胸腔镜辅助下肺癌根治术对机体氧化应激损伤的分子机制研究

Research on the molecular mechanism of oxidative stress injury induced by thoracoscopic assisted radical resection of lung cancer

目的探讨胸腔镜辅助下肺癌根治术对机体氧化应激损伤的分子机制。方法选择2019年9月至2020年9月于首都医科大学附属北京天坛医院行胸腔镜下肺癌根治术患者30例为观察组,并匹配选取30例常规开放手术肺癌患者为对照组。比较2组术前(T1)、术后即刻(T2)和术后6 h(T3)丙二醛水平,自噬标志物肌球蛋白样BCL2结合蛋白1(Beclin-1)、自噬相关基因5(ATG5)、ATG7、ATG16L,典型性自噬(CA)标志物ULK1和微管相关蛋白1轻链3相关性吞噬(LAP)标志物Rubicon水平。结果T3时点,观察组丙二醛水平低于对照组[(2.7±0.8)μmol/L比(3.9±1.1)μmol/L](P<0.001)。T3时点,观察组Beclin-1、ATG5、ATG7和ATG16L水平均低于对照组(均P<0.05)。T1、T2、T3时点,2组CA标志物ULK1表达水平比较差异均无统计学意义(均P>0.05)。T2、T3时点观察组LAP标志物Rubicon表达水平均低于对照组(均P<0.001)。结论胸腔镜辅助下肺癌根治术较常规开放手术对机体造成的氧化应激损伤更弱,LAP标志物水平较低可能是氧化应激损伤水平较低的原因之一。

Objective To explore the molecular mechanism of oxidative stress injury induced by thoracoscopic assisted radical resection of lung cancer.Methods From September 2019 to September 2020,30 patients who underwent thoracoscopic radical resection of lung cancer in Beijing Tiantan Hospital,Capital Medical University were selected as the observation group,and 30 patients with lung cancer who underwent conventional open surgery were selected as the control group.The levels of malondialdehyde,autophagy marker myosin-like BCL2 binding protein 1(Beclin-1),autophagy-related gene 5(ATG5),ATG7,ATG16L,classic autophagy(CA)marker ULK1 and Rubicon,a marker of microtubule-associated protein 1 light chain 3-associated phagocytosis(LAP),were compared between the two groups before surgery(T1),immediately after surgery(T2)and 6 h after surgery(T3).Results At T3,the level of malondialdehyde in the observation group was lower than that in the control group[(2.7±0.8)μmol/L vs(3.9±1.1)μmol/L](P<0.001).At T3,the levels of Beclin-1,ATG5,ATG7 and ATG16L in the observation group were lower than those in the control group(all P<0.05).There were no significant differences in expression levels of CA marker ULK1 between the two groups at T1,T2 and T3(all P>0.05).The expression levels of LAP marker Rubicon in the observation group were higher than those in the control group at T2 and T3(both P<0.001).Conclusion Thoracoscopic assisted radical resection of lung cancer causes less oxidative stress injury than conventional open surgery,and the lower level of LAP marker may be one of the reasons for the lower level of oxidative stress injury.