|Estrogen inhibits lipopolysaccharide-induced tumor necrosis factor-alpha release from murine macrophages|
Zhang, X., Wang, L., Zhang, H., Guo, D., Qiao, Z., Qiao, J.
|During their reproductive years, females have a lower risk for atherosclerosis as compared with age-matched males, although the mechanisms behind this are not clearly understood. Cytokines, including TNF-alpha, play an important role in the pathogenesis of atherosclerosis. We therefore evaluated whether or not there was any difference between 17beta-estradiol and testosterone in modulating TNF-alpha release from murine bone marrow-derived macrophages (BMM) in vitro. Cells were incubated with or without physiological concentrations (10exp(-10) - 10exp(-8) M) of 17beta-estradiol or testosterone for 48 h, followed by an additional 6 h in the absence or presence of lipopolysaccharide (LPS; 10 mcg/ml). The amount of TNF-alpha released into the culture medium was determined with radioimmunoassay. We found that 17beta-estradiol or testosterone alone did not affect TNF-alpha release from BMM as compared to untreated controls. Preincubation with 17beta-estradiol significantly inhibited LPS-induced TNF-alpha release by 18.15% (p < 0.05), 25.28% (p < 0.05) and 40.83% (p < 0.01) for 10exp(-10), 10exp(-9) and 10exp(-8) M of 17beta-estradiol, respectively, as compared to LPS alone. In contrast, testosterone tested for 3 concentrations did not significantly effect TNF-alpha release induced by LPS. The results indicate that 17beta-estradiol, but not testosterone, inhibits TNF-alpha release from LPS-stimulated macrophages, which may be one of the mechanisms by which estrogen protects against atherosclerosis.|
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