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.

Nesfatin-1在调节心脏功能中起重要作用。但是，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分钟建立MI的大鼠模型，再灌注前腹腔内注入20 µg / kg浓度的nesfatin-1。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。结果显示，与仅MI组相比，nesfatin-1可以显着恢复GSH含量和SOD活性，并降低MDA水平（p <.05）。同样，nesfatin-1通过抑制自噬和凋亡标记（例如caspase3和Bax  ）来促进细胞存活（p <.05）。总而言之，这些发现支持了nasfatin-1可以通过靶向氧化应激，细胞凋亡和自噬来作为治疗MI的良好候选者的想法。