What question did this study set out to answer?

To evaluate the protective effects of salidroside against lipopolysaccharide-induced myocardial injury and determine the role of the reactive oxygen species-mediated PI3K/Akt/mTOR signaling pathway.

September 14, 2017Journal of Cellular and Molecular MedicineOpen Access

Salidroside suppressing LPS‐induced myocardial injury by inhibiting ROS‐mediated PI3K/Akt/mTOR pathway in vitro and in vivo

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Authors

LCLvyi Chen PLPeng Liu XFXin Feng

Discussion

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Overview

Preclinical study demonstrates that salidroside alleviates endotoxin-induced myocardial injury in rat models and cardiac cells, suggesting therapeutic potential for inflammatory heart disease.

Key Points

To evaluate the protective effects of salidroside against lipopolysaccharide-induced myocardial injury and determine the role of the reactive oxygen species-mediated PI3K/Akt/mTOR signaling pathway.
Sprague-Dawley rats were randomly assigned to control, lipopolysaccharide (15 mg/kg), lipopolysaccharide plus dexamethasone (2 mg/kg), or lipopolysaccharide plus salidroside (20 or 40 mg/kg) groups to assess hemodynamics, myocardial histology, and serum biomarkers.
In vitro experiments utilized rat embryonic cardiomyoblast H9c2 cells exposed to lipopolysaccharide with or without salidroside and the antioxidant N-acetyl-L-cysteine.
Reactive oxygen species levels were quantified via flow cytometry, antioxidant enzymes and cytokines were measured spectrophotometrically, and pathway proteins were evaluated via Western blot.
Salidroside treatment in endotoxemic rats significantly preserved hemodynamic function, reduced cardiac damage markers (CK, LDH) and inflammatory cytokines (TNF-α, IL-6, IL-1β), and restored antioxidant enzyme activities (SOD, CAT, GSH-px).
Salidroside suppressed the expression of inflammatory mediators iNOS, COX-2, and NF-κB, alongside downregulating PI3K/Akt/mTOR pathway activation in vivo.
In H9c2 cells, salidroside and the ROS scavenger N-acetyl-L-cysteine similarly reduced intracellular reactive oxygen species generation and inhibited the downstream PI3K/Akt/mTOR signaling cascade.

Cite This Study

Chen et al. (2017) studied this question.

synapsesocial.com/papers/6a827b64ee46c620893ad4e8 https://doi.org/10.1111/jcmm.12871

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September 14, 2017Journal of Cellular and Molecular MedicineOpen Access

Salidroside suppressing LPS‐induced myocardial injury by inhibiting ROS‐mediated PI3K/Akt/mTOR pathway in vitro and in vivo

View Full Paper

Ask AI

Bookmark

Authors

LCLvyi Chen PLPeng Liu XFXin Feng

Discussion

Member takes

Overview

Preclinical study demonstrates that salidroside alleviates endotoxin-induced myocardial injury in rat models and cardiac cells, suggesting therapeutic potential for inflammatory heart disease.

Key Points

To evaluate the protective effects of salidroside against lipopolysaccharide-induced myocardial injury and determine the role of the reactive oxygen species-mediated PI3K/Akt/mTOR signaling pathway.
Sprague-Dawley rats were randomly assigned to control, lipopolysaccharide (15 mg/kg), lipopolysaccharide plus dexamethasone (2 mg/kg), or lipopolysaccharide plus salidroside (20 or 40 mg/kg) groups to assess hemodynamics, myocardial histology, and serum biomarkers.
In vitro experiments utilized rat embryonic cardiomyoblast H9c2 cells exposed to lipopolysaccharide with or without salidroside and the antioxidant N-acetyl-L-cysteine.
Reactive oxygen species levels were quantified via flow cytometry, antioxidant enzymes and cytokines were measured spectrophotometrically, and pathway proteins were evaluated via Western blot.
Salidroside treatment in endotoxemic rats significantly preserved hemodynamic function, reduced cardiac damage markers (CK, LDH) and inflammatory cytokines (TNF-α, IL-6, IL-1β), and restored antioxidant enzyme activities (SOD, CAT, GSH-px).
Salidroside suppressed the expression of inflammatory mediators iNOS, COX-2, and NF-κB, alongside downregulating PI3K/Akt/mTOR pathway activation in vivo.
In H9c2 cells, salidroside and the ROS scavenger N-acetyl-L-cysteine similarly reduced intracellular reactive oxygen species generation and inhibited the downstream PI3K/Akt/mTOR signaling cascade.

Cite This Study

Chen et al. (2017) studied this question.

synapsesocial.com/papers/6a827b64ee46c620893ad4e8 https://doi.org/10.1111/jcmm.12871

Also Consider

Synapse has enriched one closely related paper. Consider it for comparative context:

1Protective Effects of Salidroside on Epirubicin-Induced Early Left Ventricular Regional Systolic Dysfunction in Patients with Breast Cancer2012 · 62 citations

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