【摘要】 为了探索肝脏X受体（LXRα）对脂多糖（LPS）诱导的奶牛子宫内膜上皮细胞炎症反应的调节机制，研究采用小鼠体内试验及奶牛子宫内膜上皮细胞体外试验，用LXRα激动剂T0901317激活LXRα,子宫灌注0.2 mg/mL LPS 50μL,检测奶牛子宫内膜上皮细胞活性、肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）、亚硝酸盐、前列腺素E₂（PGE₂）等炎性细胞因子的表达情况，对核因子κB（NF-κB）、糖原合成酶激酶3β（GSK3β）-重组与合成蛋白（Nrf2）信号通路的影响。结果表明：10,20,40μmol/L的T0901317对奶牛子宫内膜上皮细胞没有毒性作用，对TNF-α、IL-1β、亚硝酸盐、PGE₂的表达具有极显著的抑制作用（P<0.01）,可降低磷酸化蛋白65（p-p65）、磷酸化蛋白ⅠκB（p-ⅠκB）的磷酰化水平，提高磷酸化葡萄糖合成激酶3β（p-GSK3β）、Nrf2及Nrf2调控的抗氧化因子血红素氧化酶-1（HO-1）的表达。说明LXRα可以通过调节GSK3β-Nrf2信号通路抑制LPS诱导的子宫内膜炎症。更多还原

【Abstract】 In order to explore the regulatory mechanism of liver X receptor（LXRα） on lipopolysaccharide（LPS） induced inflammatory response in dairy cow endometrial epithelial cells, in this experiment, in vivo test of mice and in vitro test of dairy cow endometrial epithelial cells were employed; LXRα was activated with LXRα agonist T0901317 and uterine perfusion of 0.2 mg/mL LPS 50 μL was carried out for the determination of dairy cow endometrial epithelial cell activity, the expression of inflammatory cytokines such as tumor necrosis factor α（TNF-α）, interleukin-1β（IL-1β）, nitrite, and prostaglandin E₂（PGE₂）, as well as its effect on nuclear factor κB（NF-κB）, glycogen synthetase kinase 3β（GSK3β）-synthetic protein（Nrf2） signaling pathways. The results showed that T0901317 of 10, 20, 40 μmol/L had no toxic effect on dairy cow endometrial epithelial cells, and had very significant inhibitory effect on the expression of TNF-α, IL-1β, nitrite and PGE₂（P<0.01）, which could reduce the phosphorylation levels of phosphorylated protein 65（p-p65） and phosphorylated protein Ⅰ κB（p-Ⅰ κB）, and increase the expression of phosphorylated glucose synthesis kinase 3β（p-GSK3β）, recombinant and Nrf2 and Nrf2-regulated antioxidant factor heme oxidase-1（HO-1）. The results suggested that LXRα could inhibit LPS-induced endometrial inflammation by regulating the GSK3β-Nrf2 signaling pathway.更多还原