氯离子通道阻断剂对肺血管内皮细胞氧化损伤的保护作用

The protective effects of chloride channel blockers on pulmonary artery endothelial cell injury induced by oxidant

目的:研究氯离子通道阻断剂在肺血管内皮细胞氧化损伤中的作用。方法:以肉联厂检疫合格的健康小牛为研究对象,过氧化氢(H2O2)诱导体外培养的牛肺动脉内皮细胞损伤,观察Cl-通道阻断剂对受损细胞细胞活力、乳酸脱氢酶(LDH)释放量、三磷酸腺苷(ATP)含量、细胞内钙离子浓度犤Ca2+犦i和DNA降解程度的影响。结果:Cl-通道阻断剂可使受损细胞的细胞活力得到提高,NPPB组和NFA组分别恢复到0.449±0.015和0.535±0.023;LDH释放量下降,分别为(12.4±0.4)%,(6.4±0.6)%。ATP含量分别回升为18.22nmol/mg蛋白质和21.96nmol/mg蛋白质,犤Ca2+犦i下降和DNA降解程度减轻。结论:Cl-通道参与了氧化剂对肺血管内皮细胞损伤的病理过程,Cl-通道阻断剂对肺血管内皮细胞的损伤具有保护作用。

AIM:To study the effect of chloride (Cl- ) channel blockers on pulmonary artery endothelial cell injury induced by oxidant H2O2. METHODS:Cultured pulmonary artery endothelial cells obtained from health calf (CAPE cells) exposed to H2O2 were used to observe the effect of Cl- channel blocker stress on cell vitality, lactate dehydrogenase (LDH) release, adenosine triphosphate (ATP) contents,i and DNA damage.RESULTS:The Cl- channel blockers (NPPB and NFA) markedly promoted cell vitality, which in NPPB group was promoted to 0.449± 0.015, and in NFA group was 0.535± 0.023. The release of LDH of part NPPB was reduced to (12.4± 0.4)% ,and that of part NFA was (6.4± 0.6)% . The ATP content was increased to 18.22 and 21.96 nmol/mg respectively, with the content of i and the DNA fragmentation of damaged cells decreased.