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March 28, 2026Phytotherapy Research

Syringin Protects Against Doxorubicin‐Induced Cardiotoxicity via Apelinr‐Dependent Activation of the Nuclear Factor‐Erythroid 2‐Related Factor 2/Heme Oxygenase‐1 Antioxidant Pathway

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Key result

Syringin attenuates doxorubicin-induced cardiotoxicity and myocardial atrophy via APJ/PI3K/AKT and NRF2/HO-1 antioxidant pathways.

Why the study?

Doxorubicin-induced cardiotoxicity mediated by oxidative stress is a major clinical challenge, and the efficacy and mechanism of syringin in this setting remain poorly defined.

Does Syringin prevent Doxorubicin-induced cardiotoxicity in a mouse model and primary cardiomyocytes?

Population

Doxorubicin-induced mouse model of cardiotoxicity and primary cardiomyocytes

Comparison

Syringin vs pravastatin (10 mg/kg) positive control and controls

Design

Preclinical animal and cellular experimental study

Authors

YLYujiang LiTWTing WangMSMing‐Yi Shen

Discussion

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Overview

Should not yet change cardio-oncology practice; extends preclinical evidence for APJ-targeted therapy in doxorubicin cardiotoxicity.

Key Points

  • The study aims to explore the cardioprotective effects of Syringin against Doxorubicin-induced cardiac injury and its underlying mechanisms.
  • Evaluated Syringin in a Dox-induced mouse model and primary cardiomyocytes.
  • Measured cardiac function using advanced echocardiography.
  • Conducted network pharmacology for pathway identification.
  • Assessed antioxidant proteins and oxidative stress markers via histology and Western blotting.
  • Performed siRNA-mediated knockdown of the apelin receptor to validate molecular targets.
  • Syringin significantly reduced myocardial atrophy and oxidative stress.
  • Syringin activated the APJ/PI3K/AKT signaling pathway, enhancing NRF2/HO-1 antioxidant response.
  • Increased levels of the antioxidant protein FGF21 were observed after treatment.
  • APJ knockdown negated the cardioprotective effects of Syringin, leading to worsened cardiac function.

Structured PICO

Does Syringin prevent Doxorubicin-induced cardiotoxicity in a mouse model and primary cardiomyocytes?

P
Population
Doxorubicin-induced mouse model of cardiotoxicity and primary cardiomyocytes
I
Intervention
Syringin
C
Comparator
Pravastatin (10 mg/kg) as positive control, and Doxorubicin alone
O
Outcome
Cardiac function, myocardial strain, myocardial atrophy, and oxidative stress markerssurrogate

Syringin is a promising natural compound for mitigating chemotherapy-induced cardiotoxicity by targeting the APJ receptor pathway.

Cite This Study

Li et al. (2026) studied this question. Syringin significantly attenuates doxorubicin-induced cardiotoxicity, myocardial atrophy, and oxidative stress by activating the APJ/PI3K/AKT and NRF2/HO-1 antioxidant signaling pathways.

synapsesocial.com/papers/69c772d98bbfbc51511e352dhttps://doi.org/10.1002/ptr.70312
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Syringaresinol Protects against Type 1 Diabetic Cardiomyopathy by Alleviating Inflammation Responses, Cardiac Fibrosis, and Oxidative Stress2020 · 64 citations
  2. 2Syringic Acid Alleviates Doxorubicin-Induced Hepatotoxicity Through PI3K/Akt-Mediated Nrf-2/HO-1 Signaling Pathways in Male Rats2025 · 3 citations
  3. 3Syringin exerts anti‐inflammatory and antioxidant effects by regulating SIRT1 signaling in rat and cell models of acute myocardial infarction2023 · 30 citations
  4. 4In-silico and In-vivo Investigations Reveal Ameliorative Potential of Myricetin Against Doxorubicin-induced Myocardial Damage via Modulation of NF-κB Signaling Pathway2025
  5. 5Sinapic Acid Ameliorates Doxorubicin-Induced Cardiotoxicity in H9c2 Cardiomyoblasts by Inhibiting Oxidative Stress Through Activation of the Nrf2 Signaling Pathway2025 · 7 citations