Objective To compare the effects of different local intervention temperatures of pressure ulcer on endoplasmic reticulum stress (ERS) and apoptosis in rats, and to provide an experimental evidence for clinical prevention and treatment of pressure ulcer. Methods The rat model of pressure ulcer was established by ischemia reperfusion, and a total of 40 SPF adult, male SD rats were divided into 4 groups: the sham group (anesthesia only, without other treatment), model group (ischemia at 22℃ for 1 h and reperfusion at 22℃ as one cycle, repeated for 5 cycles), high-temperature intervention group (ischemia at 22℃ for 1 h and reperfusion at 32℃ as one cycle, repeated for 5 cycles) and low-temperature intervention group (ischemia at 22℃ for 1 h and reperfusion at 12℃ as one cycle, repeated for 5 cycles). At the end of the experiment, muscle tissues at the sites under pressure of the rats were taken on ice. The pathological changes of skeletal muscle tissues were observed by HE staining. The expression levels of ERS-related proteins GRP78, caspase-12 and CHOP were detected by Western blot, and the expression of caspase-12 and CHOP was also observed by immunofluorescence. Moreover, apoptosis in the skeletal muscle cells was examined by TUNEL staining. Results Compared with the model group, skeletal muscle cell damages became more severe and apoptotic cells were increased in the high-temperature intervention group. Besides, the results of the immunofluorescence assay showed an increased positive expression of caspase-12 and CHOP, and the results of Western blot showed that the expression levels of GRP78, caspase-12 and CHOP were all higher than those of the model group (P < 0.05). In contrast, skeletal muscle cell damages were alliviated and apoptotic cells were reduced in the low-temperature intervention group. Meanwhile, the positive expression of caspase-12 and CHOP was decreased, as shown by immunofluorescence, and all the expression levels of GRP78, caspase-12 and CHOP detected by Western blot were lower than the control group (P < 0.05). Conclusions Local low-temperature intervention can alleviate the pressure ulcer damages in rats through inhibition of the ERS-mediated apoptotic pathway. Local high-temperature intervention may exacerbate the pressure ulcer damages in rats by activating the ERS-mediated apoptotic pathway and promoting cell apoptosis. Local low?temperature intervention may be promising in clinical prevention and treatment of pressure ulcer.