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Published on: September 28, 2015
Polydatin Protects Against the Formation of PPE-Induced Abdominal Aortic Aneurysms in Mice by Activating Nuclear
Zikang Liu1, Jinyi Zhu2, Qian Zhou1
1Department of Cardiothoracic Surgery, Jingzhou Central Hospital Affiliated to Yangtze University, Jingzhou City, Hubei Province, China.
Abstract:
Sudden death resulting from abdominal aortic aneurysm (AAA) rupture is a highly fatal cardiovascular condition. There remains an urgent need to identify innovative therapeutic strategies capable of decelerating AAA progression and rupture. Although polydatin (PLD) has been consistently shown to exert potent anti-inflammatory effects in diverse pathological contexts, its regulatory role in AAA has not yet been investigated. Using a porcine pancreatic elastase (PPE) infusion-induced AAA mouse model, we comprehensively evaluated PLD's influence on NRF2 signaling by Western blot (WB) analysis, immunohistochemistry (IHC), immunofluorescence (IF), flow cytometry (FC), and real-time quantitative PCR (RT-qPCR) tests. Our findings demonstrate that PLD robustly activates NRF2 pathway, thereby attenuating AAA formation by curbing smooth muscle cell (SMCs) phenotypic transformation and apoptosis, as well as suppressing macrophage-mediated inflammatory responses.
Insights
Polydatin (PLD) activates the NRF2 pathway, offering a potential therapeutic strategy against abdominal aortic aneurysm (AAA) rupture. This study shows PLD attenuates AAA by reducing inflammation and cell death.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pharmacology
Background:
- Abdominal aortic aneurysm (AAA) rupture is a fatal cardiovascular event with limited therapeutic options.
- Polydatin (PLD), known for anti-inflammatory properties, has not been studied for its role in AAA.
- There is an urgent need for novel therapeutic strategies to slow AAA progression.
Purpose of the Study:
- To investigate the regulatory role of polydatin (PLD) in abdominal aortic aneurysm (AAA) formation.
- To evaluate the effect of PLD on NRF2 signaling in a mouse model of AAA.
- To determine if PLD can attenuate AAA progression by modulating cellular and inflammatory responses.
Main Methods:
- A porcine pancreatic elastase (PPE) infusion-induced AAA mouse model was utilized.
- PLD's effects on NRF2 signaling were assessed using Western blot (WB), immunohistochemistry (IHC), immunofluorescence (IF), flow cytometry (FC), and RT-qPCR.
- Key cellular processes including smooth muscle cell (SMC) phenotypic transformation and apoptosis were analyzed.
Main Results:
- Polydatin (PLD) robustly activated the NRF2 signaling pathway in the AAA model.
- PLD significantly attenuated AAA formation.
- PLD curbed SMC phenotypic transformation and apoptosis and suppressed macrophage-mediated inflammation.
Conclusions:
- Polydatin (PLD) demonstrates therapeutic potential for abdominal aortic aneurysm (AAA).
- Activation of the NRF2 pathway by PLD is a key mechanism in attenuating AAA.
- PLD offers a promising strategy to mitigate AAA progression by targeting cellular dysfunction and inflammation.
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