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. 2020 Jan 10;12(1):718–739. doi: 10.18632/aging.102652

Figure 6.

Figure 6

Slicing lncRNA NONRATT023402.2 inhibited Gsto2 and Ptger3, and promoted inflammatory response in vivo. (A, B) qRT-PCR detection of NONRATT023402.2 and Gsto2 levels in rat PC12 cells transfected with NONRATT023402.2 siRNA (n = 3). (C, D) Protein levels of GSTO2, PTGER3, c-FOS, p-EERK, ERK, IL-1β, IL-6 and TNF-α in PC12 cells transfected with NONRATT023402.2 siRNA (n = 3), as determined by western blotting. The signal intensity of protein bands was quantified by densitometry and normalized to that of GAPDH. (E) Schematic representation of the regulatory mechanism of NONRATT023402.2 in PD and LID. Downregulation of NONRATT023402.2 leads to the decline of GSTO2 and PTGER3, possibly through a ceRNA-type mechanism. The decrease in GSTO2 results in increased oxidative stress in neurons and astrocytes, whereas the decrease in PTGER3 promotes inflammation in neurons; these ultimately contribute to the development of PD/LID. Data represent mean ± SEM. *P < 0.05, **P < 0.01 vs. control group; #P < 0.05, ##P < 0.01 vs. negative control (NC) group.