Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation

Bo, Qingli; Chen, Yuan-Hua; Yu, Zhen; Fu, Lin; Zhou, Yan; Zhang, Guibin; Wang, Hua; Zhang, Zhihui; D, Xu

doi:10.1016/j.mce.2016.01.004

Cited by 29 publications

(25 citation statements)

References 66 publications

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“…**P<.01 agreement with previous study, in which IL-10 was obviously increased in maternal serum, placenta, and amniotic fluid in response to LPS [35][36][37]. Pregnant mice were administered with LPS or VitD3 as in Materials and Methods.…”

supporting

confidence: 84%

“…These results are in agreement with previous study, in which IL-10 was obviously increased in maternal serum, placenta, and amniotic fluid in response to LPS. [35][36][37] The present study then investigated the effects of VitD3 on IL-10 in maternal serum. Surprisingly, VitD3 pretreatment further elevated serum IL-10 level in LPS-treated mice.…”

Section: Discussionmentioning

confidence: 99%

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Vitamin D3 pretreatment protects against lipopolysaccharide-induced early embryo loss through its anti-inflammatory effects

Zhou

Chen

et al. 2017

Am J Reprod Immunol

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supporting

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Vitamin D3 pretreatment protects against lipopolysaccharide-induced early embryo loss through its anti-inflammatory effects

Zhou

Chen

et al. 2017

Am J Reprod Immunol

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“…PPAR‐γ is also an orphan nuclear receptor. A previous report from our laboratory indicated that rosiglitazone, a specific PPAR‐γ agonist, blocked the activation of NF‐κB in mouse placentas 33 . The article found that nuclear translocation of PPAR‐γ and NF‐κB p65 was remarkably elevated in mononuclear sinusoidal trophoblast giant cells of the labyrinth layer.…”

Section: Discussionmentioning

confidence: 89%

“…Accumulative data have demonstrated that NF‐κB p65 suppresses the activity of several orphan nuclear receptors, such as pregnane X receptor (PXR) and vitamin D receptor (VDR) in human primary hepatocytes, mouse kidneys, and mouse placentas 29,31‐36 . PPAR‐γ is also an orphan nuclear receptor.…”

Section: Discussionmentioning

confidence: 99%

Association among placental 11β‐HSD2, PPAR‐γ, and NF‐κB p65 in small‐for‐gestational‐age infants: A nested case‐control study

Gan

et al. 2020

American J Rep Immunol

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Problem: 11β-Hydroxysteroid dehydrogenase 2 (11β-HSD2) catalyzes active glucocorticoids into their inactive products, preventing the passage of glucocorticoids into the fetus from maternal circulation. Peroxisome proliferator-activated receptor (PPAR)γ is a member of the nuclear receptor superfamily that regulates the expression of placental 11β-HSD2. Nuclear factor-kappa B (NF-κB) is a transcription factor that regulates inflammatory signaling. This study aimed to investigate the association among 11β-HSD2, PPAR-γ, and NF-κB p65 in small-for-gestational-age (SGA) infants. Method of study:Forty-six SGA and 46 appropriate-for-gestational-age (AGA) infants were enrolled in this study. Both newborns and placentas were weighed.Placental 11β-HSD2 levels were measured using Western blotting. Placental PPAR-γ and NF-κB p65 were detected by immunohistochemistry. Placental inflammatory cytokines were evaluated by real-time RT-PCR.Results: 11β-HSD2 levels were lower in SGA placentas than those in AGA placentas.Placental PPAR-γ-positive nuclei were less in SGA than those in AGA. By contrast, placental NF-κB p65-positive nuclei were more in SGA than those in AGA. The levels of CRP, , several inflammatory cytokines, were higher in SGA placentas. Correlation analysis showed that neonatal weight was positively associated with PPAR-γ and 11β-HSD2 in SGA placentas. By contrast, neonatal weight was inversely correlated with NF-κB p65 in SGA placentas. 11β-HSD2 was positively correlated with PPAR-γ in SGA placentas.

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“…Prostaglandins synthesized after Ptgs2 induction by LPS administration contribute to cervical ripening and other endpoints of parturition, and suppression of Ptgs2 with specific inhibitors can modulate LPS-induced PTD rate56. Pretreatment with rosiglitazone, which promotes placental synthesis of peroxisome proliferator-activated receptor-γ (PPARγ) similarly attenuates responsiveness to LPS-induced PTD, in association with suppressed NFκB signaling and reduced synthesis of TNF, IL1, IL6 and other pro-inflammatory chemokines57. Thus the current study adds to considerable evidence that TLR-driven inflammatory signaling can be attenuated to effectively reduce susceptibility to preterm birth.…”

Section: Discussionmentioning

confidence: 99%

Novel Toll-like receptor-4 antagonist (+)-naloxone protects mice from inflammation-induced preterm birth

Chin

Dorian

Hutchinson

et al. 2016

Sci Rep

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Toll-like receptor 4 (TLR4) activation by bacterial infection, or by sterile inflammatory insult is a primary trigger of spontaneous preterm birth. Here we utilize mouse models to investigate the efficacy of a novel small molecule TLR4 antagonist, (+)-naloxone, the non-opioid isomer of the opioid receptor antagonist (−)-naloxone, in infection-associated preterm birth. Treatment with (+)-naloxone prevented preterm delivery and alleviated fetal demise in utero elicited by i.p. LPS administration in late gestation. A similar effect with protection from preterm birth and perinatal death, and partial correction of reduced birth weight and postnatal mortality, was conferred by (+)-naloxone administration after intrauterine administration of heat-killed E. coli. Local induction by E. coli of inflammatory cytokine genes Il1b, Il6, Tnf and Il10 in fetal membranes was suppressed by (+)-naloxone, and cytokine expression in the placenta, and uterine myometrium and decidua, was also attenuated. These data demonstrate that inhibition of TLR4 signaling with the novel TLR4 antagonist (+)-naloxone can suppress the inflammatory cascade of preterm parturition, to prevent preterm birth and perinatal death. Further studies are warranted to investigate the utility of small molecule inhibition of TLR-driven inflammation as a component of strategies for fetal protection and delaying preterm birth in the clinical setting.

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Rosiglitazone pretreatment protects against lipopolysaccharide-induced fetal demise through inhibiting placental inflammation

Cited by 29 publications

References 66 publications

Vitamin D3 pretreatment protects against lipopolysaccharide-induced early embryo loss through its anti-inflammatory effects

Vitamin D3 pretreatment protects against lipopolysaccharide-induced early embryo loss through its anti-inflammatory effects

Association among placental 11β‐HSD2, PPAR‐γ, and NF‐κB p65 in small‐for‐gestational‐age infants: A nested case‐control study

Novel Toll-like receptor-4 antagonist (+)-naloxone protects mice from inflammation-induced preterm birth

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