ABSTRACT
AIM: To study the protective effect of tea polyphenols (TPs) on submandibular glands affected by radiation injury. METHODS: Sixty rats were randomly divided into radiation group (R-group, N = 30) and TP-pre-treated-radiation group (TPR-group, N = 30). The rats were intragastrically administered with TP or normal sodium from 14 days before radiation, continuously daily, until the experiment. All the rats in both groups were irradiated with a single exposure dose of 15 Gy gamma rays that were delivered to the head and neck areas. Ten rats of each group were anatomised on the 3rd, 6th and 30th day after irradiation, respectively. The submandibular glands of the rats were removed for the study. The morphologic changes of the submandibular glands were observed by transmission electron microscopy (TEM). The terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP)-biotin nick-end labelling (TUNEL) method was used to detect apoptosis of the submandibular glands' cells. RESULTS: Electron microscope observation of the submandibular glands showed that the lesions of the TPR-group were mild. Change in apoptosis of the cells was not obvious compared with the R-group. The cell apotosis was typical after irradiation in the R-group. Apoptosis index that was detected in the cells of submandibular glands of the TPR-group was statistically significantly decreased compared with the R-group (P < 0.01) on the 3rd, 6th and 30th day after irradiation. CONCLUSION: TP could protect submandibular glands from radiation injuries, and the protection mechanism may be realised by anti-apoptosis.
Subject(s)
Plant Extracts/therapeutic use , Polyphenols/therapeutic use , Radiation Injuries, Experimental/prevention & control , Radiation-Protective Agents/therapeutic use , Submandibular Gland/radiation effects , Tea , Animals , Apoptosis/drug effects , Apoptosis/radiation effects , Atrophy , Cell Death/drug effects , Cell Death/radiation effects , Cell Degranulation/drug effects , Cell Degranulation/radiation effects , Cell Nucleus/drug effects , Cell Nucleus/radiation effects , Extracellular Space/drug effects , Extracellular Space/radiation effects , Female , Gamma Rays , In Situ Nick-End Labeling , Microscopy, Electron, Transmission , Organelles/drug effects , Organelles/radiation effects , Radiation Dosage , Radiation Injuries, Experimental/pathology , Random Allocation , Rats , Rats, Wistar , Submandibular Gland/drug effects , Submandibular Gland/pathology , Time FactorsABSTRACT
OBJECTIVE: To study the regulation of anoikis by tyrosine kinase receptor B (TrkB) in human nasopharyngeal carcinoma lines. METHODS; Expression levels of TrkB and brain-derived neurotrophic factor (BDNF) were evaluated by RT-PCR and Western blot. Colony formation ability of C666-1 was observed in soft agar. Proliferation rate and apoptosis, that change in cells by treating the TrkB inhibitor K252a and specificity ligand BDNF respectively under suspension culture, were measured by cell counting kit-8 (CCK-8) assay and the flow cytometry assay. The expression change of TrkB, BDNF and phosphorylation of serine threonine kinase (p-Akt) were investigated by Western blot analysis. RESULTS: TrkB and BDNF were identified in C666-1 cells. C666-1 cells could be decreased the proliferation of colony in soft agar by effect of K252a, but BDNF could make the colony prolific. K252a can inhibit the expression of TrkB in C666-1, and prevent p-Akt activation. And exogenous BDNF stimulated up-regulation TrkB and p-Akt, induced anoikis resistance. CONCLUSION: TrkB inhibits anoikis in nasopharyngeal carcinoma cells. Inhibiton of TrkB by K252a can induce anoikis, and may prove particularly effective in treatment of nasopharyngeal carcinoma.
Subject(s)
Anoikis , Receptor, trkB/metabolism , Carcinoma , Cell Line, Tumor , Humans , Nasopharyngeal Carcinoma , Nasopharyngeal Neoplasms/metabolism , Nasopharyngeal Neoplasms/pathologyABSTRACT
<p><b>OBJECTIVE</b>To evaluate protective effect of minocycline,a semisynthetic tetracycline derivative on different traumatic brain injuries in rats and mice.</p><p><b>METHODS</b>The opened brain trauma was induced in rats and the closed head injury and cold brain injury were induced in mice. In 3 brain trauma models, minocycline (45 mg/kg, ip) was administered twice daily for 2 d before the operation, at 30 min before and 1 h after the operation, and once daily for 2 d following the operation (totally 8 doses in 5 d). After the operation, the behavioral alteration was observed daily, lesion area and survival neuron density were measured at the end of the experiments (14 d after the injuries).</p><p><b>RESULT</b>For rat opened traumatic injury, minocycline promoted the recovery of hindlimb motor activity (inclined board angle), but did not alter other indexes. For mouse closed head traumatic injury, minocycline reduced the neuron loss, but did not improve behavioral dysfunction. For mouse cold injury-induced trauma, minocycline reduced death rate and lesion area, but did not remarkably improve behavior and neuron loss.</p><p><b>CONCLUSION</b>Minocycline only has an incomplete neuroprotective effect on different brain traumatic injuries in rats and mice.</p>
