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. 2021 Mar 25;22(7):3367. doi: 10.3390/ijms22073367

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© 2021 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Pharmacological inhibition of the p65 pathway prevents the cellular senescence and proinflammatory paracrine transmission by small extracellular vesicles (sEV) in mesenchymal stem cells (MSCs). Quantification of the proliferation capacity using the MTT (bromide 3-(4,5-dimetiltiazol-2-il)-2,5-diphenyltetrazolium) assay in (A) recipient proliferative MSCs (Non-Se) treated with sEV from Non-Se, Senescent MSCs (DDIS and TIS) and JSH-23 (sEV-DDIS-JSH-23 and sEV-TIS-JSH-23), MG-132 (sEV-DDIS-MG-132 and sEV-TIS-MG-132) and curcumin (sEV-DDIS-Curcumin and sEV-TIS-Curcumin) and (B) recipient MSCs treated with sEV from DMSO (without TNF-α treatment); TNF-α (tumor necrosis factor alpha treatment) and inhibitor of the p65 pathway (JSH-23, MG-132 and curcumin) (sEV- TNFα-JSH-23, sEV- TNFα-MG-132 and sEV- TNFα-Curc). (C) Quantification of senescence-associated β-galactosidase activity in recipient Non-Se treated with sEV from Non-Se, Senescent MSCs (DDIS, and TIS) and JSH-23 (sEV-DDIS-JSH-23 and sEV-TIS-JSH-23), MG-132 (sEV-DDIS-MG-132 and sEV-TIS-MG-132) and curcumin (sEV-DDIS-Curcumin and sEV-TIS-Curcumin). The graphs show the mean ± SD of three independent experiments. Nonparametric Kolmogorov–Smirnov test was used to calculate the significance, and it was represented as p < 0.05 and p < 0.01. A.U: arbitrary units and MTT (bromide 3-(4,5-dimetiltiazol-2-il)-2,5-diphenyltetrazolium).

Inline graphic — Pharmacological inhibition of the p65 pathway prevents the cellular senescence and proinflammatory paracrine transmission by small extracellular vesicles (sEV) in mesenchymal stem cells (MSCs). Quantification of the proliferation capacity using the MTT (bromide 3-(4,5-dimetiltiazol-2-il)-2,5-diphenyltetrazolium) assay in (A) recipient proliferative MSCs (Non-Se) treated with sEV from Non-Se, Senescent MSCs (DDIS and TIS) and JSH-23 (sEV-DDIS-JSH-23 and sEV-TIS-JSH-23), MG-132 (sEV-DDIS-MG-132 and sEV-TIS-MG-132) and curcumin (sEV-DDIS-Curcumin and sEV-TIS-Curcumin) and (B) recipient MSCs treated with sEV from DMSO (without TNF-α treatment); TNF-α (tumor necrosis factor alpha treatment) and inhibitor of the p65 pathway (JSH-23, MG-132 and curcumin) (sEV- TNFα-JSH-23, sEV- TNFα-MG-132 and sEV- TNFα-Curc). (C) Quantification of senescence-associated β-galactosidase activity in recipient Non-Se treated with sEV from Non-Se, Senescent MSCs (DDIS, and TIS) and JSH-23 (sEV-DDIS-JSH-23 and sEV-TIS-JSH-23), MG-132 (sEV-DDIS-MG-132 and sEV-TIS-MG-132) and curcumin (sEV-DDIS-Curcumin and sEV-TIS-Curcumin). The graphs show the mean ± SD of three independent experiments. Nonparametric Kolmogorov–Smirnov test was used to calculate the significance, and it was represented as p < 0.05 and p < 0.01. A.U: arbitrary units and MTT (bromide 3-(4,5-dimetiltiazol-2-il)-2,5-diphenyltetrazolium).