OBJECTIVE: Investigated the effects of @entity898 (NAC) on endoplasmic reticulum stress of sertoli cells induced by @entity3163 ( @entity7034 ). METHODS: @entity35 sertoli cells were exposed to various concentration of (0, 6, 12, 24   g/ml) @entity3163 with or without 2 mmol/L NAC for 24 hours. The cell viability was evaluated using @entity3460 exclusion test. Intracellular reactive @entity26 species (ROS) was measured using the fluorescent probe @entity21184 . Western blot was used to test the expression of @entity21205 , PERK and @entity21206 . RESULTS: It was found that treatment with NAC (2 mmol/L) restored the reduced cell viability and excessive oxidative stress (P < 0.01). Moreover, @entity1388 exposure upregulated the expression of @entity21205 , PERK and @entity21206 protein (P <0. 01 ). NAC was also found to suppress the levels of @entity21205 , PERK and @entity21206 expression in @entity7034 -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 @entity7034 -treated sertoli cells.

[Effects. of XXXX on @entity1388 -induced endoplasmic reticulum stress in sertoli cells].

@entity21206 :: ('29467(Tax:10116)', 'Gene') :: ['CHOP'] @entity3163 :: ('MESH:D012969', 'Chemical') :: ['sodium fluoride'] @entity35 :: ('10116', 'Species') :: ['Rat'] @entity26 :: ('MESH:D010100', 'Chemical') :: ['oxygen'] @entity21205 :: ('25617(Tax:10116)', 'Gene') :: ['GRP7 8', 'GRP78'] @entity898 :: ('MESH:D000111', 'Chemical') :: ['N-acetylcysteine'] @entity21184 :: ('MESH:C029569', 'Chemical') :: ['DCFH-DA'] @entity3460 :: ('MESH:D014343', 'Chemical') :: ['trypan blue'] @entity7034 :: ('CHEBI:28741', 'Chemical') :: ['NaF'] @entity1388 :: ('MESH:D005459', 'Chemical') :: ['fluoride']
@entity898 :: (MESH:D000111,Chemical) :: ['N-acetylcysteine']
