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. 2021 Jun 7;17(1):170–177. doi: 10.4103/1673-5374.314314

Figure 3.

Figure 3

6-OHDA-induced lincRNA-p21 upregulation modulates α-synuclein expression and neurotoxicity.

(A) Reverse transcription quantitative polymerase chain reaction analysis of lincRNA-p21 expression in SH-SY5Y cells treated with 6-OHDA for 24 hours; GAPDH served as the internal control. (B) Reverse transcription quantitative polymerase chain reaction analysis of lincRNA-p21 levels in SH-SY5Y cells transfected with lincRNA-p21 siRNA for 24 hours. (C) Representative western blot and quantification data of α-synuclein in SH-SY5Y cells transfected with lincRNA-p21 siRNA and then treated with 6-OHDA for 24 hours. (D) Cell apoptosis was assessed using Annexin V-FITC/propidium iodide. The data are shown as the mean ± SD (n = 5; A, B: Student’s t-test; C, D: one-way analysis of variance followed by Bonferroni post hoc test); **P < 0.01, vs. control group; ##P < 0.01, vs. 6-OHDA treatment group; &&P < 0.01, vs. NC group. 6-OHDA: 6-Hydroxydopamine; Con: control; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; NC: negative control; siRNA: small interfering RNA; TGIF1: TG-interacting factor 1; α-syn: α-synuclein.