Buathong Norathee, Poonyachoti Sutthasinee, Deachapunya Chatsri
J Med Assoc Thai. 2015 Oct;98 Suppl 9:S31-8.
The present study aimed to investigate whether genistein, a potent phytoestrogen mainly found in soybean, modulated the expression of TLRs 2, 3, 4 and 9 proteins in human endometrial epithelial cell line RL95-2 under basal and polyinosinic-polycytidylic acid (poly I: C) stimulated conditions to mimic viral infection. The genistein effects were also compared with 17β-estradiol.
The RL95-2 cells were cultured in the estrogen-deprived media with or without poly I: C 30 min prior to incubation with genistein (10(-7), 10(-6) or 10(-5) M) or 17β-estradiol (10(-9) M) for 48 h. The TLRs protein expression was analyzed by semi-quantitative Western blot.
The cells expressed TLRs 3, 4 and 9 but a very low level of TLR2 proteins. Poly I: C significantly increased the TLRs 2 and 9 protein expressions whereas the TLRs 3 and 4 were reduced. Under basal condition, genistein at 10(-7) M increased the TLR2 while 17β-estradiol decreased the TLR4. All concentrations of genistein and 17β-estradiol attenuated the poly I: C induced increase in the TLR2. By contrast, both genistein at 10(-5) M and 17 β-estradiol further potentiated the TLR4 suppressed by poly I: C. Only 17β-estradiol was found to antagonize the poly I: C-induced changes in TLRs 3 and 9.
Taken together, the present results that genistein increased the basal TLR2 and attenuated the viral component-induced TLR2 protein expression in human endometrial epithelial cells may indicate the potential role of this soy isoflavone in promoting the uterine immune function and probably alleviating the inflammation of endometrium following pathogen
本研究旨在调查金雀异黄素（一种主要存在于大豆中的强效植物雌激素）是否在基础条件和聚肌苷酸-聚胞苷酸（poly I：C）刺激条件下调节人子宫内膜上皮细胞系RL95-2中Toll样受体（TLRs）2、3、4和9蛋白的表达，以模拟病毒感染。还将金雀异黄素的作用与17β-雌二醇进行了比较。
在与金雀异黄素（10⁻⁷、10⁻⁶或10⁻⁵M）或17β-雌二醇（10⁻⁹M）孵育48小时前30分钟，将RL95-2细胞在雌激素缺乏的培养基中培养，添加或不添加poly I：C。通过半定量蛋白质印迹法分析TLRs蛋白表达。
细胞表达TLRs 3、4和9，但TLR2蛋白水平极低。Poly I：C显著增加TLRs 2和9的蛋白表达，而TLRs 3和4减少。在基础条件下，10⁻⁷M的金雀异黄素增加TLR2，而17β-雌二醇降低TLR4。所有浓度的金雀异黄素和17β-雌二醇均减弱了poly I：C诱导的TLR2增加。相比之下，10⁻⁵M的金雀异黄素和17β-雌二醇均进一步增强了poly I：C抑制的TLR4。仅发现17β-雌二醇拮抗poly I：C诱导的TLRs 3和9的变化。
综上所述，本研究结果表明金雀异黄素增加人子宫内膜上皮细胞的基础TLR2并减弱病毒成分诱导的TLR2蛋白表达，这可能表明这种大豆异黄酮在促进子宫免疫功能以及可能减轻病原体感染后子宫内膜炎症方面的潜在作用。
