关键词: 肌细胞, 心脏, 心肺复苏, 坏死性凋亡

Abstract: Objective To explore the effect of cardiopulmonary resuscitation (CPR) on the expression of insulin-like growth factor-1 (IGF-1) and its regulatory mechanism on myocardial injury in rats. 
Methods Thirty Sprague-Dawley rats were selected and randomly divided into five groups, with 6 rats in each group. One group was randomly selected as sham operation group, and in the other four groups, cardiac arrest due to ventricular fibrillation/CPR models were established. After the successful modeling, one group was randomly selected as I/R, and the other three groups were divided into IGF-1 supplementation group, TAK-242 ［Toll-like receptor 4 (TLR4)/nuclear factor κB (NF-κB) supplementation］ inhibitor supplementation group and IGF-1 and TAK-242 supplementation group. The myocardial injury of rats in different treatment groups was detected by Evans blue staining. The expression level of IGF-1 was detected by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-qPCR). The expression levels of TLR4, NF-κB, myeloid differentiation primary response protein 88 (MyD88), receptor-interacting protein kinase 3 (RIPK3) and mixed-lineage kinase domain-like (MLKL) were detected by Western blot. The expression levels of interleukin-1β (IL-1β) and interleukin-18 (IL-18) were detected by enzyme-linked immunosorbent assay (ELISA). 
Results Compared with the sham operation group, the myocardial tissue of rats was seriously damaged after cardiac arrest and CPR, among which the model group had the most severe damage, and the IGF-1 and TAK-242 supplementation group had the least severe damage. Compared with sham operation group, the expression of IGF-1 in myocardial tissue of rats in model group was decreased significantly (P＜0.05). Compared with sham operation group, the expression levels of IL-1β and IL-18 in myocardial tissue of model rats were significantly increased, among which the expression levels of IL-1β and IL-18 were the highest in the model group and the lowest in IGF-1 and TAK-242 supplementation group (P＜0.05). Compared with sham operation group, the expression levels of TLR4, MyD88 and NF-κB p65 in model rats were significantly increased, among which the expression levels were the highest in the model group, and the lowest in IGF-1 and TAK-242 supplementation group (P＜0.05). Compared with the sham operation group, the expression levels of RIPK3 and MLKL in model rats were significantly increased, among which the expression levels of model rats were the highest in the model group and the lowest in IGF-1 and TAK-242 supplementation group (P＜0.05). Conclusion After cardiac arrest and restoration of autonomous circulation, the expression level of IGF-1 will decrease, and IGF-1 can inhibit necroptosis of myocardial cells by inhibiting TLR4/NF-κB signaling pathway, thereby reducing myocardial injury in rats.

Key words: myocytes, cardiac, cardiopulmonary resuscitation, necroptosis