RESUMO
We used immunohistochemistry to identify the localization of monoamine oxidase type B (MAOB) in the rat oxyntic mucosa. At light microscopic levels, MAOB-immunopositive cells were mostly located in the basal half of the oxyntic mucosa. By a double-labeling immunofluorescence method, it was shown that MAOB immunoreactivity was localized in almost all of histidine decarboxylase (HDC)-positive cells. Only a few MAOB-positive cells were negative for HDC. At electron microscopic levels, immunohistochemical reaction products of MAOB were detected on the mitochondrial outer membranes in cells that showed morphological characteristics of enterochromaffin-like (ECL) cells. These findings indicate that ECL cells contain MAOB in the rat. We provide a hypothesis that MAOB is involved in the inactivation mechanism of histamine that is released from ECL cells and activates parietal cells to secrete gastric acid.
Assuntos
Celulas Tipo Enterocromafim/enzimologia , Mucosa Gástrica/enzimologia , Histidina Descarboxilase/metabolismo , Mitocôndrias/metabolismo , Monoaminoxidase/metabolismo , Animais , Masculino , Microscopia Eletrônica , Coelhos , Ratos , Ratos Sprague-DawleyRESUMO
Hepatocyte growth factor/scatter factor (HGF/SF) is a multifunctional cytokine with mitogenic, motogenic, and morphogenic activities. In addition, HGF/SF inhibits the proliferation of some tumor cell lines, but its mechanism remains poorly understood. We determined in this study whether HGF/SF induces cell death of a Meth A mouse sarcoma cell line in vitro, whose proliferation is remarkably suppressed by HGF/SF. Inhibition of Meth A cell growth by HGF/SF was dose-dependent and maximal at a concentration of 30 ng/ml. The percentage of dead cells increased to 22% upon treatment with 30 ng/ml of HGF/SF for 96 h, whereas that in untreated cultures was less than 5%. Staining of these cells nuclei with Hoechst 33342 revealed condensation of the chromatin and nuclear fragmentation. Gel electrophoresis of DNA from HGF/SF-treated cells showed a typical ladder pattern. Cells with a fractional DNA content also increased five-fold in the HGF/SF-treated cultures as analyzed by flow cytometry after propidium iodide staining. These are features typical of apoptosis. Concurrent addition of 12-O-tetradecanoylphorbol 13-acetate (TPA) with HGF/SF augmented the apoptosis induced by the growth factor, while TPA alone caused little death. This enhancement was largely blocked by addition of the specific protein kinase C inhibitor GF 109203X. These results indicate that HGF/SF induced the apoptotic cell death of the Meth A sarcoma cell line and that protein kinase C activation augmented the growth factor-induced apoptosis.
Assuntos
Apoptose/efeitos dos fármacos , Fator de Crescimento de Hepatócito/farmacologia , Acetato de Tetradecanoilforbol/farmacologia , Animais , Benzimidazóis/metabolismo , Ciclo Celular/fisiologia , Sobrevivência Celular/efeitos dos fármacos , Fragmentação do DNA/efeitos dos fármacos , Replicação do DNA/efeitos dos fármacos , Citometria de Fluxo , Corantes Fluorescentes/metabolismo , Indóis/farmacologia , Maleimidas/farmacologia , Camundongos , Proteína Quinase C/antagonistas & inibidores , Células Tumorais CultivadasRESUMO
The case was a 43-year-old male who complained of anal bleeding and melena. He was diagnosed as rectal cancer with multiple liver metastases. Mile's operation with hepatic arterial cannulation was performed. This patient received 10 courses of arterial infusion chemotherapy using low-dose 5-FU, CDDP and LV. Tumor size of liver lesions significantly decreased. Internal iliac arterial cannulation was also performed for local recurrence. He received 3 courses of arterial infusion chemotherapy using the same regimen. The size of local recurrence also decreased. He had no side effect except mild epigastralgia and dermatitis around the stoma with good QOL.