RESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of Luteolin alone or combination with chemotherapentic drugs on the cytoxicity of cancer cells.</p><p><b>METHODS</b>Cultured A549, Hela, MCF-7, AGS, MGC-803, Caco2 and HepG2 cells were treated with Luteolin or the combination of Luteolin with other chemotherapeutic agents (Bexarotene, Cisplatin and Bleomycin). Cell viability was measured by MTS assay and IC(50) was calculated.</p><p><b>RESULTS</b>The IC(50) of Bexarotene to Hela cells was 2 micromol/L, but with the combination of 5 micromol/L of Luteolin that reduced to 0.2 micromol/L. However, the combination of Bexarotene and Luteolin did not show significant benefit in MGC-803, HepG2 cells, Caco2 and MCF-7 cells. The IC(50) of Cisplatin to Hela cells was over 30 micromol/L,but it decreased to 3 micromol/L in the presence of 5 micromol/L Luteolin; Luteolin also sensitized Cisplatin in MGC-803, HepG2 and A549 cells studied. The IC(50) of Bleomycin to Hela cells was over 100 micromol/L, but it was about 1 micromol/L in the presence of 5 micromol/L Luteolin. A549 cells were resistant to Bleomycin with an IC(50) of 100 micromol/L, 10 micromol/L Luteolin greatly enhanced the cytotoxicity of Bleomycin to the cells with the IC(50) of about 10 micromol/L. The inhibitions of MGC-803, HepG2, A549 and AGS cells didn't change by combination of Luteolin.</p><p><b>CONCLUSION</b>Low concentration of Luteolin has little toxic effect on the cancer cell lines tested in the study, but it can sensitize chemotherapeutic drugs in various cancer cell lines.</p>
Asunto(s)
Humanos , Antineoplásicos , Farmacología , Neoplasias de la Mama , Patología , Línea Celular Tumoral , Proliferación Celular , Sinergismo Farmacológico , Neoplasias Pulmonares , Patología , Luteolina , Farmacología , Neoplasias , PatologíaRESUMEN
<p><b>OBJECTIVE</b>To explore the mucosal protective effect on the quality of gastric ulcer healing.</p><p><b>METHODS</b>Gastric ulcers were induced in male rats by serosal application of acetic acid. Rats were gavaged for 14 days with saline, omeprazole (OME), teprenone (TEP) and TEP plus OME starting 3 days after ulcer induction. Then the tissues and blood samples were obtained and measured.</p><p><b>RESULT</b>The lower ulcer index (UI) and increased ulcer inhibition rate were observed in OME and OME+TEP groups. In TEP and OME+TEP groups, restored mucosa thickness increased, cystically dilated glands decreased, microvessels in connective tissue increased, the secretion of mucus, hexosamine, PGE(2), bFGF were enhanced, the expression of EGFR was increased.</p><p><b>CONCLUSION</b>TEP can improve the quality of gastric ulcer healing, when combined with OME,the effect is more marked.</p>
Asunto(s)
Animales , Masculino , Ratas , Ácido Acético , Antiulcerosos , Usos Terapéuticos , Diterpenos , Usos Terapéuticos , Quimioterapia Combinada , Mucosa Gástrica , Metabolismo , Patología , Omeprazol , Usos Terapéuticos , Ratas Wistar , Receptores ErbB , Prevención Secundaria , Úlcera Gástrica , Quimioterapia , Patología , Cicatrización de HeridasRESUMEN
<p><b>OBJECTIVE</b>To explore the effect of muscovite on the quality of gastric ulcer healing.</p><p><b>METHOD</b>Gastric ulcers were produced in male rats by serosal application of acetic acid. Rats were gavaged for 14 days with saline, omeprazole and muscovite starting 3 days after ulcer induction. Then the tissue and blood samples were obtained and measured.</p><p><b>RESULT</b>In the muscovite group, restored mucosa thickness increased, cystically dilated glands decreased, microvessels in connective tissue increased, the secretion of mucus, hexosamine, PGE2, EGF, bFGF were enhanced, and the express of EGFR was stronger.</p><p><b>CONCLUSION</b>Muscovite can promote the gastric ulcer healing and improve the quality of gastric ulcer healing.</p>
Asunto(s)
Animales , Masculino , Ratas , Silicatos de Aluminio , Farmacología , Dinoprostona , Sangre , Factor 2 de Crecimiento de Fibroblastos , Metabolismo , Mucosa Gástrica , Patología , Hexosaminas , Metabolismo , Materia Medica , Farmacología , Moco , Secreciones Corporales , Ratas Wistar , Receptores ErbB , Metabolismo , Úlcera Gástrica , PatologíaRESUMEN
<p><b>OBJECTIVE</b>To investigate the mechanism of isinglass in the prevention and treatment of chronic atrophic gastritis (CAG) in rats.</p><p><b>METHOD</b>Animal models of SD rats with CAG were made in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while CAG rat model was being made. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed. Then the length of the proliferation zone of the gastric mucosa and serum epidermal growth factors (EGF) and growth hormones (GH)level were studied.</p><p><b>RESULT</b>In isinglass prevention groups and high dose isinglass reverse group, the length of the proliferation zone of the gastric mucosa was very close to that in normal control group (P > 0.05), much better than model control group (P < 0.01). In low dose isinglass reverse group, it was lower than that in normal control group (P < 0.01), but much better than model control group (P < 0.01). In both prevention and reverse groups, serum EGF level was higher than that in normal (P < 0.01) and model control group (P < 0.05). Serum GH level was the same in every group (P > 0.05).</p><p><b>CONCLUSION</b>The mechanism of isinglass in the prevention and treatment of CAG rats lies in revitalizing and proliferating gastric mucosal cells by stimulating endogenous EGF secretion.</p>
Asunto(s)
Animales , Femenino , Ratas , Enfermedad Crónica , Relación Dosis-Respuesta a Droga , Factor de Crecimiento Epidérmico , Sangre , Gastritis Atrófica , Quimioterapia , Gelatina , Usos Terapéuticos , Hormona del Crecimiento , Sangre , Materia Medica , Usos Terapéuticos , Antígeno Nuclear de Célula en Proliferación , Metabolismo , Ratas Sprague-DawleyRESUMEN
<p><b>OBJECTIVE</b>To evaluate the effect of isinglass on the prevention and treatment of chronic atrophic gastritis in rats.</p><p><b>METHOD</b>Animal model of SD rats with CAG was established in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol x L(-1) sodium deoxycholate and 0.1% ammonia water. In prevention groups, sucralfate and isinglass were used as preventive therapy while we were establishing CAG rat model. In the reverse groups, sucralfate and isinglass were used to treat rats after establishment of CAG rat model. Finally all the rats were executed and pathologic changes of the gastric mucosa were studied by gross appearance and microscopy.</p><p><b>RESULT</b>In isinglass prevention groups and reverse groups, inflammation grades of gastric antrum were less than these in model control group (P < 0.01) while the means of ratios of the thickness of gastric mucosal gland and muscularis mucos (L1/L2), the number of gastric glands in 1-mm lengths of mucosal layer were much better than those in model control group (P < 0.01). They were very close to normal control group (P > 0.05).</p><p><b>CONCLUSION</b>Isinglass can prevent the gastric mucosal atrophy in the CAG model and can improve and cure the gastric mucosal atrophy of the SD rats with GAG.</p>
Asunto(s)
Animales , Masculino , Ratas , Enfermedad Crónica , Mucosa Gástrica , Patología , Gastritis Atrófica , Quimioterapia , Patología , Gelatina , Usos Terapéuticos , Materia Medica , Usos Terapéuticos , Ratas Sprague-DawleyRESUMEN
<p><b>OBJECTIVE</b>To investigate the epidermal growth factor(EGF) and epidermal growth factor receptor(EGFR) expression in atrophic gastritis in rats to explore the relationship between EGF and chronic atrophic gastritis(CAG).</p><p><b>METHODS</b>The serum EGF and gastric mucosal, EGFR level were measured in 20 rats with CAG and 20 normal controls.</p><p><b>RESULTS</b>The average EGF level (0.149+/-0.020) microg/L and 80% positive rate of EGFR expression observed in CAG group were significantly higher than those in control group[(0.043+/-0.003) microg/L and 0%,P<0.01].</p><p><b>CONCLUSION</b>The study demonstrates an association of high levels of EGF and positive EGFR expression in CAG rats. Further studies are necessary to clarify whether EGF/EGFR play a significant role in the pathogenesis of CAG.</p>