Fig 2: SIRT1 and PGC-1a were involved in MC1R-mediated neuroprotection at 24 h after SAH. Representative images and quantification of immunofluorescence and Golgi staining of (A, B) DHE; (C, D) FJC; (E, F) TUNEL; (G, H) Golgi. n = 4 for each group. Scale bar = 50 µm. Data were shown as means ± SD and compared by 1-way ANOVA, followed by the Tukey post-hoc test. *p < 0.05 vs. sham, &p < 0.05 vs. SAH + vehicle, #p < 0.05 vs. SAH + BMS-470539.

Fig 3: The potential molecular mechanisms of anti-inflammatory and neuroprotective effects through the MC1R/cAMP/PKA/Nurr1 signaling pathway post-HI

Fig 4: Knockout of PGC-1a with siRNA aggravates oxidative stress and apoptosis following SAH. (A) Representative western blot images; (B) Quantitative analyses of MC1R, p-AMPK, SIRT1, PGC-1a, UCP2, GPx, SOD, CC-3, Bcl-2, Bax. Data were shown as means ± SD, and were compared using 1-way ANOVA followed by the Tukey post hoc test. *p < 0.05 vs. sham, &p < 0.05 vs. SAH + vehicle, #p < 0.05 vs. SAH + BMS-470539.

Fig 5: BMS-470539 administration suppressed oxidative stress at 48 h post-HI, which was abolished by MC1R or Nurr1 knockout CRISPR. (a, b) Representative microphotographs of MitoSox (red) and 8-OHdG (green) staining in the ipsilateral hemisphere at 48 h post-HI. Blue was for DAPI. (c, d) Quantitative analysis of MitoSox- and 8-OHdG-positive cells. n = 6 per group. Scale bar = 100 µm. Data was represented as mean ± SD. *p < 0.05 versus sham; #p < 0.05 versus HI+vehicle; @p < 0.05 HI+BMS-470539 or HI+BMS-470539+control CRISPR; one-way ANOVA, Tukey's post hoc test.