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. 2021 Oct 21;19:332. doi: 10.1186/s12951-021-01077-y

Fig. 4.

Fig. 4

Hemin-MSC-EXO ameliorates cardiomyocyte senescence induced by SD/H challenge via inhibition of mitochondrial fission. A Representative images of the fragmented mitochondria in control, SD/H, SD/H + MSC-EXO, SD/H + Hemin-MSC-EXO, SD/H + MSC-EXO + FCCP, and SD/H + Hemin-MSC-EXO + FCCP-treated NMCMs. B Quantitative analysis of fragmented mitochondria in control, SD/H, SD/H + MSC-EXO, SD/H + Hemin-MSC-EXO, SD/H + MSC-EXO + FCCP, and SD/H + Hemin-MSC-EXO + FCCP-treated NMCMs. C Representative images of SA-β-gal staining in control, SD/H, SD/H + MSC-EXO, SD/H + Hemin-MSC-EXO, SD/H + MSC-EXO + FCCP, and SD/H + Hemin-MSC-EXO + FCCP-treated NMCMs. D Quantitative analysis of SA-β-Gal positive cells in control, SD/H, SD/H + MSC-EXO, SD/H + Hemin-MSC-EXO, SD/H + MSC-EXO + FCCP, and SD/H + Hemin-MSC-EXO + FCCP-treated NMCMs. E Western blotting and quantitative analysis of the expression level of p16, p21, p-Drp1, Drp1, Mfn1 and Mfn2 in control, SD/H, SD/H + MSC-EXO, SD/H + Hemin-MSC-EXO, SD/H + MSC-EXO + FCCP, and SD/H + Hemin-MSC-EXO + FCCP-treated NMCMs. SD/H means serum deprivation/hypoxia. n = 3 biological replicates for each group. Data are expressed as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ns = not significant