Smoking is considered to be one of the primary causes of
atherosclerosis and
vascular injury. Previous studies have shown that
nicotine in tobacco can lead to vascular
inflammation and endothelial dysfunction. Perivascular adipose tissue (PVAT) is known to secrete various types of
adipokines to maintain vascular homeostasis. The present study investigated whether nicotine‑induced PVAT malfunction can accelerate endothelial
inflammation and eventually lead to endothelial dysfunction. The levels of inflammatory
adipokines, including nuclear factor (NF)‑κB,
interleukin (IL)‑1β, IL‑6 and
tumor necrosis factor (TNF)‑α, the ICAM‑1 and VCAM‑1 adhesion molecules and secretion of
adiponectin were assessed in mature adipocytes and endothelial cells cultured alone or in co‑culture under
nicotine stimulation. It was found that
nicotine reduced the secretion of
adiponectin and stimulated secretion of the NF‑κB, IL‑1β, IL‑6 and TNF‑α inflammatory
adipokines in mature adipocytes. Although
nicotine stimulated endothelial cells to secrete IL‑1β and IL‑6, no significant increase in the secretion of TNF‑α was observed. The co‑culture of mature adipocytes with endothelial cells markedly augmented the expression of the NF‑κB, IL‑1β, IL‑6 and TNF‑α inflammatory
adipokines and the ICAM‑1 and VCAM‑1 adhesion molecules, and significantly lowered the levels of
adiponectin. These findings suggested that
nicotine induced mature adipocyte dysfunction, which caused the abnormal secretion of
adiponectin and inflammatory
adipokines, and exacerbated endothelial
inflammation. These findings also suggested a mechanism whereby
nicotine induced the secretion of
adiponectin and inflammatory
cytokines by adipocytes. The results of the present study elucidated a novel pathway induced by cigarette
smoke, which contributed to
atherosclerosis and
vascular injury.