Acute exposure to LPS induces cardiac dysfunction via the activation of the NLRP3 inflammasome DOI Creative Commons
Tshiamo T. Maluleke, Ashmeetha Manilall,

Nandi Shezi

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Oct. 17, 2024

Systemic inflammation contributes to left ventricular (LV) dysfunction, however the role of NLRP3 inflammasome in LV dysfunction acute inflammatory conditions is unclear. This study investigated (24 h) cardiac structural and functional changes vivo vitro lipopolysaccharide (LPS)-induced inflammation. LPS-treated Sprague-Dawley (SD) rats showed increased LPS metabolite abundance their LVs as measured by atmospheric pressure matrix-assisted laser desorption ionisation (AP-MALDI) mass spectrometry imaging (MSI). Echocardiography histology that LPS-exposed rats, internal diameter was decreased, with evidence macrophage infiltration oedema. However, there were no wall thickness or collagen volume. Additionally, exhibited impaired relaxation, potentially contributing decreased stroke While global systolic function preserved, exposure SD resulted myocardial deformation assessed speckle-tracking echocardiography. Exposure upregulation expression components rodents. In gene downstream cytokines IL-1β IL-18, antioxidant SOD2, elevated markers pyroptosis (GSDMD) which inhibited treatment a antagonist. LPS-induced increases apoptosic (BAX/Bcl2) not impacted antagonism. These findings suggest induced adverse is, at least part, mediated acute, high-grade states. addition, while mediates pyroptotic pathways, regulation apoptosis independent inflammasome.

Language: Английский

Acute exposure to LPS induces cardiac dysfunction via the activation of the NLRP3 inflammasome DOI Creative Commons
Tshiamo T. Maluleke, Ashmeetha Manilall,

Nandi Shezi

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: Oct. 17, 2024

Systemic inflammation contributes to left ventricular (LV) dysfunction, however the role of NLRP3 inflammasome in LV dysfunction acute inflammatory conditions is unclear. This study investigated (24 h) cardiac structural and functional changes vivo vitro lipopolysaccharide (LPS)-induced inflammation. LPS-treated Sprague-Dawley (SD) rats showed increased LPS metabolite abundance their LVs as measured by atmospheric pressure matrix-assisted laser desorption ionisation (AP-MALDI) mass spectrometry imaging (MSI). Echocardiography histology that LPS-exposed rats, internal diameter was decreased, with evidence macrophage infiltration oedema. However, there were no wall thickness or collagen volume. Additionally, exhibited impaired relaxation, potentially contributing decreased stroke While global systolic function preserved, exposure SD resulted myocardial deformation assessed speckle-tracking echocardiography. Exposure upregulation expression components rodents. In gene downstream cytokines IL-1β IL-18, antioxidant SOD2, elevated markers pyroptosis (GSDMD) which inhibited treatment a antagonist. LPS-induced increases apoptosic (BAX/Bcl2) not impacted antagonism. These findings suggest induced adverse is, at least part, mediated acute, high-grade states. addition, while mediates pyroptotic pathways, regulation apoptosis independent inflammasome.

Language: Английский

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