中文摘要：

Proteasome 禁止者涉及细胞周期控制，生长并且煽动性的发信号，和有丝分裂的细胞的 transcriptional 规定。最近的研究建议了特定的 proteasome 禁止者 MG132 可以在 vitro 压制 cardiomyocyte 肥大。然而，内在的分子的机制不是清楚的。在这研究，我们在 vivo 在心脏的肥大和相关分子的机制上调查了长期的 MG132 处理的效果。MG132 (0.1 mg/kg/day ) intraperitoneally 与腹的大动脉的 banding (AAB ) 被注射到老鼠 8 个星期。结果证明有显著地稀释的 MG132 的处理留给室(LV ) myocyte 区域， LV 重量 / 身体重量，和肺重量 / 身体重量比率，减少的 LV 心脏舒张的直径和墙厚度，并且在 AAB 老鼠的增加的部分弄短。AAB 在心脏的 myocytes 导致了 ERK1/2， JNK1，和 p38 的 phosphorylation。在 AAB 老鼠的 ERK1/2 和 JNK1 的提高的 phosphorylation 层次被 MG132 处理显著地颠倒。在结论，我们的结果建议有 MG132 的长期的处理稀释 pressure-overload-induced 心脏的肥大并且通过表明小径的 ERK1/2 和 JNK1 的规定在 AAB 老鼠改进心脏的功能。

英文摘要：

Proteasome inhibitors are involved in cell cycle control, growth and inflammatory signaling, and transcriptional regulation of mitotic cells. A recent study has suggested that specific proteasome inhibitor MG132 may suppress cardiomyocyte hypertrophy in vitro. However, the under- lying molecular mechanisms are not clear. In this study, we investigated the effects of long-term MG132 treatment on cardiac hypertrophy and the related molecular mechanisms in vivo. MG132 （0.1mg/kg/day） was intraperitoneaHy injected to rats with abdominal aortic banding （AAB） for 8 weeks. Results showed that treatment with MG132 signifi- cantly attenuated left ventricular （LV） myocyte area, LV weight/body weight, and lung weight/body weight ratios, decreased LV diastolic diameter and wall thickness, and increased fractional shortening in AAB rats. AAB induced the phosphorylation of ERK1/2, JNK1, and p38 in cardiac myocytes. The elevated phosphorylation levels of ERK1/2 and JNKI in AAB rats were significantly reversed by MG132 treatment. In conclusion, our results suggested that long-term treatment with MG132 attenuates pressure- overload-induced cardiac hypertrophy and improves cardiac function in AAB rats through regulation of ERK1/2 and JNK1 signaling pathways.