Objective: To study the protective effect of zeaxanthin on endoplasmic reticulum stress-induced apoptosis. The research was divided into blank control group， TM injury group (5 μg/mL)， zeaxanthin protection group (5 μmol/L) and injury plus protection group. The Caspase 3 activity detection kit is used for detecting changes of Caspase 3 enzyme activity. The apoptosis-related proteins PERK and CHOP， the downstream signal molecules elF2α and ATF4 of PERK， and the autophagy-related protein Beclin 1 were determined by Western Blot. The results showed that compared with the TM model group， the expressions of PERK and its downstream regulatory proteins elF2α and ATF4 after zeaxanthin treatment were significantly decreased (P<0.01)， and the level of Beclin 1 was significantly increased (P<0.01). The level of GRP78 in the zeaxanthin group was significantly higher than that in the absence of 3MA autophagy inhibitor (P<0.01). Compared with the control group， the CHOP protein expression level in the TM model group was significantly increased (P<0.01)， while the CHOP protein expression level in the zeaxanthin treatment group was significantly lower than that in the TM model group (P<0.01). Conclusion: Zeaxanthin can reduce the damage caused by endoplasmic reticulum stress and reverse the damage caused by TM to a certain extent. The mechanism is that by inhibiting the PERK pathway and further inhibiting the separation of GRP78 and ERS receptors， the level of pro-apoptotic factor CHOP is reduced， and alleviate ERS by regulating protective autophagy.