Methylthiouracil

Methylthiouracil is an antithyroid agent. Methylthiouracil suppresses the production TNF-α and IL-6, and the activation of NF-κB and ERK1/2. IC50 & Target:TNF-α, IL-6, ERK1/2, NF-κB^[1] In Vitro:HUVECs are treated with various concentrations of MTU (0-20 μM) for 6 h after the addition of LPS (100 ng/mL) for 4 h. MTU inhibits LPS-mediated hyperpermeability in endothelial cells, with the optimal effect occurring at a concentration above 5 μM. The effects of MTU are examined on HUVEC actin cytoskeletal arrangement by immunofluorescence staining of HUVEC monolayers with F-actin labeled fluorescein phalloidin. Control HUVECs exhibit a random distribution of F-actin throughout the cells, with some localization of actin filament bundles at the cell boundaries. Barrier disruption by LPS (100 ng/mL) is manifested by the formation of paracellular gaps in HUVECs. In addition, post-treatment with MTU (10 or 20 μM) results in inhibited formation of LPS-induced paracellular gaps with the formation of dense F-actin rings. To test the cytotoxicity of MTU, cellular viability assays are performed in HUVECs treated with MTU for 24 h. At concentrations up to 20 μM, MTU does not affect cell viability^[1]. In Vivo:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment.

Methylthiouracil can be used to model neurological defects. Methylthiouracil can significantly inhibit LPS-induced peritoneal dye leakage. In the mouse model, the average circulating blood volume was 72 mL/kg (average mouse weight 27 g) and the average blood volume was about 2 mL. After injection of Methylthiouracil (142 or 284 μg/kg), the dye concentration in peripheral blood reached a maximum of 10 or 20 μM, respectively. In dairy cows, after oral administration, Methylthiouracil rapidly appears in plasma, urine, and milk, and accumulates selectively in the thyroid gland. Its excretion follows a biphasic pattern. At the beginning of treatment, the level of Methylthiouracil drops rapidly within 4 days, and then the excretion rate slows down by 15-30 times. Long-term use of Methylthiouracil results in significant residues that can still be detected in the thyroid gland, muscle tissue, urine, and plasma one month after stopping administration^[1][2][3].