Department of Gynecology and Obstetrics, Wuxi Maternal and Child Health Hospital, The Affiliated Hospital of Nanjing Medical University, Wuxi, Jiangsu, 214002, China.
Department of Gynecology and Obstetrics, Wuxi Maternal and Child Health Hospital, The Affiliated Hospital of Nanjing Medical University, Wuxi, Jiangsu, 214002, China.
Biochem Biophys Res Commun. 2018 Oct 12;504(4):834-842. doi: 10.1016/j.bbrc.2018.09.035. Epub 2018 Sep 12.
Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific hepatic disorder with potentially deleterious consequences of fetuses. Although the intimate relationship between ICP and peroxisome proliferator-activated receptor γ (PPARγ) has been previously reported in physiological and pathological conditions, the detailed mechanisms in the process of intrahepatic cholestasis of pregnancy has been unclear. The aims of this study are to assess the role of PPARγ regulating the reactive oxygen species (ROS) and inflammation in the process of the ICP.
Clinical data of the pregnant women were collected. And the serum of cytokines, hepatic function, the expression of PPARγ and NF-κB were measured. The rat and fetal rat ICP model were constructed and detection of the expression of PPARγ and NF-κB, evaluation the level of ROS and inflammation.
The clinical data showed that the new-born information in severe ICP group were significantly different as compared to that in control group (P < 0.05), and part of information in mild ICP group were also difference to that in control group (P < 0.05). The expression of PPARγ and NF-κB were significantly higher in clinical pregnant women, rat, fetal rat ICP model groups and taurocholate acid (TCA) treated HTR-8/SVneo cell (P < 0.01). PPARγ inhibited the production of ROS and decreased the level of inflammation. PPARγ down-regulated the NF-κB pathway.
PPARγ provides the anti-inflammatory and protective effects in intrahepatic cholestasis of pregnancy through NF-κB pathway, which might be a probably one of the mechanisms of ICP.
妊娠肝内胆汁淤积症（ICP）是一种与妊娠相关的肝脏疾病，可能对胎儿产生有害影响。尽管已经在生理和病理条件下报道了 ICP 与过氧化物酶体增殖物激活受体γ（PPARγ）之间的密切关系，但 ICP 发生过程中的详细机制尚不清楚。本研究旨在评估 PPARγ 在调节活性氧（ROS）和炎症过程中在 ICP 中的作用。
收集孕妇的临床数据。测量细胞因子、肝功能、PPARγ 和 NF-κB 的表达。构建大鼠和胎鼠 ICP 模型，检测 PPARγ 和 NF-κB 的表达，评估 ROS 和炎症水平。
临床数据显示，重度 ICP 组的新生儿信息与对照组有显著差异（P < 0.05），轻度 ICP 组的部分信息也与对照组有差异（P < 0.05）。临床孕妇、大鼠、胎鼠 ICP 模型组和牛磺胆酸（TCA）处理的 HTR-8/SVneo 细胞中 PPARγ 和 NF-κB 的表达均显著升高（P < 0.01）。PPARγ 抑制 ROS 的产生并降低炎症水平。PPARγ 下调 NF-κB 通路。
PPARγ 通过 NF-κB 通路在妊娠肝内胆汁淤积症中提供抗炎和保护作用，这可能是 ICP 的机制之一。
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