The anti-inflammatory effects of 17B-Estradiol on RAW 264.7 Macrophages

By Rose McMullen, Olivia Pierce, and Kayla Rodriguez

Faculty Mentor: Laura Sipe PhD.


Chronic inflammation can be detrimental to the structures and functions of the body. When the body detects unknown agents, the immune system is activated to fight, destroy, and heal the body. This reaction begins with macrophage cells; macrophages detect and engulf these foreign molecules through phagocytosis and activate the TLR4 inflammatory pathway, causing the release of inflammatory cytokines. Chronic inflammation results from over-activated macrophages that constantly secrete cytokines. This continuous signaling of inflammation and activation of the immune cells can lead to a variety of diseases. 17ꞵ-estradiol (E2) is an important hormone that plays many vital roles in the body. Not only is E2 an essential sex hormone, E2 has been shown to have many important roles in regulating the immune system. E2 receptors have been shown to be expressed on many types of immune cells, such as macrophages. To investigate the anti-inflammatory effect of E2, we utilized LPS-stimulated RAW 264.7 macrophages. To determine the cell viability of the E2 treatment, we used an MTT assay, which indicated that E2 does not induce cell death in RAW 264.7 cells. To determine Nitric Oxide (NO) production, a Griess assay was conducted. From the Griess assay, we concluded that E2 treatment significantly reduced NO production in LPS-stimulated RAW 264.7 cells. While we were able to show the antimicrobial effects of E2, further research is required to determine the anti-inflammatory effects of E2.


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