| Popis: |
Background The incidence and mortality of thoracic aortic dissection(TAD) are increasing. In clinicopathological studies, macrophage, T lymphocytes and dendritic cells were found infiltrating in the aortic middle layer. Acetaldehyde dehydrogenase 2(ALDH2) gene polymorphism is associated with high incidence of hypertension in Asian populations. However, there is no clear evidence of the relationship between ALDH2 and TAD in Asians. The aim of this study was to investigate the incidence of aortic dissection in different ALDH2 genotypes and explore changes in the vascular wall. Materials and methods Three-week-old male mice were administered by freshly prepared β-aminopropionitrile(BAPN) solution dissolved in drinking water(1 g/kg/d) for 28 days to induce TAD. The animal ultrasound imaging system was used to observe the formation of arterial dissection. Subsequently, mice were killed by cervical dislocation. The aortic were fixed for HE staining and EVG staining to observe the aortic elastic fiber tears and pseudoluma formation under the microscope. Results Knockout(KO) of ALDH2 mitigated BAPN-induced TAD formation in animal studies. Ultrasound results showed that ALDH2 knockout reduced the degree of ascending aortic widening and the incidence of aortic dissection rupture. Pathological sections of multiple aortic segments showed that the protective effect of ALDH2 knockout included not only the ascending aorta but also the aortic arch and descending aorta. The expressions of NK CD56bright cells, Th17 cells, T cells and T helper cells were decreased in the ALDH2 KO mice treated with BAPN for 28 days. Conclusions ALDH2 knockout played a protective role in the aorta dissection by altering inflammatory response, immune response and protecting elastic fibers. |
