IGF‑1 inhibits palmitic acid‑induced mitochondrial apoptosis in macrophages

Insulin growth factor-1 (IGF-1) is an endocrine regulator that plays an important role in normal growth and development. IGF-1 mediated effects may result in protecting macrophages from immunometabolic response. However, it is unclear whether IGF-1 has a protective effect on fatty acid-induced macrophages damage. In the present study, THP-1 cells were differentiated into macrophages and stimulated with palmitic acid (PA) in the absence or presence of IGF-1. Macrophages apoptosis was measured by Cell Counting Kit-8 assay, flow cytometry, Hoechst 33342 staining and western blotting. The mitochondrial damage was evaluated using JC-1 staining and mitochondrial reactive oxygen species detection. The activation of mitophagy was assessed using immunofluorescence and western blotting. As a result, IGF-1 significantly restored the survival rate in macrophages, while the apoptosis was inhibited through mitochondrial pathway. In addition, IGF-1 protected the mitochondrial damage induced by PA. Furthermore, PA induced mitophagy via phosphatase and tensin homolog-induced putative kinase protein 1/Parkin, which was reversed by IGF-1. Taken together, the present study demonstrated the protective effect of IGF-1 on PA-induced mitochondrial apoptosis in macrophages, which might provide a potential therapeutic strategy for treatment of lipotoxicity.