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

Area of Science:

• Biochemistry
• Cell Biology
• Materials Science

Background:

• Chitosan, derived from chitin, possesses inherent bioactivities.
• Selenium modification enhances chitosan's bioactivity, making it a recent research focus.

Purpose of the Study:

• To investigate the inhibitory mechanism of selenium-modified chitosan (SMC) on HepG2 cells.
• To elucidate the pathways involved in SMC-induced HepG2 cell death.

Main Methods:

• MTT assays, morphological observation, and annexin V-FITC/PI staining.
• Mitochondrial membrane potential, cell cycle analysis, Western blotting, and 2-DE.
• Analysis of apoptosis-related proteins and protein expression profiles.

Main Results:

• SMC induced HepG2 cell apoptosis with cell cycle arrest in S and G2/M phases.
• Disruption of mitochondrial membrane potential and altered expression of apoptosis markers (Bcl2, Bax, cytochrome C, caspases).
• Downregulation of specific proteins including tubulin and cytochrome C oxidase subunit 5B in HepG2 cells.

Conclusions:

• SMC induces apoptosis in HepG2 cells via the mitochondrial pathway, involving cell cycle arrest.
• The findings support potential applications of SMC in the food and pharmaceutical industries.