The Inhibition of miR-873 Provides Therapeutic Benefit in a Lipopolysaccharide-Induced Neuroinflammatory Model of Parkinson’s Disease

Figure 2

The downregulation of ABCA1 by LPS via miR-873 in human glioblastoma U251 cells. The pre-miR-873 mRNA level was increased 4 h to 8 h after LPS treatment and returned to the control levels by 12 h (a); additionally, the miR-873 mRNA level was increased after LPS treatment for 12 h (b). The induction of miR-873 following LPS treatment for 24 h was eliminated by a TLR4 inhibitor (CLI-095) and a MyD88 inhibitor (ST2825) (c). The mRNA level of ABCA1 was increased 4 h after LPS treatment, but a significant decrease in ABCA1 was observed from 12 h to 24 h (d). The protein level of ABCA1 was reduced after LPS treatment for 24 h (e). Transfection of the miR-873 sponge decreased the mRNA levels of miR-873 (f). Transfection of the miR-873 sponge eliminated the increase in the ABCA1 mRNA levels 24 h after LPS treatment (g). The reduction in the ABCA1 levels was eliminated by a TLR4 inhibitor (CLI-095) and a MyD88 inhibitor (ST2825) following LPS treatment for 24 h (H). The data are expressed as the ; , , , and compared with the respective controls.

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