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Abstract
Stroke is a leading cause of long term disability and is associated with a 30% incidence of severe cognitive impairment. Sustained pro-inflammatory microglia activation contributes to, and our lab has shown that the Angiotensin II type 2 receptor (AT2R) agonist, compound 21 (C21) can prevent, the development of, PSCI. We hypothesized that activation of pro-inflammatory microglia and macrophages can be prevented with C21. This was assessed using a microglial cell line (C8-B4) and THP-1 derived macrophages. The reduction in the pro-inflammatory cell markers was assessed via RT-qPCR using the following genes, IL-1b, TNFa, and NOS2. Cells were either pre-treated, prior to LPS exposure, or post-treated after LPS treatment, with C21 (100 uM). C21 effectively reduced the expression of IL-1b in a concentration-dependent manner. Both pre- and post-treatment with C21 significantly reduced the expression of pro-inflammatory markers after LPS exposure in a mouse microglial cell line and human macrophages.