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. 2020 Nov 19;47(1):276–288. doi: 10.3892/ijmm.2020.4793

Figure 5.

Figure 5

PDCC4 relieves the pathological manifestations of preeclampsia in a rat model. (A) SBP of the four groups was evaluated on GD7, 11, 14, 16 and 18. The SBP of the rats increased significantly after treatment with LPS, and this change was rescued by PDCC4 (n=18 per group). (B) Ratio of urinary protein to creatinine in the four groups was analyzed (n=12 per group). (C) Representative pictures of fetal appearance were captured for the four groups (n=12 per group). (D) Fetal weight and the (E) numbers of live and dead fetuses in each group were determined (n=12 per group). (F) Pathological alterations of the kidneys and placentas were observed after hematoxylin and eosin staining. Black arrows indicated glomerulus in kidney (upper) and basal zone in placenta (lower). The PDCC4-treated group exhibited mild inflammation compared with the LPS-treated group in a microscopic analysis of morphology. Scale bar, 100 µm. PDCC4 decreased the expression levels of markers of endothelial dysfunction, (G) ET-1 and (H) tPA, in the rat placentas (n=12 per group). Increasing serum levels of (I) sFlt-1 and (J) sEng in each group were declined by PDCC4 (n=12 per group). (K) Immunohistochemical staining demonstrated that PDCC4 decreased proinflammatory cytokines (IL-6) and increased anti-inflammatory cytokines (IL-4) in PE rats (n=12 per group). Scale bar, 50 µm. *P<0.05, **P<0.01 and ***P<0.001 vs. negative control group; #P<0.05, ##P<0.01 and ###P<0.001 vs. PE group. SBP, systolic blood pressure; GD, gestational day; PDCC4, peptide derived from complement C4 A chain; tPA, tissue plasminogen activator; ET-1, endothelin; sFlt-1, soluble fms-like tyrosine kinase 1; sEng, soluble endoglin; NS, not significant; LPS, lipopolysaccharide; OD, optical density.