Our previous studies showed that recombinant high-density lipoprotein (rHDL) rHDL74 exhibited higher anti-inflammatory capabilities compared to wild-type rHDL (rHDLwt), while rHDL228 showed hyper-proinflammation. In this paper, we further investigated the potential mechanisms involved in their different inflammatory functions using two models: endotoxemic mice and the RAW264.7 inflammation model. Our results showed that 24 h after the injection of lipopolysaccharide (LPS), mice treated with rHDL74 had a significant decrease in plasma CRP (P<0.01 vs. rHDLwt; P<0.01 vs. LPS), MCP-1 (P<0.05 vs. rHDLwt; P<0.01 vs. LPS) and CD14 (P<0.01 vs. LPS) compared with the mice treated with rHDLwt or the controls that received LPS only. Similar to our previous study, rHDL228 increased the plasma level of CRP (P<0.05 vs. LPS) and MCP-1 (P<0.01 vs. LPS). Our immunohistochemistry and western blot analysis showed that rHDL74 inhibited the activation of NF-κB in endotoxemic mice and JNK and p38 in the RAW264.7 inflammation model, while rHDL228 exacerbated the activation of NF-κB and ERK. In summary, our data suggest that rHDL74 exhibits higher anti-inflammatory activity by decreasing inflammatory factors and inhibiting the activation of NF-κB, JNK and p38, while rHDL228 appears to be hyper-proinflammation by increasing these inflammatory factors and aggravating the activation of NF-κB and ERK.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3520896PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0051327PLOS

Publication Analysis

Top Keywords

endotoxemic mice
8
mice raw2647
8
lipid-bound apolipoprotein
4
apolipoprotein a-i
4
a-i cysteine
4
cysteine mutant
4
mutant n74c
4
n74c inhibits
4
inhibits activation
4
activation nf-κb
4

Similar Publications

Pericytes mediate neuroinflammation via Fli-1 in endotoxemia and sepsis in mice.

Inflamm Res

January 2025

Department of Pathology and Laboratory Medicine, Medical University of South Carolina, 173 Ashley Ave, Charleston, SC, 29425, USA.

Background: Sepsis-associated encephalopathy (SAE) often results from neuroinflammation. Recent studies have shown that brain platelet-derived growth factor receptor β (PDGFRβ) cells, including pericytes, may act as early sensors of infection by secreting monocyte chemoattractant protein-1 (MCP-1), which transmits inflammatory signals to the central nervous system. The erythroblast transformation-specific (ETS) transcription factor Friend leukemia virus integration 1 (Fli-1) plays a critical role in inflammation by regulating the expression of key cytokines, including MCP-1.

View Article and Find Full Text PDF

Neurotensin receptor agonist PD149163 modulates LPS-induced enterocyte apoptosis by downregulating TNFR pathway and executioner caspase 3 in endotoxemic mice: insights from in vivo and in silico study.

Naunyn Schmiedebergs Arch Pharmacol

January 2025

Department of Zoology, University of Allahabad, Senate House, University Road, Old Katra, Prayagraj, Uttar Pradesh, 211002, India.

This study was designed to evaluate the dose-dependent efficacy of neurotensin receptor-1 (NTSR1) agonist PD149163 in the amelioration of the lipopolysaccharide (LPS)-induced apoptosis in the gastrointestinal tract (GIT) of mice. PD149163 is an analogue of NTS, a GIT tri-decapeptide with anti-inflammatory and anti-oxidative effects. Swiss-albino mice (female/8 weeks/25 ± 2.

View Article and Find Full Text PDF

Purpose: Angiopoietin-1 (Ang1) mitigates inflammation as a proangiogenic growth factor. Action of Ang1 on lipopolysaccharide (LPS)-induced endotoxemic inflammation was investigated in endothelin receptor-B null Hirschsprung's disease mice (KO).

Methods: LPS or saline was injected intraperitoneally in KO (KO-LPS; n = 9, KO-sal; n = 5) and wild-type (WT) (WT-LPS; n = 6, WT-sal; n = 6) pups obtained within 24 h of birth.

View Article and Find Full Text PDF

The multistrain probiotics' efficacy in ameliorating the endotoxemic effect in Lipopolysaccharide (LPS) challenged mice was evaluated with the agonist of anti-inflammatory peptide, neurotensin (NTS), especially targeting the inflammation of the gut and liver. Swiss Albino Mice (Female, 8 weeks old) were maintained in eight groups: Group I as Control, Group II-Group V were exposed to intraperitoneal (i.p.

View Article and Find Full Text PDF

Biochanin A-mediated anti-ferroptosis is associated with reduction of septic kidney injury.

Life Sci

December 2024

Department of Food Science and Biotechnology of Animal Resources, College of Sang-Huh Life Sciences, Konkuk University, 120 Neungdong-ro, Gwangjin-gu, Seoul 05029, Republic of Korea. Electronic address:

Article Synopsis
  • - This study explored how biochanin A affects acute kidney injury related to sepsis in mice, using lipopolysaccharide to induce the condition and monitoring survival rates and kidney health over two weeks.
  • - Treatment with biochanin A improved survival rates in septic mice and reduced kidney damage by decreasing inflammatory responses and preventing cell death in kidney tissues.
  • - The research highlights biochanin A's ability to inhibit ferroptosis and its potential as a treatment for sepsis-related kidney disorders by stabilizing key biochemical parameters and influencing the expression of specific protective genes.
View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!