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Updated: Nov 3, 2025
Isolation of Human Primary Valve Cells for In vitro Disease Modeling
Published on: April 16, 2021
Protective Effects of Fucoxanthin on Hydrogen Peroxide-Induced Calcification of Heart Valve Interstitial Cells
Yi-Fen Chiang1, Chih-Hung Tsai2, Hsin-Yuan Chen1,3
1School of Nutrition and Health Sciences, College of Nutrition, Taipei Medical University, Taipei 11031, Taiwan.
Insights
Fucoxanthin (Fx), a marine carotenoid, protects heart valves from oxidative stress. This natural compound reduces cell damage, apoptosis, and calcification, showing promise for treating heart valve diseases.
Area of Science:
- Cardiovascular research
- Cell biology
- Natural product chemistry
Background:
- Cardiovascular diseases like atherosclerosis involve inflammation and oxidative stress, damaging heart cells and leading to apoptosis or calcification.
- Current treatments for heart valve disease include drugs and surgery.
- Fucoxanthin (Fx), a marine carotenoid, exhibits antioxidant, anti-inflammatory, and anti-tumor properties.
Purpose of the Study:
- To investigate the protective effects of fucoxanthin (Fx) on heart valves against oxidative stress.
- To elucidate the underlying mechanisms of Fx's action in heart valve protection.
Main Methods:
- In vitro: Rat heart valve interstitial cells were subjected to H2O2-induced oxidative stress and treated with Fx.
- In vitro analysis included cell viability, propidium iodide staining for DNA damage, Alizarin Red-S for calcification, and Western blotting for apoptosis and signaling proteins (Akt/ERK).
- In vivo: Dogs received Fx (60 mg/kg) with medical treatment for 0.5-2 years, with echocardiography assessing cardiac function.
Main Results:
- Fx significantly improved cell survival and reduced DNA damage in oxidative stress-induced rat heart valve cells.
- Fx demonstrated a protective effect against calcification and abrogated oxidative stress-induced apoptosis by modulating apoptosis-related proteins and Akt/ERK signaling.
- In vivo studies showed significant recovery in echocardiographic parameters in dogs treated with Fx.
Conclusions:
- Fucoxanthin exhibits significant protective effects against oxidative stress-induced damage in heart valve cells.
- Fx mitigates apoptosis and calcification, potentially through modulation of Akt/ERK pathways.
- Both in vitro and in vivo results suggest Fx is a promising therapeutic agent for protecting heart valves from oxidative stress-related damage.
Abstract:
Cardiovascular diseases such as atherosclerosis and aortic valve sclerosis involve inflammatory reactions triggered by various stimuli, causing increased oxidative stress. This increased oxidative stress causes damage to the heart cells, with subsequent cell apoptosis or calcification. Currently, heart valve damage or heart valve diseases are treated by drugs or surgery. Natural antioxidant products are being investigated in related research, such as fucoxanthin (Fx), which is a marine carotenoid extracted from seaweed, with strong antioxidant, anti-inflammatory, and anti-tumor properties. This study aimed to explore the protective effect of Fx on heart valves under high oxidative stress, as well as the underlying mechanism of action. Rat heart valve interstitial cells under H2O2-induced oxidative stress were treated with Fx. Fx improved cell survival and reduced oxidative stress-induced DNA damage, which was assessed by cell viability analysis and staining with propidium iodide. Alizarin Red-S analysis indicated that Fx has a protective effect against calcification. Furthermore, Western blotting revealed that Fx abrogates oxidative stress-induced apoptosis via reducing the expression of apoptosis-related proteins as well as modulate Akt/ERK-related protein expression. Notably, in vivo experiments using 26 dogs treated with 60 mg/kg of Fx in combination with medical treatment for 0.5 to 2 years showed significant recovery in their echocardiographic parameters. Collectively, these in vitro and in vivo results highlight the potential of Fx to protect heart valve cells from high oxidative stress-induced damage.
