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Hemostimulating Effects of c-Jun N-Terminal Kinase (JNK) Inhibitor during Cytostatic Myelosuppression and Mechanisms of Their Development
Bulletin of Experimental Biology and Medicine ( IF 0.7 ) Pub Date : 2020-07-01 , DOI: 10.1007/s10517-020-04880-z
G N Zyuz'kov 1 , V V Zhdanov 1 , L A Miroshnichenko 1 , E V Simanina 1 , T Yu Polyakova 1 , L A Stavrova 1 , V I Agafonov 1 , M Yu Minakova 1 , M G Danilets 1 , A A Ligacheva 1
Affiliation  

The hemostimulating effects of c-Jun N-terminal kinase (JNK) inhibitor were examined on the mouse model of myelosuppression provoked by 5-fluorouracil. Blockade of JNK during postcytostatic period accelerated recovery of granulomonocytopoiesis and erythropoiesis. It also increased the content of neutrophilic granulocytes and erythroid cells in the hematopoietic tissue and elevated the counts of neutrophils and reticulocytes in the peripheral blood. The development of these phenomena resulted from elevated content and up-regulated functional activity of bone marrow hematopoietic progenitors associated with the direct action of JNK inhibitor on these progenitors and enhanced secretion of hemopoietins by stromal elements of the hematopoiesis-inducing microenvironment.

中文翻译:

c-Jun N-末端激酶(JNK)抑制剂在骨髓抑制过程中的止血作用及其发展机制

在由 5-氟尿嘧啶引起的骨髓抑制小鼠模型上检查了 c-Jun N-末端激酶 (JNK) 抑制剂的血液刺激作用。在细胞生长停滞期阻断 JNK 可加速粒单细胞生成和红细胞生成的恢复。它还增加了造血组织中中性粒细胞和红细胞的含量,增加了外周血中性粒细胞和网织红细胞的数量。这些现象的发展是由于骨髓造血祖细胞的含量升高和功能活性上调与 JNK 抑制剂对这些祖细胞的直接作用和造血诱导微环境的基质元素增强的造血素分泌相关。
更新日期:2020-07-01
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