4.7 Article

Selenium nanoparticles fabricated in laminarin polysaccharides solutions exert their cytotoxicities in HepG2 cells by inhibiting autophagy and promoting apoptosis

Journal

INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
Volume 137, Issue -, Pages 829-835

Publisher

ELSEVIER
DOI: 10.1016/j.ijbiomac.2019.07.031

Keywords

Laminarin polysaccharides; Selenium nanoparticles; HepG2 cells; Apoptosis; Autophagy

Funding

  1. Program for the Top Young Academic Leaders of Higher Learning Institutions of Shanxi
  2. Fund for Shanxi Key Subjects Construction (FSKSC)
  3. Collaborative Innovation Center Project of Shanxi 'Astragalus' Resource Industrialization and Industrial Internationalization [HQXTCXZX2016-021]
  4. Natural Science Foundation of Shanxi Province [201601D011112]
  5. Key Research and Development Program of Shanxi Province [201603D21109]

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Selenium nanoparticles (SeNPs) have been attracting increasing attention as potential cancer therapeutic agents. In the present study, laminarin polysaccharides (LP) decorated selenium nanoparticles (LP-SeNPs) with an average diameter of ca. 60 nm were synthesized. Transmission electron microscope (TEM), laser particle analyzer, UV-visible spectrometer and Energy dispersive X-ray (EDX) spectrometer were applied to characterize the prepared SeNPs. The cytotoxicity, apoptosis, and autophagy were examined using a series of cellular assays. The results revealed that LP-SeNPs exhibited cytotoxicity against HepG2 cells with IC50 value was 23.4 +/- 2.7 mu M. After cells were treated with various concentrations of LP-SeNPs (10, 20 and 40 mu M) for 24 h, the total apoptosis rate increased to 17.4 +/- 1.6, 20.9 +/- 13 and 30.9 +/- 1.2%, respectively. Additionally, treatment of LP-SeNPs increased the expression of Box and cleaved caspase-9 but decreased the level of Bcl-2. This suggested that LP-SeNPs induced mitochondria-mediated apoptosis. Further, exposure of cells to LP-SeNPs for 12 h induced the upregulation of LC3-II and p62. Treatment of chloroquine (CQ), the inhibitors of the autophagosome, resulted in further accumulation of p62 and LC3-II. These results demonstrated that LP-SeNPs induced the activation of early autophagy, but blocked the late phase of autophagy. Inhibition of late phase of autophagy resulted in the damaged organelles cannot be cleared and aggravating apoptosis. In conclusion, these results indicated that LP-SeNPs exerted its cytotoxicity in HepG2 cells by inhibiting autophagy and inducing apoptosis. (C) 2019 Elsevier B.V. All rights reserved.

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