Increases in pregnancy success of aging mouse embryos with suppression of CXCL5‐CXCR2 signaling before embryo transfer. (a) Blastocyst formation rate of aging embryos with suppression of CXCL5‐CXCR2 signaling. In vitro fertilized zygotes from aging mice were allowed to develop into blastocysts without or with anti‐CXCL5 neutralizing antibody and/or CXCR2 antagonist. The number of embryos developed to blastocyst vs. total number of embryos are listed on top of each column. Data were shown as mean ± SE. N = 10–15 per group. (b–d) Implantation (b), abortion (c), and birth rates (d) of aging embryos treated with anti‐CXCL5 neutralizing antibody and/or CXCR2 antagonist. Cultured blastocysts were transferred to the uterus of recipient mice. On day 19.5 of pregnancy, the number of pups, the implantation sites, and the aborted fetuses were counted by sacrificing animals. The numbers listed on top of each column indicated the number of implantation site/total number of blastocysts transferred, the number of abortion site/the number of implantation site, and the number of pups/total number of blastocysts transferred, respectively. (e) Effects of CXCL5‐CXCR2 signaling suppression on pups and placentas derived from aging embryos. The weight of pups and placentas were measured on day 19.5 of pregnancy by sacrificing animals. (f) Representative images of pups and placentas in each group. Data were shown as mean ± SE. N = 10‐20 per group. *p < 0.01, vs. young control. Data were shown as mean ± SE. N = 10–15 per group. *p < 0.01, vs. aging control without anti‐CXCL5 neutralizing antibody and/or CXCR2 antagonist treatment