Protective Effect of Ganoderma atrum Polysaccharide on Acrolein-Induced Apoptosis and Autophagic Flux in IEC-6 Cells

This study was designed to explore the beneficial effect and mechanism of Ganoderma atrum (G. atrum) polysaccharide (PSG-1) on acrolein-induced IEC-6 cells. Our results indicated that PSG-1 significantly reduced the impairment of acrolein on cell viability, decreased oxidative stress, and enabled normal expression of tight junction (TJ) proteins that were inhibited by acrolein in IEC-6 cells. Furthermore, PSG-1 attenuated the elevation of microtubule-associated proteins LIGHT chain 3 (LC3) and Beclin 1-like protein 1 (Beclin 1) and increased the protein levels of phospho-mTOR (p-mTOR) and phospho-akt (p-akt), indicating that PSG-1 activated the mammalian target of rapamycin (mTOR) signaling pathway and alleviated acrolein-induced Autophagy in IEC-6 cells. Moreover, PSG-1 markedly attenuated the acrolein-induced Apoptosis, as evidenced by the increase in mitochondrial membrane potential (MMP) and B-cell lymphoma 2 (Bcl-2) expression, and the decrease in cysteine aspartate lyase (Caspase)-3 and caspase-9. In addition, Autophagy the inhibitor inhibited acrolein-induced TJ and Apoptosis of IEC-6 cells, while the Apoptosis inhibitor also inhibited acrolein-induced TJ and Autophagy, suggesting that Autophagy and Apoptosis were mutually regulated. Taken together, the present study proved that PSG-1 could protect IEC-6 cells from acrolein-induced oxidative stress and could repair TJ by inhibiting Apoptosis and autophagic flux, where Autophagy and Apoptosis were mutually regulated.