Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling
Abstract Calf Spleen Extractive Injection (CSEI), extracted from the spleen of healthy cows (within 24 hours of birth), is a small-peptide-enriched extraction and often used as an ancillary agent in cancer therapy. This study evaluated the hematopoietic function of CSEI and its underlying mechanisms...
Guardado en:
Autores principales: | , , , , , , , |
---|---|
Formato: | article |
Lenguaje: | EN |
Publicado: |
Nature Portfolio
2017
|
Materias: | |
Acceso en línea: | https://doaj.org/article/1c91100a88ba4b0783e78c15b81b1c64 |
Etiquetas: |
Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
|
id |
oai:doaj.org-article:1c91100a88ba4b0783e78c15b81b1c64 |
---|---|
record_format |
dspace |
spelling |
oai:doaj.org-article:1c91100a88ba4b0783e78c15b81b1c642021-12-02T15:06:15ZCalf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling10.1038/s41598-017-08970-32045-2322https://doaj.org/article/1c91100a88ba4b0783e78c15b81b1c642017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-08970-3https://doaj.org/toc/2045-2322Abstract Calf Spleen Extractive Injection (CSEI), extracted from the spleen of healthy cows (within 24 hours of birth), is a small-peptide-enriched extraction and often used as an ancillary agent in cancer therapy. This study evaluated the hematopoietic function of CSEI and its underlying mechanisms, principally in CHRF, K562 cells, BMNCs and a mouse model of cyclophosphamide (CTX)-induced hematopoietic suppression. CSEI promoted the proliferation and differentiation of CHRF and K562 cells, activated hematopoietic- and proliferation-related factors RSK1p90, ELK1 and c-Myc, and facilitated the expression of differentiation- and maturation-related transcription factors GATA-1, GATA-2. In the mice with hematopoietic suppression, 3 weeks of CSEI administration enhanced the bodyweights and thymus indices, suppressed the spleen indices and strongly elevated the production of HSPCs, neutrophils and B cells in bone marrow, ameliorated bone marrow cellularity, and regulated the ratio of peripheral blood cells. Proteome profiling combined with ELISA revealed that CSEI regulated the levels of cytokines, especially G-CSF and its related factors, in the spleen and plasma. Additional data revealed that CSEI promoted phosphorylation of STAT3, which was stimulated by G-CSF in both mice spleen and cultured BMNCs. Taken together, CSEI has the potential to improve hematopoietic function via the G-CSF-mediated JAK2/STAT3 signaling pathway.Wenqian LuDongxu JiaShengshu AnMing MuXinan QiaoYan LiuXin LiDi WangNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-13 (2017) |
institution |
DOAJ |
collection |
DOAJ |
language |
EN |
topic |
Medicine R Science Q |
spellingShingle |
Medicine R Science Q Wenqian Lu Dongxu Jia Shengshu An Ming Mu Xinan Qiao Yan Liu Xin Li Di Wang Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling |
description |
Abstract Calf Spleen Extractive Injection (CSEI), extracted from the spleen of healthy cows (within 24 hours of birth), is a small-peptide-enriched extraction and often used as an ancillary agent in cancer therapy. This study evaluated the hematopoietic function of CSEI and its underlying mechanisms, principally in CHRF, K562 cells, BMNCs and a mouse model of cyclophosphamide (CTX)-induced hematopoietic suppression. CSEI promoted the proliferation and differentiation of CHRF and K562 cells, activated hematopoietic- and proliferation-related factors RSK1p90, ELK1 and c-Myc, and facilitated the expression of differentiation- and maturation-related transcription factors GATA-1, GATA-2. In the mice with hematopoietic suppression, 3 weeks of CSEI administration enhanced the bodyweights and thymus indices, suppressed the spleen indices and strongly elevated the production of HSPCs, neutrophils and B cells in bone marrow, ameliorated bone marrow cellularity, and regulated the ratio of peripheral blood cells. Proteome profiling combined with ELISA revealed that CSEI regulated the levels of cytokines, especially G-CSF and its related factors, in the spleen and plasma. Additional data revealed that CSEI promoted phosphorylation of STAT3, which was stimulated by G-CSF in both mice spleen and cultured BMNCs. Taken together, CSEI has the potential to improve hematopoietic function via the G-CSF-mediated JAK2/STAT3 signaling pathway. |
format |
article |
author |
Wenqian Lu Dongxu Jia Shengshu An Ming Mu Xinan Qiao Yan Liu Xin Li Di Wang |
author_facet |
Wenqian Lu Dongxu Jia Shengshu An Ming Mu Xinan Qiao Yan Liu Xin Li Di Wang |
author_sort |
Wenqian Lu |
title |
Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling |
title_short |
Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling |
title_full |
Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling |
title_fullStr |
Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling |
title_full_unstemmed |
Calf Spleen Extractive Injection protects mice against cyclophosphamide-induced hematopoietic injury through G-CSF-mediated JAK2/STAT3 signaling |
title_sort |
calf spleen extractive injection protects mice against cyclophosphamide-induced hematopoietic injury through g-csf-mediated jak2/stat3 signaling |
publisher |
Nature Portfolio |
publishDate |
2017 |
url |
https://doaj.org/article/1c91100a88ba4b0783e78c15b81b1c64 |
work_keys_str_mv |
AT wenqianlu calfspleenextractiveinjectionprotectsmiceagainstcyclophosphamideinducedhematopoieticinjurythroughgcsfmediatedjak2stat3signaling AT dongxujia calfspleenextractiveinjectionprotectsmiceagainstcyclophosphamideinducedhematopoieticinjurythroughgcsfmediatedjak2stat3signaling AT shengshuan calfspleenextractiveinjectionprotectsmiceagainstcyclophosphamideinducedhematopoieticinjurythroughgcsfmediatedjak2stat3signaling AT mingmu calfspleenextractiveinjectionprotectsmiceagainstcyclophosphamideinducedhematopoieticinjurythroughgcsfmediatedjak2stat3signaling AT xinanqiao calfspleenextractiveinjectionprotectsmiceagainstcyclophosphamideinducedhematopoieticinjurythroughgcsfmediatedjak2stat3signaling AT yanliu calfspleenextractiveinjectionprotectsmiceagainstcyclophosphamideinducedhematopoieticinjurythroughgcsfmediatedjak2stat3signaling AT xinli calfspleenextractiveinjectionprotectsmiceagainstcyclophosphamideinducedhematopoieticinjurythroughgcsfmediatedjak2stat3signaling AT diwang calfspleenextractiveinjectionprotectsmiceagainstcyclophosphamideinducedhematopoieticinjurythroughgcsfmediatedjak2stat3signaling |
_version_ |
1718388498197643264 |