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目的:观察川芎嗪对新生大鼠支气管肺发育不良的防治作用并探讨其可能的作用机制。方法:选取80只足月新生12 h内的SD大鼠,随机分成4组,每组20只。A组:空气对照组;B组:空气+川芎嗪组;C组:高氧对照组(FiO2=60%);D组:高氧+川芎嗪组。B、D组予以川芎嗪30 mg/kg连续给药14 d。每组选取8只,计算肺湿重/干重(W/D)、肺放射状肺泡计数(RAC);免疫组织化学方法检测PECAM-1的表达水平并计算肺微血管密度(MVC);RT-PCR方法检测HIF-1α及VEGF mRNA水平;免疫组织化学染色法检测HIF-1α及VEGF蛋白水平。结果:C组肺泡及肺血管发育明显受到抑制,肺W/D值升高,RAC、MVC值较A组和B组均明显减少[W/D:(5.64±0.31)vs(4.92±0.19)、(4.91±0.06);RAC值:(4.75±0.71)vs(9.00±0.76)、(9.03±0.76);MVC:(45.30±2.05)vs(48.70±0.83)、(48.60±1.49),P<0.05];C组肺组织HIF-1α、VEGF表达较A组明显减少,D组肺组织HIF-1α、VEGF表达较C组有所增加,差异均有统计学意义(P<0.05)。结论:川芎嗪对新生鼠支气管肺发育不良有一定的防治作用,其机制可能与川芎嗪激活HIF-1α-VEGF通路,从而改善肺泡和肺微血管发育有关。
Objective: To observe the preventive and therapeutic effects of ligustrazine on bronchopulmonary dysplasia in neonatal rats and to explore its possible mechanism. Methods: Eighty SD neonatal rats were randomly divided into 4 groups (20 rats in each group). Group A: air control group; Group B: air + ligustrazine group; Group C: high oxygen control group (FiO2 = 60%); Group D: hyperoxia + ligustrazine group. B, D group were given ligustrazine 30 mg / kg for 14 days. Eight rats in each group were selected and the lung wet weight / dry weight (W / D) and pulmonary alveolar count (RAC) were calculated. The expression of PECAM-1 was detected by immunohistochemistry and the pulmonary microvessel density (MVC) Methods The levels of HIF-1α and VEGF mRNA were detected by immunohistochemistry. The protein levels of HIF-1α and VEGF were detected by immunohistochemical staining. Results: Alveolar and pulmonary vascular development were significantly inhibited in group C and the W / D of lung was increased. The values of RAC and MVC were significantly lower than those in group A and group B [W / D: (5.64 ± 0.31) vs (4.92 ± 0.19) , (4.91 ± 0.06), (4.75 ± 0.71) vs (9.00 ± 0.76), (9.03 ± 0.76), MVC: (45.30 ± 2.05) vs (48.70 ± 0.83), (48.60 ± 1.49), P < 0.05]. The expression of HIF-1α and VEGF in group C was significantly lower than that in group A, while the expression of HIF-1α and VEGF in group D was higher than that in group C (P <0.05). CONCLUSION: Tetramethylpyrazine may play a preventive and therapeutic role in bronchopulmonary dysplasia in neonatal rats. The mechanism may be related to the activation of HIF-1α-VEGF pathway by ligustrazine and the improvement of alveolar and pulmonary microvascular development.