Layer-specific strain for assessing the effect of naringin on systolic myocardial dysfunction induced by sepsis and its underlying mechanisms

Sun, Lijuan; Qiao, Wei; Ye, Xiao; Ren, Weidong

doi:10.1177/0300060520986369

Cited by 5 publications

(3 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In these researches, NAR treatment reduced infarct size compared to the non-treatet group. Moreover, NAR was reported to show its protective role through inhibition of inflammatory response [15], oxidative stress [16], and preservation of mitochondrial structure [17]. Here, the cell viability in cell group treated with NAR at dose of 80 µM and 160 µM was not significantly different (p>0,05).…”

Section: Nar Reduces H9c2 Cell Death In Hr Injurymentioning

confidence: 69%

Naringin Effectively Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury

Thu¹,

Yen²

2021

NST

View full text Add to dashboard Cite

This study was conducted to evaluate the protective effect of Naringin (NAR) on H9C2 cardiomyocytes in hypoxia/reoxygenation (HR) injury in vitro induced by the hypoxia chamber. Methods: H9C2 cells were grown under normal (control) and HR conditions. The viability, cardiolipin content and mitochondrial membrane potential of H9C2 cells in experimental groups were analyzed by using suitable kits. Results: The obtained results showed that the addition of Naringin (16÷160 µM) significantly increased the survival rate of H9C2 cells under HR conditions. In particular, NAR had the highest efficiency in preserving mitochondrial function at concentrations of 80 µM and 160 µM. In HR-exposed H9C2 cell group, the cardiolipin content and mitochondrial membrane potential values of H9C2 cells were decreased sharply with that of control (71,64±1,37% and 68,12±2,78%, p<0,05). Interestingly, mitochondrial cardiolipin contents were signigicantly increased in H9C2 cells post-hypoxic treated wtih NAR at dose of 80 µM 160 µM to 87,76±1,89% and 81,09±1,21%. Additionally, post-hypoxic supplementation of NAR at concentration of 80 µM and 160 µM effectively increased mitochondrial membrane potential values. Conclusion: The obtained results are preliminary data on the effects of NAR in protecting mitochondrial-targeted cardiomyocytes against HR injury.

show abstract

Section: Nar Reduces H9c2 Cell Death In Hr Injurymentioning

confidence: 69%

Naringin Effectively Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury

Thu¹,

Yen²

2021

NST

View full text Add to dashboard Cite

show abstract

“…In LPS-treated adipose-derived stem cells, the expression of KEAP1 is significantly increased and correlates with a drop in the expression of Nrf2 as well as decreased levels of antioxidant enzymes 58 . In septic cardiomyopathy, administration of naringin was shown to suppress KEAP1 expression and therefore restore the expression of Nrf2, leading to improved mitochondrial function 59 . Our results showed that sepsis does not alter cardiac KEAP1 expression, but induces instead its phosphorylation at T85 through upregulation of STK3.…”

Section: Discussionmentioning

confidence: 99%

Serine/threonine kinase 3 promotes oxidative stress and mitochondrial damage in septic cardiomyopathy through inducing Kelch-like ECH-associated protein 1 phosphorylation and nuclear factor erythroid 2-related factor 2 degradation

Zhu¹,

Dai²,

Liu³

et al. 2023

Int. J. Biol. Sci.

View full text Add to dashboard Cite

Serine/threonine kinases (STK3) is a core component of the Hippo pathway and modulates oxidative stress and inflammatory responses in cardiovascular diseases. However, its potential role in septic cardiomyopathy remains undefined. STK3-mediated phosphorylation of Kelch-like ECH-associated protein 1 (KEAP1) was shown to suppress antioxidant gene transcription controlled by nuclear factor erythroid 2-related factor 2 (Nrf2) in macrophages. To explore whether STK3 induces KEAP1-mediated suppression of Nrf2 in septic cardiomyopathy, wild-type and global STK3 knockout (STK3 -/- ) mice were treated with LPS. LPS treatment upregulated cardiac STK3 expression. STK3 deletion attenuated myocardial inflammation and cardiomyocyte death, and improved myocardial structure and function. In LPS-challenged HL-1 cardiomyocytes, shRNA-mediated STK3 knockdown normalized mitochondrial membrane potential and ATP production, attenuated apoptosis, and rescued antioxidant gene expression by preventing Nrf2 downregulation. Co-IP, docking analysis, western blotting, and immunofluorescence assays further showed that STK3 binds and phosphorylates KEAP1, promoting Nrf2 downregulation. Accordingly, transfection of phosphodefective KEAP1 mutant protein in cardiomyocyte restored Nrf2 expression and mitochondrial performance upon LPS, while expression of a phosphomimetic KEAP1 mutant abolished the mitochondria-protective and pro-survival effects of STK3 deletion. These findings suggest that STK3 upregulation contributes to septic cardiomyopathy by phosphorylating KEAP1 to promote Nrf2 degradation and suppression of the antioxidant response.

show abstract

“…More than 95% of sepsis is caused by bacterial infection, and the release of endotoxin lipopolysaccharides (LPS) caused by bacterial infection is the main factor leading to sepsis ( Sun et al, 2021 ). When the body is invaded by LPS, Toll-like receptor 4 on the surface of macrophages recognizes LPS and activates intracellular signal transduction of macrophages to produce a large number of pro-inflammatory cytokines, such as TNF-a, IL-1β, IL-6, IL-12, etc.…”

Section: Introductionmentioning

confidence: 99%

The preventative effects of Lactococcus Lactis metabolites against LPS-induced sepsis

Fu,

Zhang,

Yue

et al. 2024

Front. Microbiol.

View full text Add to dashboard Cite

IntroductionSepsis is a syndrome of organ dysfunction caused by a dysregulated host response to infection and septic shock. Currently, antibiotic therapy is the standard treatment for sepsis, but it can lead to drug resistance. The disturbance of the gut microbiota which is affected by sepsis could lead to the development of organ failure. It is reported that probiotics could shape the gut microbiota, potentially controlling a variety of intestinal diseases and promoting whole-body health.MethodsIn this study, we evaluated the preventive effects of intra- and extracellular products of probiotics on sepsis. The extracellular products of Lactococcus lactis (L. lactis) were identified through the in vivo cell experiments. The preventive effect and mechanism of L. lactis extracellular products on mouse sepsis were further explored through HE staining, mouse survival rate measurement, chip analysis, etc.ResultsL. lactis extracellular products increase cell survival and significantly reduce inflammatory factors secreted in a cellular sepsis model. In in vivo experiments in mice, our samples attenuated sepsis-induced pulmonary edema and inflammatory infiltrates in the lungs of mice, and reduced mortality and inflammatory factor levels within the serum of mice. Finally, the mechanism of sepsis prevention by lactic acid bacteria is suggested. Extracellular products of L. lactis could effectively prevent sepsis episodes.DiscussionIn animal experiments, we reported that extracellular products of L. lactis can effectively prevent sepsis, and preliminarily discussed the pathological mechanism, which provides more ideas for the prevention of sepsis. In the future, probiotics may be considered a new way to prevent sepsis.

show abstract

Layer-specific strain for assessing the effect of naringin on systolic myocardial dysfunction induced by sepsis and its underlying mechanisms

Cited by 5 publications

References 36 publications

Naringin Effectively Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury

Naringin Effectively Protects Cardiomyocytes Against Hypoxia/Reoxygenation Injury

Serine/threonine kinase 3 promotes oxidative stress and mitochondrial damage in septic cardiomyopathy through inducing Kelch-like ECH-associated protein 1 phosphorylation and nuclear factor erythroid 2-related factor 2 degradation

The preventative effects of Lactococcus Lactis metabolites against LPS-induced sepsis

Contact Info

Product

Resources

About