Objective       To investigate the mechanism of oxidative damage caused by sodium fluoride (NaF) through detecting inflammation-related factors and signaling pathway molecules in rats.       Methods       NaF poisoning model was established. Thirty adult female SD rats

which had no difference in age and weight

were randomly divided into 3 groups (10 in each group)

and then fed with pure water (control group)

100 mg/L NaF (100 mg/L NaF-exposed group) and 200 mg/L NaF (200 mg/L NaF-exposed group)

respectively

for 180 days. Inflammation-related factors Cox-2

ICAM-1

TNF-α and IL-1β were measured by Western blotting and immunohistochemistry

and oxidative stress-related factors ROS

MDA

SOD

CAT and GSH were detected by ELISA. In addition

signaling pathway molecules P38

ERK

JNK and PI3K were analyzed by Western blot.       Results       Cox-2

ICAM-1

TNF-α and IL-1β were highly expressed in the endometria of the rats exposed to NaF (P0.05). The levels of ROS

SOD

CAT and GSH were higher in the NaF-exposed groups

but the MDA level was lower compared with the control group (P0.05). In the NaF-exposed groups

phosphorylation levels of P38 and JNK were significantly increased. Though ERK and PI3K proteins and their phosphorylation levels were also increased in the NaF-exposed groups

there was no significant difference between the NaF-exposed groups and the control group.       Conclusion       NaF activates P38 and JNK via induction of oxidative stress to promote inflammation of the endometria in the rats.