study of [131] iodine labeling of indomethacin, its in vivo biological distribution in Lewis-bearing lung cancer, and its induction of apoptosis in lung cancer

To study the synthesis of [131] iodine [I] labeled histamine-indomethacin [His-IN], its in vivo distribution in Lewis-bearing mice, and its effects on suppression of Lewis lung cancer growth and induction of apoptosis. The present study was carried out in the Experimental Research Center, Sheng Jing Hospital of China Medical University Hospital, Shenyang China between December 2008 and October 2009. Chemical synthesis of His-IN was carried out. Ninety-five C57 mice were allocated into 12 groups, and a series of experiments including the in vivo biological distribution of [131] I-His-IN in C57 mice bearing Lewis lung cancer was explored, and the therapeutic effects of IN and [131] I-His-IN in lung cancer-bearing mice were assessed through tumor suppression experiments, flow cytometry, and detection of tumor necrosis factor. The [131] I-His-IN radionuclide count ratio of the tumor site and surrounding region significantly increased with time, namely, the retention time of [131] I-His-IN radionuclide was longer in the tumor site. A 3.0 mg/kg and 3.5 mg/kg [131] I-His-IN, as well as 3.0 mg/kg and 3.5 mg/kg IN all had tumor suppression and apoptosis induction effects on tumors, among which the 3.5 mg/kg [131] I-His-IN group had significant differences compared with all other groups. The [131] I-His-IN not only retains the tumor-affinity property of IN, the synergistic effect of these 2 also enhances the tumor suppression and pro-apoptotic function

Ranitidina, inhibidor de la permeabilidad vascular en la rata / Inhibitory effects of ranitidine on the vascular permeability in rat

La alta afinidad de la ranitidina hacia el receptor histaminérgico H2 y la sospecha de su participación en cambios de permeabilidad vascular, nos motivo a investigar si la ranitidina tiene efectos inhibitorios sobre los cambios en la permeabilidad provocados por la histamina. Para lograr este objetivo, se utilizaron 3 lotes de ratas variedad Wistar: Lote control, lote histamina y lote ranitidina + histamina. Se determinaron las concentraciones de proteínas totales, albúmina, sodio y cloro como indicadores de cambios en la permeabilidad vascular. Nuestros resultados demuestran parcialmente, que la ranitidina inhibe los incrementos de permeabilidad provocados por la histamina. Aunque clásicamente se ha atribuido al receptor H1, la regulación de la permeabilidad inducida por histamina, es probable que el receptor H2 también este involucrado tal como se demostró en este trabajo al bloquear su activación con ranitidina