Extracellular Histones Exacerbate Heat Stroke-Induced Liver Injury by Triggering Hepatocyte Pyroptosis and Liver Injury Via the Tlr9-Nlrp3 Pathway DOI
Yue Li, Huan Li,

Youqing Tang

et al.

Published: Jan. 1, 2023

Background: Severe heat stroke is often complicated by multiple organ failure, including liver injury. Recent evidence indicates that the underlying mechanism constitutes sterile inflammation triggered cell damage, in which hepatocyte NOD-like receptor family pyrin domain-containing 3 inflammasome activation and pyroptosis play key roles. As extracellular histones act as damage-associated molecular patterns mediate tissue toxicity inflammation, we aimed to investigate whether contribute inducing following stroke, promoting development of injury, elucidate potential mechanisms. Methods: Exogenous were administered AML-12 murine hepatocytes or male aged 8~12 week mice hyperthermic treatment (at 39°C a chamber with 60% relative humidity). Prior exposure, endogenous neutralized using neutralizing antibodies, inflammasomes inhibited RNA silencing, Toll-like 9 was modulated pharmacological agonist antagonist. Inflammasome assembly, caspase-1 activation, histological changes, enzyme levels measured. Statistical comparison more than two groups performed one-way ANOVA Tukey’s post-hoc testing. The correlations analyzed Pearson’s correlation test. All experiments repeated thrice. A p-value < 0.05 considered significant. Results: Heat induced histone release into space at correlating Moreover, augmented stroke-induced injury both vitro vivo dose- time-dependent manner, whereas conferred protection stroke. Histones mediated through signaling pathway, resulted inflammation. Conclusions: Our findings show are critical mediators aggravate setting. Therefore, suggest therapeutic targets limit death

Language: Английский

STAT3 inhibition ameliorates renal interstitial inflammation in MRL/lpr mice with diffuse proliferative lupus nephritis DOI Creative Commons

Jianfen Zhu,

Yijing Chen, Yulan Chen

et al.

Renal Failure, Journal Year: 2024, Volume and Issue: 46(1)

Published: May 27, 2024

Acute kidney injury (AKI) is one of the most common and severe clinical syndromes diffuse proliferative lupus nephritis (DPLN), which poor prognosis indicated by aggravated renal function deterioration. However, specific therapy mechanisms AKI in DPLN remain to be explored.

Language: Английский

Citations

0

Fecal Proteome Profile in Dogs Suffering from Different Hepatobiliary Disorders and Comparison with Controls DOI Creative Commons
Matteo Cerquetella, Sara Mangiaterra,

Francesco Pinnella

et al.

Animals, Journal Year: 2023, Volume and Issue: 13(14), P. 2343 - 2343

Published: July 18, 2023

In the present study, fecal proteomes of clinically healthy dogs (HD = n. 10), showing clinical, ultrasonographic, and/or laboratory evidence different hepatobiliary dysfunction (DHD and suffering from chronic hepatitis (CHD 10) were investigated with an Ultimate 3000 nanoUPLC system, coupled to Orbitrap Fusion Lumos Tribrid mass spectrometer. Fifty-two proteins canine origin identified qualitatively in three study groups, quantitative differences found 55 when comparing groups. Quantitatively, a total 41 36 differentially abundant DHD CHD groups compared control HD, 38 resulted dysregulated group as group. Among various proteins, differently fibronectin haptoglobin more feces than ones, leading us hypothesize its possible diagnostic/monitoring role hepatitis. On other hand, trefoil factor 2 was increased dogs. Our results show that analysis proteome is very promising field case disorders, it able highlight both qualitative among included. Results need be confirmed western blotting further studies.

Language: Английский

Citations

0

Extracellular Histones Exacerbate Heat Stroke-Induced Liver Injury by Triggering Hepatocyte Pyroptosis and Liver Injury Via the Tlr9-Nlrp3 Pathway DOI
Yue Li, Huan Li,

Youqing Tang

et al.

Published: Jan. 1, 2023

Background: Severe heat stroke is often complicated by multiple organ failure, including liver injury. Recent evidence indicates that the underlying mechanism constitutes sterile inflammation triggered cell damage, in which hepatocyte NOD-like receptor family pyrin domain-containing 3 inflammasome activation and pyroptosis play key roles. As extracellular histones act as damage-associated molecular patterns mediate tissue toxicity inflammation, we aimed to investigate whether contribute inducing following stroke, promoting development of injury, elucidate potential mechanisms. Methods: Exogenous were administered AML-12 murine hepatocytes or male aged 8~12 week mice hyperthermic treatment (at 39°C a chamber with 60% relative humidity). Prior exposure, endogenous neutralized using neutralizing antibodies, inflammasomes inhibited RNA silencing, Toll-like 9 was modulated pharmacological agonist antagonist. Inflammasome assembly, caspase-1 activation, histological changes, enzyme levels measured. Statistical comparison more than two groups performed one-way ANOVA Tukey’s post-hoc testing. The correlations analyzed Pearson’s correlation test. All experiments repeated thrice. A p-value < 0.05 considered significant. Results: Heat induced histone release into space at correlating Moreover, augmented stroke-induced injury both vitro vivo dose- time-dependent manner, whereas conferred protection stroke. Histones mediated through signaling pathway, resulted inflammation. Conclusions: Our findings show are critical mediators aggravate setting. Therefore, suggest therapeutic targets limit death

Language: Английский

Citations

0