Cichoric acid from extracted Echinacea purpurea induces the proliferation and apoptosis of peripheral blood mononuclear cells from yaks
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Keywords

apoptosis
Cichoric acid
cytokine
Echinacea pururea
grazing yaks
peripheral blood mononuclear cells
proliferation
transcription factors.

How to Cite

1.
Wang M- jie, Raza SHA, Wu Q, Xue C- hua, Liu J- hua, Zhang L- fei, Zhang W- ying, Wang A- chao, Wu H. Cichoric acid from extracted Echinacea purpurea induces the proliferation and apoptosis of peripheral blood mononuclear cells from yaks. Electron. J. Biotechnol. [Internet]. 2020 Sep. 15 [cited 2024 Sep. 9];47. Available from: https://preprints.pucv.cl/index.php/ejbiotechnology/article/view/2020.06.003

Abstract

Background: Cichoric acid (CA) is extracted from Echinacea purpurea. It is well known and widely used for its immunological function. However, the effect of CA on peripheral blood mononuclear cells (PBMCs) from yaks is still unclear. This study investigated the potential influences of CA on the proliferation, cytokine induction, and apoptosis of PBMCs from Datong yak in vivo, and aimed to provide a basis for exploring the pharmacological activities of CA on yaks.

 

Results: In this study, CA promoted PBMCs proliferation by combining concanavalin A (Con A) and exhibited a dose-dependent effect as demonstrated by a Cell Counting Kit-8. The concentration of 60 μg/ml CA was the best and promoted the transformation from the G0/G1 phase to the S and G2/M phases with Con A. Furthermore, 60 μg/ml CA significantly increased IL-2, IL-6, and IFN-γ levels and PCNA, CDK4 and Bcl-2 expression levels, but it significantly inhibited the TP53, Bax, and Caspase-3 expression levels. Transcriptome analysis revealed a total of 6807 differentially expressed genes (DEGs) between the CA treatment and control groups. Of these genes, 3788 were significantly upregulated and 3019 were downregulated. Gene Ontology and pathway analysis revealed that DEGs were enriched in cell proliferation and immune function signaling pathways. The expression level of some transcription factors (BTB, Ras, RRM_1, and zf-C2H2) and genes (CCNF, CCND1, and CDK4) related to PBMCs proliferation in yaks were significantly promoted after CA treatment. By contrast, anti-proliferation-associated genes (TP53 and CDKN1A) were inhibited.

 

Conclusions: In summary, CA could regulate the immune function of yaks by promoting proliferation and inhibiting inflammation and apoptosis of PBMCs.

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