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目的观察碱性成纤维细胞生长因子(bFGF)和血管内皮生长因子(VEGF)对大鼠肺气肿模型动脉血气和肺组织病理学的影响,探讨 bFGF、VEGF 修复肺泡的机制及肺气肿新的发病机制。方法 Wistar 大鼠24只,随机分为 bFGF 组、VEGF 组、对照组和健康对照组4组。bFGF 组、VEGF 组、对照组大鼠气管内一次性注入猪胰弹性蛋白酶(PPE)(250 U/kg)复制肺气肿模型,健康对照组以生理盐水对照,4周后模型制成,bFGF 组、VEGF 组气管内分别注入 bFGF(400 U/只)和 VEGF(2μg/只),对照组和健康对照组注入生理盐水,每周1次,连续3次。4周后对比大鼠动脉血气和肺泡形态学变化,免疫组化法检测 CD34~+细胞个数确定肺毛细血管增生情况。结果各组血气分析差异均无统计学意义;bFGF 组、VEGF 组平均肺泡数(MAN)分别为[(43±8)/视野、(44±9)/视野],均明显多于对照组[(30±6)/视野](P<0.01);平均肺泡面积(MAA)分别为(9856±1864)μm~2、(9804±1929)μm~2,均明显小于对照组[(14 525±3408)μm~2](P<0.01);平均内衬间隔(MLI)分别为(196±38)μm、(194±38)μm,均明显小于对照组[(288±68)μm](P<0.01);CD34~+阳性细胞相对面积分别为3.7%±1.3%、2.6%±1.2%,均明显多于对照组(0.8%±0.7%)(P<0.05)。结论bFGF 和 VEGF 能促进肺毛细血管再生,修复肺气肿的病变。肺毛细血管的损伤可能在肺气肿的发生发展中扮演了重要角色。
Objective To observe the effects of basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) on arterial blood gas and lung histopathology in rats with emphysema, and to explore the mechanisms of bFGF and VEGF in alveolar repair and emphysema The pathogenesis. Methods Twenty-four Wistar rats were randomly divided into bFGF group, VEGF group, control group and healthy control group. Rats in bFGF group, VEGF group and control group were intraperitoneally injected with porcine pancreatic elastase (PPE) (250 U / kg) to establish a model of emphysema. The rats in normal control group were treated with normal saline, 4 weeks later, bFGF In the VEGF group, bFGF (400 U / body) and VEGF (2 μg / body) were injected intratracheally into the trachea. The control group and the healthy control group were injected with normal saline once a week for 3 times. The arterial blood gas and alveolar morphology were compared after 4 weeks, and the number of CD34 + cells was detected by immunohistochemistry to determine the pulmonary capillary hyperplasia. Results There was no significant difference in blood gas analysis between groups. The mean alveolar number (MAN) of bFGF group and VEGF group was significantly higher than that of control group [(43 ± 8) / (44 ± 9) / field, (30 ± 6) / field of vision (P <0.01). The mean alveolar area (MAA) was (9856 ± 1864) μm 2 and (9804 ± 1929) μm 2, (P <0.01). The mean liner interval (MLI) was (196 ± 38) μm and (194 ± 38) μm, which were significantly lower than those in the control group [(288 ± 68) μm] <0.01). The relative area of CD34 ~ + positive cells were 3.7% ± 1.3% and 2.6% ± 1.2% respectively, which were significantly higher than that of the control group (0.8% ± 0.7%) (P <0.05). Conclusions bFGF and VEGF can promote the regeneration of pulmonary capillaries and repair the pathological changes of emphysema. Pulmonary capillaries may play an important role in the development of emphysema.