山莨菪碱和己酮可可碱对内毒素诱导大鼠心肌组织细胞间黏附分子-1的抑制作用

目的研究山莨菪碱（654—2）和己酮可可碱（PTX）对内毒素诱导大鼠心肌组织细胞间黏附分子-1（ICAM-1）的抑制作用。方法将健康Wistar大鼠按随机数字表法分为对照组、模型组、654—2组、PTX组和654—2＋PTX组，每组各时间点6只。经尾静脉注射脂多糖（LPS）5mg／kg制备动物模型。于术后0、2、4、6、8和10h不同时间点分别处死大鼠取心肌组织，采用蛋白质免疫印迹法（Western blotting）检测心肌组织ICAM-1蛋白的表达。结果注射LPS6h时大鼠心肌组织ICAM-1蛋白的表达明显升高（P〈0．01），随后ICAM-1蛋白的表达逐渐下降，至10h时仍有表达（P〈0．05）。654—2及PTX干预后均可减少心肌组织ICAM-1蛋白的表达（P均〈O．01），且654—2与PTX联合使用可使心肌组织ICAM-1蛋白的表达减少更显著，与单用654—2和PTX比较差异均有统计学意义（P均〈0．05）。结论654—2和PTX联合使用可明显抑制内毒素诱导的大鼠心肌组织ICAM-1蛋白的表达，从而起到对心肌组织的保护作用。

Inhibitory effects of anisodamine and pentoxifylline on the expression of lipopolysaccharide -induced intercellular adhesion molecule - 1 in rat cardiac muscle

OBJECTIVE: To investigate the inhibitory effects of anisodamine (654-2) and pentoxifylline (PTX) on the expression of lipopolysaccharide (LPS)-induced intercellular adhesion molecule-1 (ICAM-1) in rat cardiac muscle in vivo. METHODS: The animals were randomly divided into five groups (each n=6): (1) normal control group, (2) model group, (3) 654-2 treated group, (4) PTX treated group and (5) 654-2+PTX treated group. The errdotoxemia model was reproduced by intravenous injection LPS 5 mg/kg. The expression of ICAM-1 protein in rat cardiac muscle was assayed by Western blotting at 0, 2, 4, 6, 8, 10 hours after intravenous LPS injection. Then the expression of ICAM-1 protein in different groups was assayed at different time points. RESULTS: The changes in expression of ICAM-1 in rat cardiac muscle after LPS injection were in a time-dependent pattern, gradually elevating to approach the peak at 6 th, then it lowered, but it still appeared at 10 hours (P<0.05). Western blotting also showed that ICAM-1 protein with decreased with pre-treatment of 654-2 or PTX respectively (both P<0.01). It was reduced to a much lower level when the animals were pretreated with a combination of 654-2 and PTX, compared with the group of 654-2 alone or PTX alone (both P<0.05). CONCLUSION: The combination of 654-2 and PTX may play a protective role in rat against injury to cardiac muscle induced by LPS in vivo via inhibiting the production of ICAM-1 protein.