[Effect of Hispidulin on Proliferation and Apoptosis of Leukemia K562 Cells by Up-Regulating IL-37]

Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2023 Oct;31(5):1322-1326. doi: 10.19746/j.cnki.issn.1009-2137.2023.05.011.
[Article in Chinese]

Abstract

Objective: To investigate the effect and underlying mechanism of hispidulin on the proliferation and apoptosis of leukemia K562 cells.

Methods: K562 cells were cultured in vitro and treated with 0, 5, 25 or 100 μmol/L hispidulin for 24 h. Cell proliferation and apoptosis were detected by CCK-8 and flow cytometry, respectively. Western blot was used to assess the expression of Bax, Bcl-2 and interleukin (IL)-37 proteins. Bone marrow mononuclear cells were extracted from 17 chronic myeloid leukemia patients and 21 healthy individuals by Ficoll-Hypaque density gradient method, and the expression of IL-37 protein was measured by Western blot. K562 cells with IL-37 overexpression or knockdown were constructed, and then treated with 0 or 100 μmol/L hispidulin for 24 h. Cell proliferation, apoptosis and protein expression of Bax and Bcl-2 were determined in the same way as above.

Results: After K562 cells were treated with hispidulin, the cell inhibition rate, apoptosis rate, and the protein expression of Bax and IL-37 were significantly increased (P <0.05), but the cell proliferation and expression of Bcl-2 protein were decreased (P <0.05). The expression of IL-37 protein in bone marrow mononuclear cells of the leukemia patient was 0.24±0.03, which was significantly lower than 0.91±0.05 of healthy controls (P <0.05). Overexpression of IL-37 significantly promoted inhibition rate, apoptosis rate, and expression of Bax protein in K562 cells (P <0.05), but suppressed the expression of Bcl-2 protein (P <0.05). In addition, knockdown of IL-37 could reverse the effects of hispidulin on proliferation and apoptosis of K562 cells.

Conclusion: Hispidulin inhibits the proliferation and induces apoptosis of leukemia K562 cells, which may be related to the up-regulation of IL-37 protein in cells.

题目: 高车前素通过上调IL-37影响白血病K562细胞增殖和凋亡的实验研究.

目的: 探讨高车前素对白血病K562细胞增殖和凋亡的影响及可能机制。.

方法: 体外培养K562细胞,分别用高车前素0、5、25、100 μmol/L作用24 h,CCK-8法检测细胞增殖,流式细胞术检测细胞凋亡,蛋白质印迹法检测Bax、Bcl-2和白细胞介素(IL)-37蛋白表达。利用Ficoll-Hypaque密度梯度法提取17例慢性髓系白血病患者和21例健康体检者骨髓单个核细胞,蛋白质印迹法检测IL-37蛋白表达。构建过表达或敲减IL-37的K562细胞,再用高车前素0、100 μmol/L作用24 h,上述相同方法观察细胞增殖、凋亡及Bax和Bcl-2蛋白表达。.

结果: K562细胞经高车前素干预后,细胞增殖抑制率、凋亡率及Bax和IL-37蛋白表达均显著升高(P <0.05),而Bcl-2蛋白表达显著降低(P < 0.05)。白血病患者骨髓单个核细胞中IL-37蛋白表达量为0.24±0.03,显著低于健康体检者的0.91±0.05(P <0.05)。过表达IL-37能显著增加K562细胞增殖抑制率、凋亡率及Bax蛋白表达(P <0.05),而降低Bcl-2蛋白表达(P <0.05)。敲减IL-37能逆转高车前素对K562细胞增殖和凋亡的影响。.

结论: 高车前素抑制白血病K562细胞增殖,并诱导细胞凋亡,这可能与其上调细胞中IL-37蛋白表达有关。.

Keywords: apoptosis; hispidulin; interleukin-37; leukemia; proliferation.

Publication types

  • English Abstract

MeSH terms

  • Apoptosis*
  • Cell Proliferation
  • Humans
  • K562 Cells
  • Leukemia*
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein / pharmacology

Substances

  • bcl-2-Associated X Protein
  • hispidulin
  • Proto-Oncogene Proteins c-bcl-2