ReferenceID 2199
Liquiritin Attenuates Lipopolysaccharides-Induced Cardiomyocyte Injury via an AMP-Activated Protein Kinase-Dependent Signaling Pathway
Front Pharmacol
Background: Liquiritin (LIQ) is a traditional Chinese medicine that has been reported to regulate inflammation, oxidative stress and cell apoptosis. However, the beneficial effects of LIQ in lipopolysaccharides (LPS)-ind
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Record Fields
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- Reference Id
- 2199
- Evidence Id
- 18789
- Core Evidence Id
- 18789
- Source Reference Id
- 4442
- Herb2 Reference Id
- HBREF005239
- Subject Paper Key
- HBIN033383_34054527
- Pubmed Id
- 34054527
- Doi
- 10.3389/fphar.2021.648688
- Paper Title
- Liquiritin Attenuates Lipopolysaccharides-Induced Cardiomyocyte Injury via an AMP-Activated Protein Kinase-Dependent Signaling Pathway
- Paper Abstract
- Background: Liquiritin (LIQ) is a traditional Chinese medicine that has been reported to regulate inflammation, oxidative stress and cell apoptosis. However, the beneficial effects of LIQ in lipopolysaccharides (LPS)-induced septic cardiomyopathy (SCM) has not been reported. The primary goal of this study was to investigate the effects of LIQ in LPS-induced SCM model. Methods: Mice were pre-treated with LIQ for 7 days before they were injected with LPS (10 mg/kg) for inducing SCM model. Echocardiographic analysis was used to evaluate cardiac function after 12 h of LPS injection. Thereafter, mice were sacrificed to collect hearts for molecular and histopathologic assays by RT-PCR, western-blots, immunohistochemical and terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) staining analysis respectively. AMPKalpha2 knockout (AMPKalpha2-/-) mice were used to elucidate the mechanism of LIQ Neonatal rat cardiomyocytes (NRCMs) treated with or without LPS were used to further investigate the roles and mechanisms of LIQ in vitro experiments. Results: LIQ administration attenuated LPS-induced mouse cardiac dysfunction and reduced mortality, based upon the restoration of EF, FS, LVEDs, heart rate, dp/dt max and dp/dt min deteriorated by LPS treatment. LIQ treatment also reduced mRNA expression of TNFalpha, IL-6 and IL-1beta, inhibited inflammatory cell migration, suppressed cardiac oxidative stress and apoptosis, and improved metabolism. Mechanistically, LIQ enhanced the phosphorylation of AMP-activated protein kinase alpha2 (AMPKalpha2) and decreased the phosphorylation of mTORC1, IkappaBalpha and NFkappaB/p65. Importantly, the beneficial roles of LIQ were not observed in AMPKalpha2 knockout model, nor were they observed in vitro model after inhibiting AMPK activity with an AMPK inhibitor. Conclusion: We have demonstrated that LIQ exerts its protective effects in an SCM model induced by LPS administration. LIQ reduced inflammation, oxidative stress, apoptosis and metabolic alterations via regulating AMPKalpha2 dependent signaling pathway. Thus, LIQ might be a potential treatment or adjuvant for SCM treatment.
- Journal
- Front Pharmacol
- Publish Year
- 2021
- Experiment Subject
- mouse; rat
- Experiment Type
- Animal Experiment
- Phenotype Related
- Septic Cardiomyopathy; Cardiac Dysfunction
- Paper Title Cn
- Paper Title En
- Liquiritin Attenuates Lipopolysaccharides-Induced Cardiomyocyte Injury via an AMP-Activated Protein Kinase-Dependent Signaling Pathway
- Bilingual Status
- semi_complete