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. 2022 Feb 1;13(2):3724–3738. doi: 10.1080/21655979.2022.2029066

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© 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 7. — (a). the senescence-associated β-galactosidase (SA β-gal)-positive cell ratio were significantly reduced by uridine treatment. (b). The senescence-related markers (p16, p21 and p53) were down-regulated by uridine treatment. (c). MTT assay indicated that the uridine treatment increased cell proliferation ability of the senescent GES-1 and RGM-1 cell. (d). uridine treatment effected the cell cycle. The data are shown as means ± SEM. Asterisks indicate significant differences (P < 0.05).

Figure 7. — (a). the senescence-associated β-galactosidase (SA β-gal)-positive cell ratio were significantly reduced by uridine treatment. (b). The senescence-related markers (p16, p21 and p53) were down-regulated by uridine treatment. (c). MTT assay indicated that the uridine treatment increased cell proliferation ability of the senescent GES-1 and RGM-1 cell. (d). uridine treatment effected the cell cycle. The data are shown as means ± SEM. Asterisks indicate significant differences (P < 0.05).