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Reprod Toxicol ; 60: 148-55, 2016 04.
Article in English | MEDLINE | ID: mdl-26686910

ABSTRACT

ß-cryptoxanthin (CX), a major carotenoid pigment, can inhibit inflammatory gene expression in mice with nonalcoholic steatohepatitis. In the present study, we examined the anti-inflammatory effects of CX on lipopolysaccharide (LPS)-induced inflammation in mouse primary Sertoli cells and the possible molecular mechanisms behind its effects. The results showed that CX significantly inhibited LPS-induced decreases in cell viability and in the percentage of apoptotic cells. Moreover, CX inhibited the LPS-induced up-regulation of tumor necrosis factor α (TNF-α), interleukin-10 (IL-10), interleukin-6 (IL-6) and interleukin-1ß (IL-1ß) in Sertoli cells. In addition, CX significantly limited the LPS-induced down-regulation of AR, HSF2, CREB, FSHR, INHBB and ABP in Sertoli cells. Western blot analysis showed that CX significantly suppressed NF-κB (p65) activation as well as MAPK phosphorylation. All the results suggested that CX suppressed inflammation, possibly associated with the NF-κB activation and MAPK of phosphorylation. Thus, CX may possess therapeutic potential against inflammation-related diseases.


Subject(s)
Anti-Inflammatory Agents/pharmacology , Beta-Cryptoxanthin/pharmacology , Sertoli Cells/drug effects , Animals , Apoptosis/drug effects , Cell Survival/drug effects , Cytokines/genetics , Lipopolysaccharides , Male , Mice , Mitogen-Activated Protein Kinases/metabolism , NF-kappa B/metabolism , Phosphorylation/drug effects , RNA, Messenger/metabolism , Sertoli Cells/metabolism , Spermatogenesis/genetics
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