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. 2021 Jan 1;11(5):2247–2262. doi: 10.7150/thno.51666

Figure 7.

Figure 7

Activation of NMDAR leads to lipid accumulation through impairing FAO. (A) Representative images of Oil Red O staining in AML-12 hepatocytes treated with PA or/with MK-801 for 24 h (Scale bars = 50 μm). (B) TG content in AML-12 hepatocytes treated with PA or/with MK-801 for 24 h (n = 5). (C) Representative images of Oil Red O staining in AML-12 hepatocytes treated with NMDA for 24 h (Scale bars = 50 μm). (D) TG content in AML-12 hepatocytes treated with NMDA for 24 h was examined (n = 5). (E) RT-PCR analysis of genes involved in fatty acid oxidation in AML-12 hepatocytes treated with NMDA (n = 6). (F) RT-PCR analysis of genes involved in fatty acid synthesis in AML-12 hepatocytes treated with NMDA (n = 6). (G) RT-PCR analysis of genes involved in fatty acid oxidation in livers from mice treated with NMDA for 6 months (n = 5). (H) RT-PCR analysis of genes involved in fatty acid synthesis in livers from mice treated with NMDA for 6 months (n = 5). (I) TG content in HepG2 hepatocytes treated with NMDA for 24 h (n = 5). (J) RT-PCR analysis of genes involved in fatty acid oxidation in HepG2 hepatocytes treated with NMDA (n = 6). *P < 0.05, **P < 0.01, ***P < 0.001. All data are presented as the mean ± SEM.