The oxidation of low-density lipoproteins (oxLDL) is considered as a key step in the development of atherosclerosis. Oxysterols such as 7-ketocholesterol (7-KC) have been reported to be partially responsible for the cytotoxicity of oxLDL and induce endoplasmic reticulum (ER) stress which eventually causes apoptosis. We aimed to investigate whether ER stress is induced by 7-KC and can be prevented by the kimchi methanol extract (KME) in RAW264.7 macrophage cells. ER stress induced by 7-KC was characterized by the activation of ER stress markers (GRP78, CHOP, and ATF6). ER stress could aggravate macrophage apoptosis, as assessed by caspase-3 activity. ER stress and apoptosis were inhibited by the KME and glutathione (GSH). We conclude that 7-KC causes aberrant ER stress and apoptosis, all of which are inhibited by KME and GSH. The inhibitory expression of ER stress markers highlights its new protective role against oxLDL-induced ER stress, apoptosis, and subsequent atherosclerosis.