Allicin Alleviates Aortic Dissection Progression via p38/MAPK/NF-κB Signaling Pathways
| Author | Chang Ren | en |
| Author | Wuyi Wu Ban | en |
| Author | Ru Chen | en |
| Author | Jun Gu | en |
| Author | Liying Wu Qiu | en |
| Author | Lei Song | en |
| Issued Date | 2025-11-30 | en |
| Abstract | Background and Objectives: This study investigates the therapeutic potential of allicin, a sulfur compound derived from garlic, in addressing aortic dissection (AD), a severe cardiovascular condition characterized by the separation of the aortic wall layers. Methods: The AD mouse model induced by β-aminopropionitrile (BAPN) was used to evaluate the effect of allicin on the disease. Meanwhile, in vitro cell experiments were conducted to investigate the effect of allicin on platelet-derived growth factor-BB (PDGF-BB)-induced mouse vascular smooth muscle cells (VSMCs). Results: Allicin treatment significantly reduced the incidence of AD from 70% to 40% (P < 0.01) and improved the survival rate to 70% (P < 0.05) in BAPN-induced mice. It markedly reduced the maximal aortic internal diameter (BAPN: 2.15 ± 0.18 mm vs. The BAPN + allicin: 1.68 ± 0.15 mm, P < 0.01). Molecular analyses demonstrated that allicin significantly upregulated the expression of contractile markers [smooth muscle protein 22-α (SM22α) and alpha-smooth muscle actin (α-SMA), P < 0.01] and downregulated the synthetic marker osteopontin (OPN, P < 0.01). Furthermore, allicin mitigated oxidative stress by increasing superoxide dismutase (SOD) activity and reducing malondialdehyde (MDA) levels (P < 0.05), and alleviated inflammation by decreasing the levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) (P < 0.05). These beneficial effects are likely mediated through the inhibition of the p38 mitogen-activated protein kinase (p38/MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways. Conclusions: These findings suggest that allicin may effectively slow AD progression by targeting key pathological processes, including VSMC phenotypic transformation, extracellular matrix (ECM) degradation, and inflammation. | en |
| DOI | https://doi.org/10.5812/jjnpp-165405 | en |
| Keyword | Aortic Dissection | en |
| Keyword | Allicin | en |
| Keyword | Vascular Smooth Muscle Cell Phenotype Switch | en |
| Keyword | P38/MAPK | en |
| Keyword | NF-κB | en |
| Publisher | Brieflands | en |
| Title | Allicin Alleviates Aortic Dissection Progression via p38/MAPK/NF-κB Signaling Pathways | en |
| Type | Research Article | en |