Research Paper Volume 13, Issue 10 pp 13788—13806

Redd1 knockdown prevents doxorubicin-induced cardiac senescence

Dox exposure upregulates Redd1 in cardiomyocytes via p38 MAPK signaling. (A) Detection of Redd1 expression by q-PCR and western blotting in Dox-treated H9c2 cardiomyocytes pretreated with the p38 MAPK inhibitor SB203580 (2 μM). (n = 4 per group). (B, C) Effect of Redd1 overexpression on p16INK4a and p21 protein levels in Dox-challenged H9c2 cardiomyocytes pretreated with SB203580 (n = 4 per group). (D–G) Effect of Redd1 overexpression on IL-1β, IL-6, IL-12, and TNFα mRNA in Dox-challenged H9c2 cardiomyocytes pretreated with SB203580 (n = 4 per group). Data are mean ± SEM. *p &p #p

Figure 4. Dox exposure upregulates Redd1 in cardiomyocytes via p38 MAPK signaling. (A) Detection of Redd1 expression by q-PCR and western blotting in Dox-treated H9c2 cardiomyocytes pretreated with the p38 MAPK inhibitor SB203580 (2 μM). (n = 4 per group). (B, C) Effect of Redd1 overexpression on p16INK4a and p21 protein levels in Dox-challenged H9c2 cardiomyocytes pretreated with SB203580 (n = 4 per group). (DG) Effect of Redd1 overexpression on IL-1β, IL-6, IL-12, and TNFα mRNA in Dox-challenged H9c2 cardiomyocytes pretreated with SB203580 (n = 4 per group). Data are mean ± SEM. *p < 0.05 vs. control group. &p < 0.05 vs. Dox group. #p < 0.05 vs. Dox+SB203580 group.