Fine particulate matter (PM2 5) with diameters of less than 2.5 |xm can lead to many diseases in human.According to the results of epidemiological studies, PM25 can injury human reproductive system, hut the mechanism of reproductive injury is rarely reported.This study aimed to investigate the protective effect and mechanism of curcumin (CRC) on short-term exposure to PM2 5-induced rat uterine injury.Fifty Sprague-Dawley rats were randomly divided into control group, P.\l2 5 exposure group, PM15 +CRC-L group, PM2 5+CRC-H group and PM2 5 + VE group, which all were administered for 30 days.After a short-term exposure, PM2 s induced atrophy of endometrial epithelial cells and structural damage of endometrial glands and stromal cells.At the same time, these conditions were improved after administered with curcumin and VE.The results of TUNEL detection showed that the cell apoptosis rate (48.81 ±8.27)% in PM2 s exposure group was significantly higher than that in control group (P<0.05).Compared to PM25 exposure group, the uterine cell apoptosis rates in two curcumin groups were attenuated, and the cell apoptosis rate was significantly decreased in PM>5+CRC-H group (P<0.05).Compared to control group, the levels of reactive oxygen species (ROS) were significantly higher (P< 0.05) and the level of total antioxidant capacity (T-AOC) was significantly lower (P<0.05) in PM15 exposure group.However, curcumin and VE could attenuate PM2 5- induced oxidative stress in rat uterus.CRC and VE inhibited proteins phosphorylation of ASK 1, JNK, p38 and activation of caspase-3 induced by PM25(P<0.05).Moreover, curcumin significantly inhibited the protein expression levels of p-ASKl, p-JNK, p-p38 and cleaved caspase-3 induced by PM25.In conclusion, curcumin attenuates short-term exposure to PIV12 5-induced uterine injury by inhibiting the signal pathway of JNK-p38-caspase-3 mediated by ASK 1.