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目的探讨抗血管内皮生长因子抗体(anti-VEGF antibody)对转化生长因子β(TGF-β)或多西环素(doxycyc line,Doxy)所诱导的胸腔积液增多和胸膜粘连作用的影响。方法28只新西兰大白兔随机分4组:TGF-β对照组、TGF-β抗体组、Doxy对照组和Doxy抗体组,每组7只。在放置胸导管后,TGF-β对照组经胸腔内注入TGF-β5.0μg;TGF-β抗体组在胸腔内注入TGF-β前24 h先予以静脉注射抗血管内皮生长因子抗体10 mg/kg。Doxy对照组胸腔内注射Doxy 10 mg/kg;Doxy抗体组在胸腔内注入Doxy前24 h先予以静脉注射抗血管内皮生长因子抗体10 mg/kg。在TGF-β或Doxy注射后的24、48、72 h分别收集胸腔积液并计量,测定胸腔积液中白细胞数、蛋白及乳酸脱氢酶(LDH)含量。2周后杀死实验兔并作胸膜粘连评分,通过免疫组化染色对胸膜组织中血管新生程度做定量分析。结果4组实验兔所产生的胸腔积液量,胸腔积液中白细胞数、蛋白量及LDH水平差异无统计学意义(P>0.05)。胸膜粘连评分TGF-β对照组为(7.7±0.8)分,TGF-β抗体组为(4.4±2.4)分;Doxy对照组为(6.0±1.7)分,Doxy抗体组为(2.0±0.9)分。胸膜组织中新生血管密度TGF-β对照组为(4.9±0.4)%,TGF-β抗体组为(2.9±0.7)%;Doxy对照组为(6.9±2.2)%,Doxy抗体组为(2.2±0.9)%。两抗体干预组的胸膜粘连评分和血管新生程度均显著低于对照组(P<0.05)。结论抗血管内皮生长因子抗体显著抑制了TGF-β或Doxy所诱导的胸膜粘连,提示VEGF和血管新生可能在胸膜固定术中起重要作用。
Objective To investigate the effect of anti-VEGF antibody on pleural effusion and pleural adhesion induced by transforming growth factor β (TGF-β) or doxycycline (Doxy). Methods Twenty-eight New Zealand white rabbits were randomly divided into 4 groups: TGF-β control group, TGF-β antibody group, Doxy control group and Doxy antibody group. After the thoracic duct was placed, the TGF-β control group was injected with TGF-β5.0 μg intrathoracically. The TGF-β antibody group was injected intravenously with anti-VEGF antibody 10 mg / kg . The Doxy control group was injected intrathoracially with Doxy 10 mg / kg. The Doxy antibody group was intravenously injected with anti-VEGF antibody 10 mg / kg 24 hours before Doxy injection into the thorax. Pleural effusion was collected 24 hours, 48 hours and 72 hours after injection of TGF-β or Doxy, respectively. The number of white blood cells, protein and lactate dehydrogenase (LDH) in pleural effusion were measured. After 2 weeks, the experimental rabbits were sacrificed and the pleural adhesion score was scored. The degree of angiogenesis in the pleural tissue was quantitatively analyzed by immunohistochemistry. Results There was no significant difference in pleural effusion volume, leukocyte count, protein level and LDH level in pleural effusion between experimental rabbits in 4 groups (P> 0.05). The pleural adhesion score was (7.7 ± 0.8) in the TGF-β control group and (4.4 ± 2.4) in the TGF-β antibody group, (6.0 ± 1.7) in the Doxy control group and (2.0 ± 0.9) in the Doxy antibody group . The neovascular density in pleural tissue was (4.9 ± 0.4)% in TGF-β control group and (2.9 ± 0.7)% in TGF-β antibody group and (6.9 ± 2.2)% in Doxy control group and 0.9)%. The pleural adhesion score and angiogenesis were significantly lower in the two antibody intervention groups than in the control group (P <0.05). Conclusion Anti-VEGF antibody significantly inhibits pleural adhesion induced by TGF-β or Doxy, suggesting that VEGF and angiogenesis may play an important role in pleurodesis.