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硒修饰壳聚糖诱导 HepG2 细胞凋亡及差异蛋白分析
Authors Sun SJ, Deng P, Peng CE, Ji HY, Mao LF, Peng LZ
Received 4 August 2022
Accepted for publication 10 November 2022
Published 28 November 2022 Volume 2022:14 Pages 3335—3345
DOI https://doi.org/10.2147/CMAR.S382546
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Ahmet Emre Eşkazan
Introduction: Chitosan is the product of the natural polysaccharide chitin removing part of the acetyl group, and exhibits various physiological and bioactive functions. Selenium modification has been proved to further enhance the chitosan bioactivities, and has been a hot topic recently.
Methods: The present study aimed to investigate the potential inhibitory mechanism of selenium-modified chitosan (SMC) on HepG2 cells through MTT assays, morphological observation, annexin V–FITC/PI double staining, mitochondrial membrane potential determination, cell-cycle detection, Western blotting, and two-dimensional gel electrophoresis (2-DE).
Results: The results indicated that SMC can induce HepG2 cell apoptosis with the cell cycle arrested in the S and G2/M phases and gradual disruption of mitochondrial membrane potential, reduce the expression of Bcl2, and improve the expression of Bax, cytochrome C, cleaved caspase 9, and cleaved caspase 3. Also, 2-DE results showed that tubulin α1 B chain, myosin regulatory light chain 12A, calmodulin, UPF0568 protein chromosome 14 open reading frame 166, and the cytochrome C oxidase subunit 5B of HepG2 cells were downregulated in HepG2 cells after SMC treatment.
Discussion: These data suggested that HepG2 cells induced apoptosis after SMC treatment via blocking the cell cycle in the S and G2/M phases, which might be mediated through the mitochondrial apoptotic pathway. These results could be of benefit to future practical applications of SMC in the food and drug fields.
Keywords: selenium-modified chitosan, antihepatoma activity, mitochondrial apoptotic pathway, differential protein analysis