LIU Yawen, ZHAO Qun, ZHENG Haowen, KONG Xiang, SONG Jingzhe. Expressions and significance of CXC chemokine ligand 12 and human cartilage glycoprotein-39 in serum and placental tissues of patients with preeclampsia[J]. Journal of Clinical Medicine in Practice, 2022, 26(9): 16-19. DOI: 10.7619/jcmp.20220392
Citation: LIU Yawen, ZHAO Qun, ZHENG Haowen, KONG Xiang, SONG Jingzhe. Expressions and significance of CXC chemokine ligand 12 and human cartilage glycoprotein-39 in serum and placental tissues of patients with preeclampsia[J]. Journal of Clinical Medicine in Practice, 2022, 26(9): 16-19. DOI: 10.7619/jcmp.20220392

Expressions and significance of CXC chemokine ligand 12 and human cartilage glycoprotein-39 in serum and placental tissues of patients with preeclampsia

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  • Received Date: February 08, 2022
  • Available Online: April 18, 2022
  • Published Date: May 14, 2022
  •   Objective  To analyze the expressions of CXC chemokine ligand 12 (CXCL12) and human cartilage glycoprotein-39 (YKL-40) in serum and placental tissues of normal pregnant women and pregnant women with preeclampsia (PE).
      Methods  The serum concentrations of CXCL12 and YKL-40 in 50 normal pregnant women (control group) and 50 pregnant women with PE (PE group) were measured by enzyme-linked immunosorbent assay (ELISA), and the protein expression levels of CXCL12 and YKL-40 in placenta were detected by two-step immunohistochemistry (IHC).
      Results  The systolic blood pressure, diastolic blood pressure and 24-hour urinary protein quantification in the PE group were significantly higher than those in the control group, while the birth weight of newborns was significantly lower than that in the control group (P<0.05). The levels of serum CXCL12 and YKL-40 in the PE group were significantly higher than those in the control group (P<0.05). IHC found that the expression intensities of CXCL12 and YKL-40 in placental tissues of the PE group were significantly higher than those of the control group (P<0.05).
      Conclusion  CXCL12 and YKL-40 are highly expressed in PE patients, which suggests that the pathogenesis of PE is related to vascular endothelial lesions and inflammatory stimulation.
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