The molecular basis of vessel damage i?nduced by cigarette smoke exposure and new treatment approach: Alpha-linolenic acid

Exposure to cigarette smoke causes vessel damage. And mechanisim of this damage has not yet been clearly identified. Therefore in the present study we aimed to invastigate the wheter vessel damage due to the cigarette smoke exposure will be prevented by the alpha-linolenic acid which has antiinflammatory effect in mice. In experimental study, mice (Swis albino, male age: 8 weeks) separated into some groups such as controls (with and without cigarette smoke exposure) alpha-linolenic acid (with and without cigarette smoke exposure) and indomethacin (with and without cigarette smoke exposure). The cigarette smoke application continued 5 days in a week during two mounths. In the end of two mounths, the mice were killed by cervical dislocation and their blood and thoracic aortas were isolated. Some of isolated aorts used in organ bath experiments for testing endothelial functions. The tissues were precontracted with phenilephrine then relaxed with acetylcholine. Treatment with alfa-linolenic acid increased acetylcholine relaxations. Smoke treatment decreased acetylcholine relaxation. Smoke with alpha-linolenic acid treatment increased acetylcholine relaxations versus just smoke treatment. For testing smooth muscle functions the tissues were precontracted with KCl then relaxed papaverine. There were no variations between testing groups. Other parts of thoracic aortas were used to determine endothelial nitricoxide sythase, cyclooxigenase-2 and phospholypase A2 enzymes levels. Smoke exposure caused rising in cyclooxigenase-2 and phospholypase A2 levels. This rising inhibited with alfa-linolenic acid treatment. Smoke exposure decreased eNOS levels. But this result was not istatistically significant. Using cigarette and smoke exposure is risk factor of cardiovascular disease. Our study showed that alpha-linolenic acid rich diets can decrease the risk of this disease