Benzylurea Protects hPDLFs Against LPS‐Induced Mitochondrial Dysfunction Through MTCH2 DOI
Li Liu,

Jing Bai,

Jiyun Wang

et al.

Oral Diseases, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 3, 2024

ABSTRACT Objective The aim of this study is to explore the mechanism benzylurea in inflammatory injury human periodontal ligament fibroblasts (hPDLFs). Methods An inflammation model hPDLFs was established using LPS. Nuclear transport nuclear transcription factor‐κB (NF‐κB), secretion cytokines, and morphology distribution F‐actin were determined. Mitochondrial function assessed by measuring mitochondrial membrane potential (MMP), permeability transition pore (mPTP), reactive oxygen species (ROS) levels. expression carrier homolog 2 (MTCH2) Cytochrome b5 type B (CYB5B) detected. Results Benzylurea alleviated effects lipopolysaccharide (LPS) on proliferation apoptosis hPDLFs. It reduced release cytokines inhibited NF‐κB translocation. improved regulating MMP preventing excessive mPTP opening. Furthermore, LPS elevated MTCH2 CYB5B However, these can be benzylurea. altered directly affected expression, activation translocation NF‐κB. Conclusion may act as an effector MTCH2, with enhancing protecting from LPS‐induced through MTCH2.

Language: Английский

The role of programmed cell death in organ dysfunction induced by opportunistic pathogens DOI Creative Commons
Wang Yangyanqiu, Li Weng, Xunyao Wu

et al.

Critical Care, Journal Year: 2025, Volume and Issue: 29(1)

Published: Jan. 24, 2025

Sepsis is a life-threatening condition resulting from pathogen infection and characterized by organ dysfunction. Programmed cell death (PCD) during sepsis has been associated with the development of multiple dysfunction syndrome (MODS), impacting various physiological systems including respiratory, cardiovascular, renal, neurological, hematological, hepatic, intestinal systems. It well-established that infections lead to immune dysregulation, which subsequently contributes MODS in sepsis. However, recent evidence suggests sepsis-related opportunistic pathogens can directly induce failure promoting PCD parenchymal cells each affected organ. This study provides an overview damaged induction host pathogens, proposing innovative strategies for preventing

Language: Английский

Citations

0
Increased Trophoblast Cell Ferroptosis via HMGB1/ACSL4 Pathway Is Associated with Spontaneous Abortion DOI Creative Commons
Yishan Dong, Yong Li, Wenjie Tang

et al.

Reproductive Sciences, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 24, 2025

Abstract Introduction Trophoblast cells undergo ferroptosis in pregnancy-related diseases. HMGB1 participates pathological ferroptosis. However, whether lipopolysaccharide (LPS) -mediated expression induces the of trophoblast and further spontaneous abortion (SA) remains unknown. Methods ACSL4 were measured villous tissues from 20 women with SA elective abortion. Human HTR-8/SVneo treated LPS to establish an vitro model. The hallmarks including MDA, GSH, Fe 2+ ROS detected using indicated assay kits. Results levels significantly higher than those normal control group. interacts stabilizes promote cells. Conversely, and/or inhibition attenuated LPS-induced Conclusions An HMGB1/ACSL4 axis is engaged cells, may be targeted design treatments preventing SA.

Language: Английский

Citations

0
JNK inhibition mitigates sepsis-associated encephalopathy via attenuation of neuroinflammation, oxidative stress and apoptosis DOI

Riya Gagnani,

Harshita Singh, Manisha Suri

et al.

Metabolic Brain Disease, Journal Year: 2025, Volume and Issue: 40(3)

Published: March 13, 2025

Language: Английский

Citations

0
Neuroprotective Effect of Maresin-1 in Rotenone-Induced Parkinson’s Disease in Rats: The Putative Role of the JAK/STAT Pathway DOI Creative Commons
Suzan A Khodir, Eman Sweed,

Manar A. Faried

et al.

Neurochemical Research, Journal Year: 2024, Volume and Issue: 50(1)

Published: Nov. 22, 2024

Abstract Exposure to rotenone results in similar pathophysiological features as Parkinson’s disease. Inflammation and oxidative stress are essential PD pathogenesis. Maresin-1 has potent anti-inflammatory properties promotes the regression of inflammation function. The current study aimed evaluate protective effects (MaR1) (ROT)-induced whether this role is associated with initiation Janus kinase (JAK)-signal transducers activator transcription (STAT) signaling pathway. Thirty male Wister rats were classified into control, ROT-treated, ROT + MaR1-treated groups. Rats underwent rotarod, open field, grip strength, stepping tests part their motor behavioral evaluation. Serum glial cell-derived neurotrophic factor (GDNF) striatal dopamine, acetylcholine, malondialdehyde (MDA), reduced glutathione (GSH), TNF-α, IL-6, IL-1β evaluated. Expression JAK1 STAT3 genes was assessed striatum. Then, tissue subjected histological immunohistochemical evaluation for caspase-3, GFAP, NF-kB. administrated group showed significant impairment. This accompanied by levels GDNF dopamine increased well augmented inflammatory biomarkers antioxidant activity. Inflammatory pathways (JAK1/STAT3, NF-kB) upregulated. Histopathological changes upregulation GFAP immunopositive reaction observed. Remarkably, MaR1 treatment effectively alleviated behavior, histopathological changes, biochemical alterations induced ROT. exerts against ROT-induced its anti-inflammatory, antiapoptotic, properties. mechanisms action may involve modulation such JAK/STAT.

Language: Английский

Citations

3
Hyperoside attenuates sepsis-induced acute lung injury by Nrf2 activation and ferroptosis inhibition DOI

Kuida Chen,

Shipeng Lu, Ke Shi

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 145, P. 113734 - 113734

Published: Dec. 10, 2024

Language: Английский

Citations

2
Pharmacodynamic Insights into Maresin 1: Enhancing Flap Viability via the Keap1/Nrf2 Axis to Control ROS-Driven Apoptosis and Ferroptosis DOI Creative Commons

Pin Fang,

Sheng Cheng, Yingying Lai

et al.

European Journal of Pharmaceutical Sciences, Journal Year: 2024, Volume and Issue: 203, P. 106923 - 106923

Published: Oct. 3, 2024

Language: Английский

Citations

1
Maresin1 Inhibits Ferroptosis via the Nrf2/SLC7A11/GPX4 Pathway to Protect Against Sepsis-Induced Acute Liver Injury DOI Creative Commons

Yongjing Guo,

Huimin Chen, Jian Sun

et al.

Journal of Inflammation Research, Journal Year: 2024, Volume and Issue: Volume 17, P. 11041 - 11053

Published: Dec. 1, 2024

Maresin 1 (MaR1) is a specialized pro-resolving mediator with anti-inflammatory properties that promotes tissue repair. This study aims to investigate the molecular involvement of MaR1 in protecting against sepsis-induced acute liver injury (SI-ALI).

Language: Английский

Citations

1
Benzylurea Protects hPDLFs Against LPS‐Induced Mitochondrial Dysfunction Through MTCH2 DOI
Li Liu,

Jing Bai,

Jiyun Wang

et al.

Oral Diseases, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 3, 2024

ABSTRACT Objective The aim of this study is to explore the mechanism benzylurea in inflammatory injury human periodontal ligament fibroblasts (hPDLFs). Methods An inflammation model hPDLFs was established using LPS. Nuclear transport nuclear transcription factor‐κB (NF‐κB), secretion cytokines, and morphology distribution F‐actin were determined. Mitochondrial function assessed by measuring mitochondrial membrane potential (MMP), permeability transition pore (mPTP), reactive oxygen species (ROS) levels. expression carrier homolog 2 (MTCH2) Cytochrome b5 type B (CYB5B) detected. Results Benzylurea alleviated effects lipopolysaccharide (LPS) on proliferation apoptosis hPDLFs. It reduced release cytokines inhibited NF‐κB translocation. improved regulating MMP preventing excessive mPTP opening. Furthermore, LPS elevated MTCH2 CYB5B However, these can be benzylurea. altered directly affected expression, activation translocation NF‐κB. Conclusion may act as an effector MTCH2, with enhancing protecting from LPS‐induced through MTCH2.

Language: Английский

Citations

0