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Last update 08 May 2025

fetal inflammatory response syndrome

Last update 08 May 2025

Basic Info

Synonyms

FIRS fetal inflammatory response syndrome, LPS-induced FIRS, LPS-induced fetal inflammatory response syndrome

+ [7]

Introduction-

Drugs associated with fetal inflammatory response syndrome

Resatorvid

Target

TLR4

Mechanism

TLR4 antagonists

Active Org.

Yaqrit Ltd.

Originator Org.

Takeda Pharmaceutical Co., Ltd.

Active Indication

Acute-On-Chronic Liver Failure [+2]

Inactive Indication

fetal inflammatory response syndrome [+4]

Drug Highest PhasePhase 2

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

BI-653048

Target

Mechanism

GR modulators

Active Org.-

Originator Org.

Boehringer Ingelheim GmbH

Active Indication-

Inactive Indication

Arthritis [+2]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with fetal inflammatory response syndrome

ChiCTR2500095884

/ SuspendedNot ApplicableIIT

Correlation analysis Between Fetal Inflammatory Response Syndrome and Brain Injury in Premature Infants

Start Date20 Jan 2025

Sponsor / Collaborator-

NCT05717933

/ Not yet recruitingNot ApplicableIIT

Thyroid Function Among Pediatric Patients With Type 1 Diabetes Mellitus at Firs Presentation, From Patients' Characteristics to Disease Severity

Thyroid function among pediatric patients with type1 diabetes mellitus at the first presentation, from patients' characteristics to disease severity

Start Date01 Feb 2023

Sponsor / Collaborator

Assiut University

ChiCTR2100052175

/ SuspendedNot ApplicableIIT

Association Between Fetal Inflammatory Response Syndrome and Bronchopulmonary Dysplasia in Premature Infants: A Case-Control Study

Start Date20 Oct 2021

Sponsor / Collaborator-

100 Clinical Results associated with fetal inflammatory response syndrome

100 Translational Medicine associated with fetal inflammatory response syndrome

0 Patents (Medical) associated with fetal inflammatory response syndrome

1,174

Literatures (Medical) associated with fetal inflammatory response syndrome

01 Dec 2025·Inflammation Research

Luteolin modulates liver macrophage subtype polarization and play protective role in sepsis induced acute hepatic injury

Article

Author: Deng, Liangyong ; Kuang, Gang ; Ye, Lin ; Yu, Qiulei ; Fan, Jing ; Wang, Liuyang

BACKGROUNDLuteolin has an anti-inflammatory effect, but the mechanism has not been elucidated in sepsis-induced acute hepatic injury (AHI). The purpose of this study was to investigate the effects and potential mechanisms of luteolin on sepsis-induced AHI.METHODSIn this study, we utilized both wild-type (WT) mice and Toll-like receptor 4 (TLR4)-deficient (TLR4^-/-) mice alongside RAW264.7 cells. We constructed a CLP-induced AHI mouse model to study the effects of luteolin on liver inflammation, survival and liver macrophage subtypes in mice. In addition, we extracted mouse serum, mouse bone marrow-derived macrophages (BMDMs) and liver tissue and analysed the effects of luteolin on macrophage polarization subtypes and downstream inflammatory cytokines by flow cytometry, ELISA, Western blotting (WB) and qPCR. To further verify the effect of luteolin on macrophage polarization and explore the possible potential mechanism, we used a CLP-induced AHI mouse model and LPS-stimulated RAW 264.7 macrophages to assess the effect of luteolin on macrophage polarization; the expression of TNF-α and IL-10 in the cell culture supernatant; and the expression of iNOS, ARG-1, NF-κB (P65), p-P65 and MyD88 by flow cytometry, ELISA, immunohistochemistry and Western blotting.RESULTSWe found that luteolin reduced liver injury and inflammatory response and improved the survival rate of mice. Luteolin modulated the macrophage subtype proportion, promoted the change of macrophages from a proinflammatory M1 phenotype to an anti-inflammatory M2 phenotype, and reduced the inflammatory response both in vivo and in vitro. Moreover, luteolin reduced the expression of NF-κB (p-P65), TLR4 and MyD88. By integrating the predictions from network pharmacology with the in vitro and in vivo experimental results, it was determined that the mechanism by which luteolin alleviates sepsis-induced acute hepatic injury is closely related to the TLR4/MyD88/NF-κB pathway.CONCLUSIONSThe results of this study suggest that luteolin helps alleviate liver injury, reduces the expression of proinflammatory cytokines and promotes the expression of anti-inflammatory factors in sepsis-induced acute hepatic injury. This effect may be related to the regulation of macrophage polarization by luteolin through the TLR4/MyD88/NF-κB signalling pathway.

01 Jun 2025·Current Computer-Aided Drug Design

Xuebijing Exerts Protective Effects on Myocardial Cells by Upregulating TRIM16 and Inhibiting Oxidative Stress and Apoptosis

Article

Author: Meng, Xiaoyan ; Xue, Peng ; Xi, Zhaoqing ; Yan, Xinming

Objective:This study utilized transcriptomic sequencing combined with cellular and animal models to explore the potential mechanisms of Xuebijing in treating sepsis-induced myocardial dysfunction, also known as sepsis-induced myocardial injury.Methods:We investigated potential targets and regulatory mechanisms of XBJ injection using network pharmacology and RNA sequencing. The effects of XBJ on oxidative stress and apoptosis levels in human cardiac myocytes (AC16) and C57BL/6 mice exposed to lipopolysaccharide (LPS) were evaluated by Enzyme-Linked Immunosorbent Assay (ELISA), fluorescent probe, Fluorescent Quantitative Polymerase Chain Reaction (qPCR), Western Blot, Transmission Electron Microscopy, oxidative stress-related indicators detection kit, flow cytometry, and Immunohistochemistry (IHC).Results:First, it was verified that XBJ can reduce the deformation of AC16 cardiomyocytes induced by LPS and the production and secretion of ROS (P <0.01). The transcriptome sequencing results showed that the TRIM16 gene was significantly increased after XBJ treatment, and the data of KEGG and GO analyses demonstrated that XBJ could inhibit the pathway expression of oxidative stress damage in AC16 cells, and PCR verified that XBJ could indeed increase the expression level of TRIM16 gene in AC16 cells (P <0.01). Basic animal and cell experiments showed that LPS could inhibit the expression of TRIM16 and NRF2 in cardiomyocytes (P <0.05) and promote the expression of Keap1 (P <0.01), while XBJ could significantly upregulate the expression levels of TRIM16 and NRF2 (P <0.01) and inhibit the expression of Keap1 (P <0.01), thereby affecting the expression levels of downstream proinflammatory cytokines and alleviating LPS-induced oxidative stress damage. In addition, XBJ also inhibited the expression of the pro-apoptotic proteins Bax and c-caspase3 (P <0.01), promoted the expression of the anti-apoptotic protein Bcl2 (P <0.01), and reduced LPS-induced apoptosis by upregulating TRIM16.Conclusion:Our comprehensive data demonstrated that TRIM16 is a key gene in the therapeutic action of Xuebijing in sepsis-induced myocardial dysfunction, protecting myocardial cells from injury through antioxidative stress and anti-apoptotic mechanisms.

01 Jun 2025·Journal of Reproductive Immunology

Melatonin alleviates endometrial fibrosis in bovine endometritis by regulating TGF-β/Smad and MAPK signaling pathways via MT2

Article

Author: Song, Liangli ; Jiang, Yue ; Qiao, Limin ; Xiao, Longfei ; Chen, Xingyi ; Yao, Hua ; Du, Xianghong ; Zhou, Yi ; Fang, Zihao

Bovine endometritis can lead to abnormal endometrial function and fibrosis, resulting in difficulties in successful embryo implantation and intrauterine adhesions. Melatonin is well known for its profitable effects against inflammation and pathological fibrosis in discrepant organs. Considering the potential therapeutic benefits of melatonin, this study aimed to investigate its effects on endometrial fibrosis in cows with endometritis. Firstly, we evaluated the expression patterns of various factors associated with fibrosis, such as transforming growth factor-β1 (TGF-β1), extracellular matrix (ECM)-related markers (COL1A1 and COL3A1), epithelial-mesenchymal transformation (EMT)-related proteins (α-SMA and Vimentin) in healthy and endometritis-affected bovine uterine tissues. The results showed that diseased tissues presented significantly higher TGF-β1 expression, ECM production, and EMT progression versus normal tissues. Moreover, we established an LPS-induced fibrosis model in endometrial stromal cells (ESCs), and found that melatonin inhibited the fibrosis process of ESCs in a dose-dependent manner. The MT2 inhibitor 4P-PDOT blocked the antifibrotic effects of melatonin and inhibited the phosphorylation of Smad2/3, ERK1/2, and JNK1/2 in LPS-induced fibrosis of ESCs, but not P38 MAPK. These data implied that melatonin supplementation attenuated LPS-induced fibrosis in ESCs by modulating the inhibition of TGF-β/Smad, ERK, and JNK signaling pathways via MT2.

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