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PPARγ provides anti-inflammatory and protective effects in intrahepatic cholestasis of pregnancy through NF-κB pathway
- Zhang, Yan, Huang, Xiaoping, Zhou, Jie, Yin, Yongxiang, Zhang, Ting, Chen, Daozhen
- Biochemical and biophysical research communications 2018 v.504 no.4 pp. 834-842
- blood serum, cytokines, fetus, inflammation, intrahepatic cholestasis, liver function, models, peroxisome proliferator-activated receptors, pregnancy, pregnant women, protective effect, rats, reactive oxygen species, transcription factor NF-kappa B
- 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.