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目的:研究表皮细胞生长因子(epidermal growth factor,EGF)对吸入性损伤大鼠的肺泡Ⅱ型细胞(alveolar typeⅡcell,ATⅡ)增殖和肺水转运功能的影响。方法:清洁级雄性 SD 大鼠160只,160～180g。随机分为四组:Ⅰ组:正常对照(n=10);Ⅱ组:单纯 EGF 给药;Ⅲ组:单纯吸入性损伤;Ⅳ组:吸入性损伤+EGF 治疗。Ⅱ、Ⅲ、Ⅳ组各分为24、48、72、120、168h 五个亚组(n=10)。Ⅲ组和Ⅳ组的大鼠先造成烟雾吸入性损伤。Ⅱ组和Ⅳ组(伤后立即)用特殊针头经气管喷入 EGF(100μg/kg)。每组中6只大鼠用于检测肺泡液体清除率(alveolarliquid clearance,ALC),4只用于病理形态学观察和尿嘧啶脱氧核苷(bromodeoxyuridine,BrdU)免疫组化检查。结果:烟雾吸入性损伤可以导致各级支气管管壁水肿,肺泡壁破坏,肺泡腔内液体聚积,肺泡隔水肿。外源性EGF 显著增加新增殖 ATⅡ数量。正常大鼠 ALC 为(22.07±3.67)%。气管滴入 EGF 后48、72和120h 的 ALC显著升高,分别为[(43.37±11.04)%,(P<0.01);(41.75±7.02)%,(P<0.01);(35.86±4.09)%,(P<0.05)],168h 后恢复正常水平。吸入性损伤后 ALC 在第24h 下降36.7%,其他时间点 ALC 也有不同程度减少。EGF 治疗可以使吸入性损伤大鼠的 ALC 在48h 后即可恢复到正常水平[(25.25±3.66)%]。结论:外源性 EGF经气管喷入,能有效刺激 ATⅡ的增殖,提高肺泡液体转运能力,有助于修复吸入性损伤大鼠的肺泡组织,减轻或消除肺水肿。
Objective: To investigate the effects of epidermal growth factor (EGF) on the proliferation and pulmonary function of alveolar type Ⅱ cell (AT Ⅱ) in rats with inhalation injury. Methods: 160 male SD rats of clean grade, 160 ~ 180g. Group Ⅰ: normal control (n = 10); group Ⅱ: simple EGF administration; group Ⅲ: simple inhalation injury; group Ⅳ: inhalation injury + EGF treatment. Groups Ⅱ, Ⅲ and Ⅳ were divided into five subgroups: 24, 48, 72, 120 and 168h (n = 10). Rats in group III and group IV first caused smoke inhalation injury. Group Ⅱ and group Ⅳ (immediately after injury) were injected intratracheally with EGF (100μg / kg) by special needle. Six rats in each group were used to detect alveolar fluid clearance (ALC), four were used for histopathological observation and bromodeoxyuridine (BrdU) immunohistochemistry. Results: Inhalation of smoke could lead to bronchial wall edema, destruction of alveolar wall, accumulation of alveolar fluid and alveolar septa. Exogenous EGF significantly increased the number of newly proliferating ATⅡ. Normal rat ALC was (22.07 ± 3.67)%. The ALC at 48, 72 and 120 h after intratracheal instillation were significantly higher than those in the control group (43.37 ± 11.04%, P <0.01, 41.75 ± 7.02, P <0.01, 35.86 ± 4.09, %, (P <0.05)], returned to normal after 168h. ALC decreased 36.7% at 24 hours after inhalation injury, and ALC decreased at different time points. EGF treatment can restore the normal level of ALC in rats with inhalation injury after 48h [(25.25 ± 3.66)%]. Conclusion: Exogenous EGF transmucosal injection can effectively stimulate the proliferation of AT Ⅱ, improve the ability of alveolar fluid transport, repair alveolar tissue in rats with inhalation injury and reduce or eliminate pulmonary edema.