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Lipid storage droplet protein 5 (LSDP5) is specifically expressed in tissues with high oxidative metabolism such as liver and heart. The present study aimed to explored the role of LSDP5 in sodium palmitate‑induced lipotoxicity in LO2 normal human liver cells. LO2 cells were treated with various concentrations of sodium palmitate (25, 50, 75, 100, 125 and 150 µmol/l) for 12, 24 and 48 h, and cell viability was determined by Cell Counting Kit‑8. Subsequently, LO2 cells were exposed to 100 µmol/l sodium palmitate for 48 h to induce lipotoxicity (Model). Lipotoxicity Model LO2 cells were also transfected with pCMV5‑LSDP5 overexpression vector, and reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP) and apoptotic rates were measured. The contents of non‑esterified fatty acid (NEFA), malondialdehyde (MDA) and superoxide dismutase (SOD) were also measured. The expression levels of LSDP5, and apoptosis‑, mitochondrial‑, lipid metabolism‑related factors were detected using reverse transcription‑quantitative polymerase chain reaction and western blot assays. The results indicated that sodium palmitate exposure inhibited cell viability and induced lipotoxicity in LO2 cells. LSDP5 overexpression decreased ROS and apoptotic rates, and reduced NEFA and MDA content. LSDP5 transfection rescued the loss of MMP and elevated SOD content in lipotoxicity Model LO2 cells. In addition, LSDP5 upregulated the expression levels of B‑cell lymphoma‑2, acetyl‑CoA carboxylase1/2 and fatty acid synthase (Fas), whereas the expression levels of activated‑caspase‑3, Bcl‑2‑associated X protein, cytochrome c, cytochrome c oxidase subunits IV, carnitine palmitoyltransferase 1a and peroxisome proliferator‑activated receptors α levels were downregulated. LSDP5 may produce a protective effect on sodium palmitate‑induced lipotoxicity in LO2 cells by regulating lipid metabolism‑related factors.

molecular medicine reports

Lipid storage droplet protein 5 reduces sodium palmitate‑induced lipotoxicity in human normal liver cells by regulating lipid metabolism‑related factors