Effect of Electronic Cigarette and Moderate Intensity Aerobic Physical Exercise to IL-6, IL-15, and FSTL-1 Protein Expression and Fragmentation of Aortic Elastic Lamina of Wistar Rats

E-cigarettes may contribute to aortic stiffness through inflammation and elastic lamina fragmentation. Inflammation triggers IL-6, IL-15, and FSTL-1 production in oxidative cells. Moderate-intensity aerobic exercise also increases these cytokines; however, it confers cardiovascular benefits. This study investigates the effects of e-cigarettes and aerobic exercise on IL-6, IL-15, FSTL-1, and aortic elastic lamina fragmentation in male Wistar rats. Rats were divided into four groups: control, exercise, e-cigarette, and combined e-cigarette plus exercise. After six weeks, aortic tissue was analyzed for cytokine expression using Western blot and for elastic lamina fragmentation using Elastic-Van Gieson staining. E-cigarette exposure significantly increased IL-6 (1.14 ± 0.362) and IL-15 (1.07 ± 0.252) compared to the control group (IL-6: 0.48 ± 0.103, p = 0.002; IL-15: 0.49 ± 0.091, p < 0.001). Exercise also increased IL-6 (0.72 ± 0.200, p = 0.017) and IL-15 (0.69 ± 0.211, p = 0.046). Aortic fragmentation was significantly higher in the e-cigarette group (11.00 ± 3.46) compared to the control (4.71 ± 2.69, p = 0.003) and combined groups (5.86 ± 2.54, p = 0.008). Elastic lamina fragmentation positively correlated with IL-6 (r = 0.772, p = 0.001) and IL-15 (r = 0.688, p = 0.009). FSTL-1 expression was inversely correlated with fragmentation in the e-cigarette groups (r = –0.564, p = 0.036). E-cigarettes promote inflammation and aortic damage, whereas exercise reduces elastic lamina fragmentation. FSTL-1 may have a protective role in limiting aortic damage.