Abstract

Nesfatin-1 plays an important role in the modulation of heart performance. However, it remains unclear how nesfatin-1 contributes to cell survival in acute myocardial infarction (MI). A rat model of MI was established via ligation of left anterior descending coronary artery (LAD) for 30 min and 20 µg/kg concentration of nesfatin-1 was intraperitoneally infused prior to reperfusion. At 24 h after reperfusion, oxidative stress markers, the expression of caspase3, beclin-1, pro-inflammatory cytokines, and the mRNA levels of Bax and Bcl-2 were evaluated. Results showed that nesfatin-1 markedly restored GSH content and SOD activity as well as reduced MDA levels compared to only the MI group (p < .05). Likewise, nesfatin-1 contributed to cell survival by inhibiting autophagy and apoptosis markers such as caspase3 and Bax (p < .05). Collectively, these findings support the idea that nasfatin-1 can be used as a good candidate to treat MI by targeting oxidative stress, apoptosis, and autophagy.

摘要

Nesfatin-1 在调节心脏性能方面起着重要作用。然而，尚不清楚 nesfatin-1 如何促进急性心肌梗死 (MI) 中的细胞存活。通过结扎左冠状动脉前降支 (LAD) 30 分钟和 20 µg/kg 浓度的 nesfatin-1 在再灌注前腹膜内输注 MI 大鼠模型。再灌注后 24 小时，评估氧化应激标志物、caspase3、beclin-1、促炎细胞因子的表达以及 Bax 和 Bcl-2 的 mRNA 水平。结果表明，与仅 MI 组相比，nesfatin-1 显着恢复了 GSH 含量和 SOD 活性，并降低了 MDA 水平（p < .05)。同样，nesfatin-1 通过抑制自噬和细胞凋亡标志物如 caspase3 和 Bax 促进细胞存活 ( p  < .05)。总的来说，这些发现支持了 nasfatin-1 可以作为通过靶向氧化应激、细胞凋亡和自噬来治疗 MI 的良好候选者的观点。