Selenium-Modified Chitosan Induces HepG2 Cell Apoptosis and Differential Protein Analysis

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 alpha 1 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.

Automated summary

The study found that selenium-modified chitosan (SMC) can induce apoptosis in HepG2 cells, arrest the cell cycle in the S and G2/M phases, disrupt mitochondrial membrane potential, decrease Bcl-2 expression, increase Bax, cytochrome C, cleaved caspase 9, and cleaved caspase 3 expression. Additionally, 2-DE results showed downregulation of specific proteins in HepG2 cells after SMC treatment.