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目的:探讨视黄酸(RA)对放射性肺损伤模型大鼠支气管肺泡灌洗液(BALF)细胞数和EGFR及肺泡表面活性蛋白A(SP-A)表达的影响。方法:80只Wister大鼠随机分为正常对照组(A组)、单纯给药组(B组)、单纯照射组(C组)和照射加给药组(D组),C、D组大鼠行6MVX射线15Gy全胸野照射,B、D组给予20mg/(kg·d)RA制剂灌服,于照射后第1、2、4和8周行支气管肺泡灌洗及留取肺组织行HE、Masson染色及免疫组化法检测EGFR表达,蛋白质印迹法检测肺组织中SP-A蛋白表达。结果:放射组大鼠全胸单次15Gy照射后可以建立急性放射性肺损伤动物模型。与D组相比,C组BALF总数升高,肺内炎性渗出增多,胶原纤维增加,EGFR表达增强,以第4、8周最显著(P<0.01),C组各时间段SP-A蛋白表达均明显下降(P<0.001),以第1、8周最明显,第2、4周出现回升。B与C组各时间段相比SP-A蛋白表达差异无统计学意义。D组SP-A蛋白表达与C组比第1、8周差异无统计学意义,第2、4周均高于照射组(P<0.05),但仍低于正常组。结论:RA通过降低炎性细胞渗出,削弱EGFR和促进SP-A表达,预防放射性肺损伤的发生、发展。
Objective: To investigate the effect of retinoic acid (RA) on the number of cells and the expression of EGFR and alveolar surfactant protein A (SP-A) in bronchoalveolar lavage fluid (BALF) in radiation-induced lung injury in rats. Methods: Eighty Wistar rats were randomly divided into normal control group (group A), simple administration group (group B), simple irradiation group (group C) and irradiation plus medication group (group D) Rats were irradiated with 6MV X-rays at 15Gy full chest field. Groups B and D were given 20 mg / (kg · d) RA, and bronchoalveolar lavage and lung tissue were taken at 1, 2, 4 and 8 weeks after irradiation The expression of EGFR was detected by HE, Masson staining and immunohistochemistry. The expression of SP-A in lung tissue was detected by Western blotting. Results: The rat model of acute radiation-induced lung injury can be established after a single irradiation of 15Gy in the whole chest. Compared with group D, the total number of BALF in group C increased, inflammatory exudation increased, collagen fibers increased and EGFR expression increased in group C (P <0.01) A protein expression were significantly decreased (P <0.001), the first 1,8 weeks of the most obvious, the first 2,4 weeks recovery. There was no significant difference in SP-A protein expression between B and C groups at different time points. The protein expression of SP-A in group D was not significantly different from that in group C at week 1 and week 8, and was significantly higher at week 2 and 4 than that of group C (P <0.05). Conclusion: RA can prevent the occurrence and development of radiation-induced lung injury by decreasing inflammatory cell exudation, weakening EGFR and promoting SP-A expression.