“…PPARγ, a transcription factor involved in glycolipid metabolism 87 , is involved in placental cell metabolism, anti-inflammatory pathways, and oxidative stress 88 . PPARγ can regulate NFκB signal, inhibit its DNA binding activity, and promote its degradation 89 90 . In multiple studies, PPARgamma appears to be downregulated in the placenta of PE patients 91 92 .…”
Section: Pro-inflammatory or Anti-inflammatory Factors Affect Nfκb Si...mentioning
The high prevalence of preeclampsia (PE) is a major cause of maternal and fetal mortality and affects the long-term prognosis of both mother and baby. Termination of pregnancy is currently the only effective treatment for PE, so there is an urgent need for research into its pathogenesis and the development of new therapeutic approaches. The NFκB family of transcription factors has an essential role in inflammation and innate immunity. In this review, we summarize the role of NFκB in normal and preeclampsia pregnancies, the role of NFκB in existing treatment strategies, and potential NFκB treatment strategies.
“…PPARγ, a transcription factor involved in glycolipid metabolism 87 , is involved in placental cell metabolism, anti-inflammatory pathways, and oxidative stress 88 . PPARγ can regulate NFκB signal, inhibit its DNA binding activity, and promote its degradation 89 90 . In multiple studies, PPARgamma appears to be downregulated in the placenta of PE patients 91 92 .…”
Section: Pro-inflammatory or Anti-inflammatory Factors Affect Nfκb Si...mentioning
The high prevalence of preeclampsia (PE) is a major cause of maternal and fetal mortality and affects the long-term prognosis of both mother and baby. Termination of pregnancy is currently the only effective treatment for PE, so there is an urgent need for research into its pathogenesis and the development of new therapeutic approaches. The NFκB family of transcription factors has an essential role in inflammation and innate immunity. In this review, we summarize the role of NFκB in normal and preeclampsia pregnancies, the role of NFκB in existing treatment strategies, and potential NFκB treatment strategies.
“…Alzheimer’s disease (AD) is a cerebral neurodegenerative disease with memory loss and cognitive decline as the main clinical symptoms [ 1 ]. Currently, the etiology of AD remains unclear and there are no effective measures for its clinical prevention and treatment [ 2 ].…”
Aim: We investigated the effects and targets of gastrodin (GAS) for improving cognitive ability in Alzheimer's disease (AD). Methods: The targets and mechanisms of GAS were analyzed by network pharmacology. Morris water and eight-arm radial mazes were used to detect the behaviors of 7-months-old APP/PS1 mice. The levels of IBA-1 and PPARγ were examined by histochemical staining, nerve cells were detected by Nissl staining, inflammatory cytokines were measured by ELISA, and protein expressions were monitored by Western blotting. The neurobehavioral effects of GAS on mice were detected after siRNA silencing of PPARγ. Microglia were cultured in vitro and Aβ1-42 was used to simulate the pathology of AD. After treatment with GAS, the levels of inflammatory cytokines and proteins were assayed. Results: Network pharmacological analysis revealed that PPARγ was the action target of GAS. By stimulating PPARγ, GAS inhibited NF-κB signaling activation and decreased neuroinflammation and microglial activation, thereby ameliorating the cognitive ability of AD mice. After silencing PPARγ, GAS could not further improve such cognitive ability. Cellular-level results demonstrated that GAS inhibited microglial injury, reduced tissue inflammation, and activated PPARγ. Conclusions: GAS can regulate microglia-mediated inflammatory response by stimulating PPARγ and inhibiting NF-κB activation, representing a mechanism whereby it improves the cognitive behavior of AD.
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