Date of Award
With the number of cases of cardiovascular diseases, which are most commonly caused by atherosclerosis, continuously rising, it is important to see how different lifestyle factors can contribute to one’s health. If limiting the amount of social stress an individual experiences can cause a decrease in the prevalence of these diseases, it will be important for physicians to encourage patients to avoid possible stressors or determine ways to cope with psychosocial stress in order to decrease their risks for such diseases. In this study, Clenbuterol, a β2 adrenergic agonist, was used to activate the β2 adrenergic receptor on macrophages in order to mimic one way in which macrophages may be affected during an instance of psychosocial stress. The expression of the cholesterol uptake gene CD36 was examined and the cholesterol uptake in aggregated-LDL treated macrophages was measured. Macrophage inflammatory responses to LPS in the presence of Clenbuterol were also examined. It was determined that while CD36 levels increased in macrophages treated with Clenbuterol, no difference in cholesterol levels was observed compared with untreated macrophages. It was also found that a Clenbuterol pretreatment caused increased expression of proinflammatory cytokines such as MCP1 and IL-1β, while cotreatment with Clenbuterol caused the opposite effect (a decrease in these cytokines).
Wood, Crystal Alece, "The Effects of β2 Adrenergic Receptor Activation on Macrophage Cholesterol Accumulation and Inflammatory Responses" (2016). Senior Theses. 71.