Extended Data Fig. 9: Late life intervention with PCC1 does not alter the cause of death, but restrains the SASP and reduces oxidative stress.
From: The flavonoid procyanidin C1 has senotherapeutic activity and increases lifespan in mice
(a-b) Pie charts depicting the ultimate causes of death of C57BL/6 J mice (males and females) that had undergone vehicle (a) or PCC1 (b) biweekly treatment starting from 24-27 months of age. Note there was no significant difference between vehicle- and PCC1-treated groups upon analysis using either Chi-square or Fisher’s exact tests. (c-e) qRT-PCR profiling of the SASP and senescence marker expression in tissues of solid organs, including liver (c), lung (d) and prostate (e) collected from young (6-month-old, untreated), aged (24-27-month-old) vehicle-treated and aged (24-27-month-old) PCC1-treated animals, respectively. (f) Measurement of circulating levels of hallmark SASP factors IL6, CSF2 and MCP-1 in mouse blood by ELISA assays. (g) Quantification of SASP and senescence marker expression in CD3+ peripheral T cells of experimental mice described in c-f. (h) Examination of 4-hydroxynonenal (HNE) adducts, a marker of lipid peroxidation and oxidative stress by ELISA measurement with tissue lysates of the liver. (i) Determination of the ratio of reduced (GSH) to oxidized (GSSG) glutathione measured as an index oxidative stress. Data are shown as mean ± SD and derive from 3 biological replicates (n = 3 independent assays for c-i). P values were calculated by two-sided t-test. ^, P > 0.05. *, P < 0.05. **, P < 0.01. ***, P < 0.001.
