Abdominal aortic aneurysm (AAA) is a vascular disease characterized by chronic inflammation in the infrarenal aorta. Epidemiologic data have clearly linked tobacco smoking to aneurysm formation and a faster rate of expansion. It suggested that nicotine, one of the main ingredients of tobacco, has been suggested to be associated with AAA development and rupture. In the condition where no established drugs are available; therefore, an effective approach to prevent the vascular damage from nicotine consumption may be the use of dietary functional food factors. However, little is known about the relationship between dietary components and AAA. In this study, we estimated the effect of dietary deoxyribonucleic acid (DNA) on the vascular wall. After habituation for 5 d, the mice were divided into four groups: control diet and distilled water group (C), DNA-Na diet and distilled water group (DNA), control diet and 0.5 mg/mL nicotine solution group (C-Nic), DNA-Na diet, and 0.5 mg/mL nicotine solution group (DNA-Nic). The dietary DNA attenuated the degradation of elastin fibers induced by nicotine administration. The areas stained positive for MMP-2 in the DNA-Nic group were significantly suppressed compared to C-Nic mice. These data suggest that the dietary DNA may prevent the weakening of the aortic wall via inhibition of the MMP-2-dependent pathway. In conclusion, we have revealed the protective effect of dietary DNA on the vascular pathology of nicotine-administrated mice. A nucleic acid-rich diet might be useful for people who consume nicotine via smoking, chewing tobacco, or nicotine patches.

Introduction Abdominal aortic aneurysm AAA is a vascular disease characterized by chronic inflammation in the vascular wall and progressive dilation of the abdominal aorta. Previous reports indicated that the development of AAA is associated with advanced age, male sex, smoking, and hypertension 1, 2. The mortality rate due to AAA rupture is very high, and therapeutic drugs to prevent the progression and rupture of AAA have not been established 3. The development of AAA involves various factors 4 6 , including the weakening of the vascular walls due to inflammation and the degradation of fibers. Immune cells, such as monocytes and macrophages, release inflammatory cytokines, including monocyte chemoattractant protein-1 MCP-1 and tumor necrosis factor-α that activate matrix metalloproteinases MMPs 7. Consequently, MMPs degrade the elastin and collagen fibers that play an integral role in the

Introduction Abdominal aortic aneurysm AAA , characterized as a chronic inflammation of the vascular wall coupled with progressive abdominal aorta distention, is considered to be associated with age, male sex, smoking and hypertension. AAA is responsible for high death rates due to ruptures caused by AAA 1. At present, pharmacological treatments for AAA development and rupture are not available. AAA leads to infiltration of the vascular wall by inflammatory cells, such as lymphocytes and macrophages, resulting in the release of inflammatory mediators and free radicals as well as a loss of elastin and collagen in the media and adventitia due to matrix metalloproteinases MMPs , all of which contribute to a reduction in vascular wall strength 2. Cigarette smoking has been linked to deaths caused by cardiovascular dysfunction worldwide 3. Cigarette smoking, in particular, is a primary risk factor for AAA and a major cause of death from cardiovascular disease globally 3, 4. Nic

Abdominal aortic aneurysm (AAA) is a vascular disease characterized by weakening of vascular walls and progressive dilation of the abdominal aorta. Nicotine, the main component of tobacco, is reportedly associated with the development and rupture of AAA. It is desirable to attenuate the destructive effect of nicotine on vascular walls, using dietary food components. However, effective methods for preventing AAA progression using dietary food components remain unestablished. This study focuses on proanthocyanidins, well known for their potent antioxidant activity. We speculated that proanthocyanidins can suppress nicotine-induced weakening of vascular walls. To estimate the effect of black soybean seed coat extract (BSSCE), rich in proanthocyanidins, on nicotine-induced weakening of the aortic wall, mice were divided into four groups: the control diet and distilled water group (named C), BSSCE solution diet and distilled water group (named B), control diet and 0.5 mg/mL nicotine solution group (named CN), and BSSCE solution diet and 0.5 mg/mL nicotine solution group (named BN). Nicotine-induced degradation of elastin and collagen fibers were significantly suppressed in BN group. The positive areas for matrix metalloproteinase (MMP)-2 and oxidative stress in BN group were significantly decreased compared to those in CN group. These results suggest that proanthocyanidins-rich BSSCE can prevent the weakening of the aortic wall via inhibiting MMP-2 upregulation.