ABSTRACT
AIM OF THE STUDY: Sanazole and gemcitabine have been proven clinically as hypoxic cell radiosensitisers. This study was conducted to determine the radiation enhancing effects of sanazole and gemcitabine when administered together at relevant concentrations into hypoxic human MCF-7 and HeLa cells. MATERIAL AND METHODS: A 3-(4,5 dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay was used to evaluate the number of surviving cells. Cell cycle was determined by flow cytometry. Cell surviving fractions were determined by the standard in vitro colony formation assay. RESULTS: The cell colony formation assay indicated that the radiosensitivity of hypoxic MCF-7 and HeLa cells was enhanced by sanazole or gemcitabine. The combination of the two drugs displayed significant radiation enhancing effects at the irradiation doses of 6, 8, and 10 Gy in both cell lines, which were arrested in the S phase. CONCLUSIONS: This study indicated that the co-administration of the two drugs may result in a beneficial gain in radio-therapy for hypoxic breast cancer and cervical cancer.
ABSTRACT
PURPOSE: This study was conducted to determine the synergistic radiation sensitizing effects of the combination of sanazole and irinotecan in hypoxic cervical cancer HeLa human tumor cell line. METHODS: The 3-(4,5 dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay was used to evaluate the number of surviving cells. Cell cycle was determined by flow cytometry. Surviving cell fractions were determined by the standard in vitro colony formation assay. RESULTS: The MTT assay showed that the presence of irinotecan with or without sanazole reduced significantly the cells' viability. Flow cytometry demonstrated that the combination of sanazole and irinotecan led to more HeLa cells blocked in G(2) phase. Cell colony formation assay indicated that the radiosensitivity of hypoxic HeLa cells was enhanced by sanazole and/or irinotecan. CONCLUSION: This study showed that the radiation enhancing effects produced by the combination sanazole and irinotecan was significant in hypoxic HeLa cells, which were arrested in the G(2) phase of the cell cycle. This study may provide a new combination modality of radiosensitizers in the radiotherapy of cervical cancer.
Subject(s)
Camptothecin/analogs & derivatives , Radiation Tolerance/drug effects , Radiation-Sensitizing Agents/pharmacology , Triazoles/pharmacology , Uterine Cervical Neoplasms/pathology , Antineoplastic Combined Chemotherapy Protocols , Apoptosis/drug effects , Apoptosis/radiation effects , Camptothecin/pharmacology , Cell Cycle/drug effects , Cell Cycle/radiation effects , Cell Proliferation/drug effects , Cell Proliferation/radiation effects , Female , Flow Cytometry , Gamma Rays , Humans , Hypoxia , Irinotecan , Tumor Cells, Cultured , Uterine Cervical Neoplasms/drug therapy , Uterine Cervical Neoplasms/radiotherapyABSTRACT
Recent studies have shown that the c-Jun N-terminal kinase (JNK) signaling pathway is involved in dopaminergic neuronal degeneration, and direct blockade of JNK by specific inhibitors may prevent or effectively slow the progression of Parkinson disease (PD). Previous studies have revealed that the natural phenolic compound curcumin can reduce inflammation and oxidation, which makes it a potential therapeutic agent for neurodegenerative diseases. In this study, we investigated whether curcumin protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP) or 1-methyl-4-phenylpyridnium ion- (MPP(+)) induced dopaminergic neurotoxicity in C57BL/6N mice or SH-SY5Y cells by inhibiting JNK pathways both in vivo and in vitro. Curcumin treatment significantly improved behavioral deficits, and enhanced the survival of tyrosine hydroxylase-positive neurons in the substantia nigra (SN) in the MPTP-induced PD model mice. Most importantly, curcumin treatment significantly inhibited MPTP/MPP(+)-induced phosphorylation of JNK1/2 and c-Jun, and cleaved caspase-3. Our study suggests that the neuroprotective effect of curcumin is not related simply to its antiinflammatory and antioxidant properties, but involves other mechanisms, particularly by targeting the JNK pathways.
Subject(s)
Curcumin/pharmacology , Dopamine/metabolism , JNK Mitogen-Activated Protein Kinases/antagonists & inhibitors , MAP Kinase Signaling System/drug effects , Neurons/enzymology , Neurons/pathology , 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine , Animals , Astrocytes/drug effects , Astrocytes/enzymology , Astrocytes/pathology , Behavior, Animal/drug effects , Caspase 3/metabolism , Cell Death/drug effects , Cell Line , Curcumin/therapeutic use , Enzyme Activation/drug effects , Humans , JNK Mitogen-Activated Protein Kinases/metabolism , Male , Mice , Mice, Inbred C57BL , Nerve Degeneration/chemically induced , Nerve Degeneration/drug therapy , Nerve Degeneration/prevention & control , Neurons/drug effects , Proto-Oncogene Proteins c-jun/metabolism , Substantia Nigra/drug effects , Substantia Nigra/enzymology , Substantia Nigra/pathologyABSTRACT
OBJECTIVE: To explore the relationship between immunochemical level of salivary and caries in children aged 4-6 years old. METHODS: Two groups were assorted as patients with caries and without caries. Every group included 45 people. Measurements of salivary secretory immunoglobulin A (SIgA)were performed by using radio-immunoassay and single agar diffusion assay. The levels of lysozyme (LZ), alkaline phosphatase (ALP) and lactic dehydrogenase (LDH) were studied with colorimetry and turbidimentry. RESULTS: The levels of LDH, SigA, ALP, LZ had significant difference between the two groups (P < 0.05). The level of LDH between patients and peoples without caries had little difference (P > 0.05). CONCLUSION: The incidence of caries is associated with age, and it may have association with immunochemical levels of salivary.
