Role And Mechanisms Of Sympathetic/Parasympathetic Neurotransmitters In Atherogenesis

Autonomic nervous system ( sympathetic/parasympathetic ) dysfunction is involved in the induction of AS. Intimal hyperplasia could be induced by adventitia injury. So an animal model of vascular adventitial injury established by combining collogenase digestion and mechanical dissection was used to induce artery denervation and preadipocyte was cultured in vitro to find out the role of neurotransmitter in the development of AS. In the experiment, HE staining was used to reveal morphological changes in vessels after adventitial injury, HPLC to observe the level change of NE and Ach, immunohistochemistry and western blot to detect NF-κB p65 in the artery and cell nucleus, ELISA to measure cytokines in cell supernatant and Annexin V for cell apoptosis. The results showed that there were intimal hyperplasia lesions in vessels with adventitial injury but not in controls. The levels of NE and Ach in the injured artery were elevated for a short time while NF-κB p65 was also elevated. NE and Ach could increase the secretion of IL-6 while inhibiting IL-10 by promoting the translocation of NF-κB p65. Treatment with Tongxl could inhibit intimal lesions and reduce the level of NF-κB p65. All these results leads to these conclusions: 1. vascular adventitia denervation is involved in the pathological process of intimal hyperplasia; 2. secondly, ANS dysfunction contributes to the AS process by promoting the inflammation response in the local artery; 3. ANS dysfunction could also promote the inflammation in other tissues.