OBJECTIVE: Investigated the effects of N-acetylcysteine (NAC) on endoplasmic reticulum stress of sertoli cells induced by sodium fluoride (NaF). METHODS: Rat sertoli cells were exposed to various concentration of (0, 6, 12, 24 µg/ml) sodium fluoride with or without 2 mmol/L NAC for 24 hours. The cell viability was evaluated using trypan blue exclusion test. Intracellular reactive oxygen species (ROS) was measured using the fluorescent probe DCFH-DA. Western blot was used to test the expression of GRP78, PERK and CHOP. RESULTS: It was found that treatment with NAC (2 mmol/L) restored the reduced cell viability and excessive oxidative stress (P < 0.01). Moreover, fluoride exposure upregulated the expression of GRP7 8, PERK and CHOP protein (P <0. 01 ). NAC was also found to suppress the levels of GRP78, PERK and CHOP expression in NaF-treated cells (p<0.01). CONCLUSION: Endoplasmic reticulum stress signaling pathways were activated by ROS, and NAC attenuate endoplasmic reticulum stress through inhibiting the levels of ROS in NaF-treated sertoli cells.
OBJECTIVE: Investigated the effects of N-acetylcysteine (NAC) on endoplasmic reticulum stress of sertoli cells induced by sodium fluoride (NaF). METHODS:Rat sertoli cells were exposed to various concentration of (0, 6, 12, 24 µg/ml) sodium fluoride with or without 2 mmol/L NAC for 24 hours. The cell viability was evaluated using trypan blue exclusion test. Intracellular reactive oxygen species (ROS) was measured using the fluorescent probe DCFH-DA. Western blot was used to test the expression of GRP78, PERK and CHOP. RESULTS: It was found that treatment with NAC (2 mmol/L) restored the reduced cell viability and excessive oxidative stress (P < 0.01). Moreover, fluoride exposure upregulated the expression of GRP7 8, PERK and CHOP protein (P <0. 01 ). NAC was also found to suppress the levels of GRP78, PERK and CHOP expression in NaF-treated cells (p<0.01). CONCLUSION: Endoplasmic reticulum stress signaling pathways were activated by ROS, and NAC attenuate endoplasmic reticulum stress through inhibiting the levels of ROS in NaF-treated sertoli cells.