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[Atractylenolide I Can Induce Apoptosis of U266 Cells and Enhance Bortezomib Effect]. | LitMetric

AI Article Synopsis

  • Atractylenolide I inhibits the growth and promotes apoptosis of U266 cells, showing a dose-dependent effect.
  • The combination of atractylenolide I and bortezomib significantly enhances the inhibition of U266 cell proliferation compared to either drug alone.
  • Mechanistic studies suggest that this combined effect may involve the mitochondrial pathway and regulation of specific gene expressions related to the JAK2/STAT3 signaling pathway.

Article Abstract

Objective: To investigate the effect of atractylenolide I on proliferation and apoptosis of U266 cells, and anti-multiple myeloma effect of bortezomib.

Methods: Bortezomib, bortezomib combined atractylenolide I and atractylenolide I at different concentrations were added into U266 cells respectively, cellular proliferation toxicity was evaluated by CCK-8 assay, apoptosis and cell cycle were detected by using flow cytometry with Annexin V-FITC/PI staining. RT-PCR and Western blot analysis were used to detect the mRNA and protein levels of targeting gene Caspase-3,Caspase-9,BCL-2,BAX,JAK2,STAT3 and IL-6, respectively.

Results: The proliferation of U266 cells could inhibited by atractylenolide I, and the apoptosis of U266 cells could be promoted by atractylenolide I, also, which showed a dose-dependent manner(P<0.00; r=0.99). Moreover, the atractylenolide I could regulat the mitochondrial pathway(P<0.01). The combination of 2 drugs could strengther the inhibition of U266 cell proliferation significantly, and the expression level of IL-6,JAK2,STAT3 and BCL-2 mRNA and protein could be decreased by single drug and 2 drugs both(P<0.01).

Conclusion: Atractylenolide I significantly inhibits the proliferation of U266 cells and promotes their apoptosis. At the same time, it acts synergistically with bortezomib, which may be related to mitochondrial pathway, and probably related to the regulating of IL-6, JAK2 and STAT3 gene expression in signal pathway of JAK2/STAT3.

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Source
http://dx.doi.org/10.19746/j.cnki.issn.1009-2137.2020.01.030DOI Listing

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