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. 2020 Mar 10;10:4446. doi: 10.1038/s41598-020-61441-0

Figure 1.

Figure 1

The effects of hUCBCs on the IL-8-mediated signalling pathway include the upregulation of Cxcl2 and CXCR2 expression, p38 activation, and subsequent degradation of IκB in the HI mouse brain. (a) The mRNA level of mouse Cxcl2, the IL-8 homologue was upregulated at 1 h post-hUCBC treatment according to RT-PCR analysis of the HI mouse brain (n = 5). (b) The upregulation of Cxcl2 expression after hUCBC administration in the HI mouse brain was consistent and significant according to real-time PCR assays 1 h post-hUCBC injection (n = 7). (c) The levels of mouse CXCR2 (the receptor for Cxcl2), p-p38, IκB, and ß-actin in the sham, HI, and hUCBC groups sacrificed on post-hUCBC days 1 and 3 were assayed using Western blotting to observe the consecutive changes after Cxcl2 upregulation. The level of CXCR2 was upregulated in parallel with p38 activation and the successive degradation of IκB after hUCBC administration. (d) The graph depicts the band intensity in p-p38 Western blotting. The data were obtained from triplicate results. Data are shown as the mean ± SEM (n = 5). Asterisks (*) indicate significant differences (*p < 0.05, **p < 0.01, one-way ANOVA) between groups. HI, hypoxic-ischaemic brain injury; hUCBCs, human umbilical cord blood mononuclear cells; UCB, HI mice subjected to hUCBC treatment.