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. 2016 Jan 20;17(1):134. doi: 10.3390/ijms17010134

Figure 1.

Figure 1

Metabolic syndrome-very low density lipoproteins (MetS-VLDL) is cytotoxic and provokes oxidative stress, with greater internalization in HL-1 atrial myocytes. (A) HL-1 cells were treated with normal-VLDL or MetS-VLDL at different test concentrations (3.125, 6.25, 12.5 and 25 mg/dL) for 24 h. OD values at 450 nm indicating viability were significantly lower in the msVLDL group (* p < 0.05; n = 4 for each group); (B) HL-1 cells treated with MetS-VLDL showed significantly reduced cell viability (% of control) with a concentration of 25 mg/mL (** p < 0.01; n = 4); (C) DCF fluorescence (excitation at 480 nm and emission at 520 nm) indicated total cytosolic oxidant activity (values of % control; n = 3 for each group). MetS-VLDL significantly increased oxidative stress at 25 mg/dL (* p < 0.05; ** p < 0.01); (D) Representative images for control, nVLDL, msVLDL, and msVLDL with VLDL receptor (VLDLR) antibody (msVLDL + Ab) groups (n = 3 for each group); (E) Internalization of DiI-labeled VLDL particles (red) increased in size and number in MetS-VLDL treated HL-1 cells (msVLDL) compared to normal-VLDL treated cells (nVLDL) (* p < 0.05, n = 3). Pre-treatment with VLDLR Ab for 24 h reduced internalization (* p < 0.05).