粉防己碱对缺氧／复氧乳鼠心肌细胞前炎症因子的影响

目的：研究粉防己碱对离体培养的大鼠心肌细胞在缺氧／复氧条件下对前炎症因子：肿瘤坏死因子（TNF—α）、自细胞介素-1（IL-1G）、白细胞介素-6（IL-6）的影响。方法：乳鼠心肌细胞体外培养心肌细胞成功后，随机分为三组：对照组、缺氧／复氧（A／R）组、粉防己碱（Tet）组。对照组：不进行A／R处理，正常情况下持续培养26h；A／R组：在高纯度氩气，无糖无血清培养基条件下培养2h，复氧开始时加入0．9％盐水，再复氧培养24h；Tet组：预先给予终浓度为30μmol／L的Tet孵育60min，再在无血清低糖DMEM培养基缺氧孵育2h，然后继续复氧培养24h；检测各组在复氧24h后的TNF-α、IL-1β、IL－6的水平。结果：试验24h后A／R组、Tet组前炎症因子TNF－α（682．65±32．59）、（388．94±17．22）]，IL～1β189．11±8．29），（109．46±7．62）]，IL－6（78．45±2，74）、（40．91±1．53）]水平（pg／ml）均较对照组的（211．44±14．20），（59．64±2．43），（23．99±3.24）]显著升高（P〈0．01），Tet组前炎症因子TNF—α、IL-1β、IL-6水平均分别显著低于A／R组的（P〈0．01）。结论：Tet可以抑制IKB—α磷酸化，显著减少前炎症因子TNF—α、IL-6的产生，减轻心肌缺血／再灌注损伤。

Effect of tetrandrine on anoxiareoxygenation-induced release of proinflammatory factors in cultured cardiocyte of neonate rats

Objective： To investigate the effect of tetrandrine on anoxia/reoxygenation （A/R） induced proinflammatory factors： TNF-α, IL--1β, IL-6 in cultured cardiocytes of neonate rates. Methods： After cardiocytes were success- fully cultured in vitro, it were randomly divided into three groups： control group, A/R group, tetrandrine （Tet） group. Control group not treated with A/R, continuous incubated 26h under normal circumstance. In A/R group, cells were incubated in non-saccharide, non-serum culture medium 2h, which saturate by 95% argon gases; then reoxygenation incubate followed, cells were incubated in normal circumstance 24h. In Tet group the procedure of anoxia/reoxygenation was same to A/R group, but added Tet （30μmol/L） into culture fluid and incubated 60 min before anoxia beginning. TNF-α, IL-1β, IL-6 were detected after reoxygenation 24h. Results： After test 24h the proin- flammatoryfactors TNF-α （682.65±32.59）, （388.94±17.22）], IL-1β 189.11±8. 29）, （109.46±7.62）], and IL-6 （78.45±2, 74）, （40. 91±1.53）] levels （pg/ml） increased significantly in A/R group, Tet group, respectively compared with those of control group （211.44±14.20）, （59. 64±2.43）, （23. 99±3.24） pg/ml], P〈0.01 all. The TNF-α, IL-1β, and IL-6 levels of Tet group were significant lower than those of A/R group （P〈 0.01 all）. Conclusion： Tet can attenuate myocardial ischemia/reperfusion injury. Its machanism may be through inhibition the IκB-α phosphorylation and reduce the harmful cytokine TNF-α and IL-6.