RESUMEN
OBJECTIVE: It is agreed that methimazole (MMI) can be administered to induce hypothyroidism. However, there are conflicting data about its effect on thyroid function and development in rats through different administrations. In the present study, we established and compared differences of the rat hypothyroid model induced by MMI added to drinking water or given through an intragastric tube. METHODS: Sixty-four male Wistar rats were randomly divided into seven groups. Methimazole was added to the drinking water (0.025%, 0.04% or 0.1% wt/vol), or through intragastric gavage (5 mg/100 g body weight (bw) or 8 mg/100 g bw) one time each day for 21 days. The rats were weighed every seven days. Blood samples were taken in order to detect the concentrations of serum triiodothyronine (T3), thyroxine (T4) and thyrotropin (TSH) at the end of the experiments. RESULTS: Our results indicate that the effect of methimazole on a rat's thyroid function and body weight is similar in both the group given 0.1% concentration in drinking water and the group which received 8 mg/100 g bw once daily through the intragastric tube. Also, a similar effect was observed in the 0.025%, 0.04% and 5 mg/100 g bw groups. CONCLUSION: These findings suggest that a relationship between the concentration of MMI by oral administration and the dose of it through intragastric administration could exist, and may contribute to inducing hypothyroidism in rats.
RESUMEN
Notch signaling is an evolutionarily ancient, highly conserved pathway important for deciding cell fate, cellular development, differentiation, proliferation, apoptosis, adhesion, and epithelial-to-mesenchymal transition. Notch signaling is also critical in mammalian cardiogenesis, as mutations in this signaling pathway are linked to human congenital heart disease. Furthermore, Notch signaling can repair myocardial injury by promoting myocardial regeneration, protecting ischemic myocardium, inducing angiogenesis, and negatively regulating cardiac fibroblast-myofibroblast transformation. This review provides an update on the known roles of Notch signaling in the mammalian heart. The goal is to assist in developing strategies to influence Notch signaling and optimize myocardial injury repair.