantly lower than that of the control group [(44.557 ± 173.30), (102.687 ± 4.74.56) , (2 1976.51 ± 74 2 1.01) pg ml], the difference was significant (P <0.05). The content of Flt1 in serum of mice exposed to [2 36 9.5 6 ± 381.70] pg ml] Which was significantly higher than that of the control group [(1898.0 ± 45.69) pg ml] (P <0.05). The expression of VEGF mRNA in the lung of the mice was decreased. CONCLUSION: Phosgene exposure to the respiratory tract can cause apoptosis of primary lung type II cells in pulmonary edema, decrease the levels of serum VEGF, lung VEGF and Flt1, and decrease the expression of VEGFmRNA in the lung.