Vitamin B6 attenuates aortic dissection by inhibiting pathological remodeling of the aortic extracellular matrix

Aortic dissection (AD) is a serious medical condition characterized by a tear in the inner lining of the aorta that can lead to life-threatening complications and carries a high mortality rate. Vitamin B6 (B6) is a vital micronutrient required to maintain normal physiological function and has been reported to protect against various vascular diseases. However, its effects on AD remain insufficiently characterized.

To investigate the potential therapeutic effects and mechanisms of B6 in a β-aminopropionitrile (BAPN)-induced mouse model of AD.

A BAPN-induced AD model was established in 3-week-old C57BL/6J mice. B6 (50 mg/kg/day) was administered for four weeks, and body weight and mortality were recorded daily. Gross anatomical examination and histological staining were used to evaluate aortic morphology and elastin integrity. Western blotting and immunofluorescence were performed to assess changes in extracellular matrix (ECM) components in vivo and in vitro. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) levels were measured as indicators of oxidative stress.

B6 supplementation significantly attenuated AD, as evidenced by reduced AD incidence, improved survival, preservation of aortic architecture, and decreased elastin degradation. B6 also exerted antioxidant effects, alleviating oxidative stress, which was associated with inhibition of smooth muscle cell phenotypic switching and reduced ECM degradation.

B6 treatment may slow AD progression by protecting the aortic ECM from pathological remodeling through its antioxidant effects. These findings suggest that B6 supplementation may represent a promising therapeutic strategy for the prevention and treatment of AD.