Skip to main content
. 2022 Jun 27;33(11):451–462. doi: 10.1097/WNR.0000000000001803

Fig. 6.

Fig. 6

Involvement of the Nrf2/HO-1 signaling pathway in the NGR1-induced attenuation of neuronal inflammation after SCI. (a) The representative image of Western Blot analysis for IL-6, IL-1β, and TNF-α in the Sham + vehicle, SCI + vehicle, SCI + NGR1, and SCI + NGR1 + ML385 groups at 21 days after SCI. (b–d) Quantitative analysis of IL-6/actin, IL-1β/actin, and TNF-α/actin in each group. N = 3. Data are represented as mean ± SEM. *P < 0.05 vs. the Sham + vehicle group; #P < 0.05 vs. the SCI + vehicle group; &P < 0.05 vs. the SCI + NGR1 group. (e–g) Quantitative analysis of the mRNA expression of IL-6, IL-1β, and TNF-α in each group. N = 3. Data are represented as mean ± SEM. One-way analysis of ANOVA with Turkey’s post hoc tests was used. *P < 0.05 vs. the Sham + vehicle group; #P < 0.05 vs. the SCI + NGR1 group; &P < 0.05 vs. the SCI + NGR1 group. ANOVA, analysis of variance; HO-1, heme oxygenase-1; NGR1, notoginsenoside R1; Nrf2, nuclear factor erythroid 2 related factor 2; SCI, spinal cord injury.