1. Academic Validation
  2. IGF‑1 inhibits palmitic acid‑induced mitochondrial apoptosis in macrophages

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

  • Mol Med Rep. 2023 Dec;28(6):234. doi: 10.3892/mmr.2023.13121.
Wanying Tang 1 Ming Zhang 2 Yu Wang 2 Dan Ma 3 Mi Hu 1 Yangkai Zhang 1 Huiling Lin 1 Weiwei Jiang 4 Yuxin Ouyang 1 Liping Jiang 5 Pingping He 6 Guojun Zhao 2 Xinping Ouyang 1
Affiliations

Affiliations

  • 1 Department of Physiology, Institute of Neuroscience Research, Hengyang Key Laboratory of Neurodegeneration and Cognitive Impairment, University of South China, Hengyang, Hunan 421001, P.R. China.
  • 2 Institute of Cardiovascular Disease, The Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan, Guangdong 511500, P.R. China.
  • 3 School of Pharmacy Zunyi Medical University, Zunyi, Guizhou 563000, P.R. China.
  • 4 Department of Organ Transplantation, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
  • 5 Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.
  • 6 The Research Center of Reproduction and Translational Medicine of Hunan Province, Department of Physiology, Medical College, Hunan Normal University, Changsha, Hunan 410081, P.R. China.
Abstract

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.

Keywords

apoptosis; insulin growth factor; macrophages; mitochondria; palmitic acid.

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