Comparative study on effect of mesenchymal stem cells and endothelial progenitor cells on treatment of experimental CCL4-induced liver fibrosis

被引:16
作者
Abdelgwad, Marwa [1 ]
Ewaiss, Manal [2 ,3 ]
Sabry, Dina [1 ]
Khalifa, Warda A. [4 ]
Altaib, Zeinab M. [5 ]
Alhelf, Maha [1 ]
机构
[1] Cairo Univ, Fac Med, Dept Med Biochem & Mol Biol, Giza, Egypt
[2] Beni Suef Univ, Fac Med, Dept Biochem & Mol Biol, Bani Suwayf, Egypt
[3] Al Jouf Univ, Med Coll, Al Jawf, Saudi Arabia
[4] Sebha Univ, Fac Sci, Dept Biotechnol, Sabha, Libya
[5] Helwan Univ, Helwan Fac Med, Dept Histol & Cell Biol, Cairo, Egypt
关键词
CCl4 liver fibrosis; umbilical cord blood EPCs; bone marrow mesenchymal stem cell; CARBON-TETRACHLORIDE; GROWTH-FACTOR; PARTIAL-HEPATECTOMY; HEPATIC-FIBROSIS; RAT-LIVER; ANGIOGENESIS; CIRRHOSIS; TRANSPLANTATION; THERAPY; REGENERATION;
D O I
10.1080/13813455.2020.1752256
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background: We speculated impacts of BM-MSCs and UC-EPCs on reversal of hepatic injury induced by carbon tetrachloride (CCl4). Fifty adult rats were divided into five groups: control group, CCl4A group, CCl4B group, CCl4/BM-MSCs group and CCl4/UC-EPCs group. Blood samples were driven to measure concentration of albumin and ALT. Quantitative expression of HGF, TGF-beta, MMP-2, and VEGF were assessed by PCR. Histological and immunohistochemistry examination of the liver tissue were performed. Results: There was elevating albumin (p < .05) and reducing ALT (p < .05) concentrations in groups treated with BM-MSCs and UC-EPCs compared to untreated CCL4A&B groups. UC-EPCs treated group have significantly higher MMP-2 and VEGF (p < .01) genes expression than BM-MSCs treated group. Furthermore, UC-EPCs were more valuable than BMMSCs in increasing gene expression of HGF (p < .05) and immunohistochemistry of alpha-SMA and Ki-67 (p < .01). BM-MSCs have significantly lower TGF-beta (p < .00) compared to UC-EPCs. Conclusion: This study highlighted on liver regeneration role of both UC-EPCs and BM-MSCs in liver fibrosis.
引用
收藏
页码:1071 / 1080
页数:10
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