共轭亚油酸通过在水牛颗粒细胞中抑制核因子-κB（NF-κB）经过过氧化物酶体增殖物激活受体γ（PPARγ）的易位，减轻脂多糖（LPS）诱导的促炎基因表达。
Conjugated linoleic acids attenuate LPS-induced pro-inflammatory gene expression by inhibiting the NF-κB translocation through PPARγ in buffalo granulosa cells.
作者信息
Yenuganti Vengala Rao, Ravinder Ravinder, Singh Dheer
机构信息
Molecular Endocrinology Laboratory, Animal Biochemistry Division, National Dairy Research Institute, Karnal, India.
出版信息
Am J Reprod Immunol. 2014 Sep;72(3):296-304. doi: 10.1111/aji.12261. Epub 2014 May 5.
PROBLEM
In granulosa cells, TLR4-mediated LPS-induced immune response interferes with ovarian granulosa cell function.
METHOD OF STUDY
LPS-induced pro-inflammatory gene expression was monitored by real-time PCR and NF-κB was determined by the immuno-blotting and immuno-staining in granulosa cells in vitro.
RESULTS
The LPS (1 μg/mL) increased pro-inflammatory gene expression which was reverted back by treatment with TLR4 signaling inhibitor. Cotreatment of CLA (10 μm) with LPS did not show any effect on LPS-induced pro-inflammatory gene expression but granulosa cells pre-treated with CLA for 24 hr, attenuated LPS-induced pro-inflammatory gene expression and nuclear NF-κB. GW9662, a PPARγ-inhibitor, further increased the expression of pro-inflammatory genes.
CONCLUSION
The present findings reiterated that pre-treatment with CLA can prevent LPS-induced granulosa cells dysfunction.
问题
在颗粒细胞中，Toll样受体4（TLR4）介导的脂多糖（LPS）诱导的免疫反应会干扰卵巢颗粒细胞功能。
研究方法
通过实时聚合酶链反应（PCR）监测LPS诱导的促炎基因表达，并通过免疫印迹和免疫染色法在体外颗粒细胞中测定核因子κB（NF-κB）。
结果
LPS（1μg/mL）增加了促炎基因表达，而用TLR4信号抑制剂处理可使其恢复。共轭亚油酸（CLA，10μm）与LPS共同处理对LPS诱导的促炎基因表达没有任何影响，但预先用CLA处理24小时的颗粒细胞可减弱LPS诱导的促炎基因表达和核NF-κB。PPARγ抑制剂GW9662进一步增加了促炎基因的表达。
结论
目前的研究结果重申，预先用CLA处理可预防LPS诱导的颗粒细胞功能障碍。
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