Abstract:Objective To investigate the effects of aloe-emodin on apoptosis of gastric cancer SGC-7901 cells induced by Calnexin/Calreticulin circulating and endoplasmic reticulum stress (ERS). Methods The gastric cancer SGC-7901 cells were respectively cultured in MEM medium of inactivated fetal bovine serum (control group), 10 μmol/L aloe-emodin (low dose group), 30 μmol/L aloe-emodin (middle dose group) and 50 μmol/L aloe-emodin (high dose group) for 30 minutes. Cell Counting Kit-8 (CCK-8) was used to detect cell proliferation rates after cell culture for 24 hours, 48 hours and 72 hours. Transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) was used to detect cell apoptosis. Real-time quantitative polymerase chain reaction assay (qRT-PCR) was used to detect the expressions of calnexin, calreticulin, glucose regulated protein 78 (GRP78), inositol-requiring enzyme 1 (IRE1) and CCAAT enhancer binding protein homologous protein (CHOP) mRNAs. Western blotting method was used to detect the expressions of calnexin, calreticulin, GRP78, IRE1and CHOP proteins. Results Compared with control group, cell proliferation rate and cell apoptosis index in low dose group remained unchanged (all P>0.05), and they increased significantly in middle dose group and high dose group(all P<0.05). Compared with control group, the expression levels of calnexin, calreticulin, GRP78, IRE1, CHOP proteins and mRNAs in low dose group remained unchanged (all P>0.05), while the expression levels of calnexin and calreticulin proteins and mRNAs decreased significantly, GRP78, IRE1, CHOP proteins and mRNAs expression levels increased significantly in middle dose group and high dose group(all P<0.05). Conclusion Aloe-emodin can induce apoptosis and reduce cell proliferation rate possibly through influencing the Calnexin/Calreticulin cycle of SGC-7901 cells, activating GRP78/IRE1/CHOP signaling pathway and aggravating ERS of gastric cancer cells.