BACKGROUND: The aims of this study were to investigate the effects of mercaptoethanol treatment on the expression of mediators of oxidative stress, inflammation, and extracellular matrix (ECM) degeneration in a mouse aortic dissection (AD) model.

MATERIAL AND METHODS: Twenty-four 8-month-old C57BL/6J mice were divided into three groups and studied for two weeks: 1) the aortic dissection (AD) Model group (N=8) underwent intraperitoneal injection of angiotensin II (Ang II) (5 ml/kg) three times every 24 h; 2) the mercaptoethanol Treated group (N=8) were given oral mercaptoethanol (2.5 mM); the Normal group (N=8) underwent intraperitoneal injection of noradrenaline (5 mg/kg) three times every 24 h. Sections of mouse aorta were prepared for histology with hematoxylin and eosin (H&E) staining; immunohistochemistry was performed to detect levels of: nuclear factor (erythroid-derived 2)-like 2 (NFE2L2), nuclear factor κB (NF-κB), p65, superoxide dismutase-1 (SOD1), glutamate cysteine ligase catalytic subunit (GCLC), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), and matrix metalloproteinase-9 (MMP9). Quantitative reverse transcription-polymerase chain reaction (RT-PCR) evaluated mRNA expression of SOD1, GCLC, TNF-α, IL-1β, and MMP9.

RESULTS: Mercaptoethanol treatment inhibited Ang II-induced aortic dissection in AD mice, as shown histologically. Mercaptoethanol treatment reduced the expression levels of NFE2L2, NF-κB, p65, TNF-α, IL-1β and increased the expression levels of SOD1, MMP9, and GCLC.

CONCLUSIONS: In an AD mouse model, mercaptoethanol treatment inhibited thoracic and abdominal aortic dissection and reduced aortic tissue expression of mediators of oxidative stress and inflammation and increased the activation of ECM signaling pathways.

Keywords: Carotid Artery, Internal, Dissection