The purpose of this study is to investigate the mechanism of alternative responses to low dose irradiation for neuronal cell proliferation in the dentate gyrus of rats. To determine the effect of a single exposure to radiation, rats were irradiated with a single dose of 0.1, 1, 10 or 20 Gy. To determine the effect of the cumulative dose, the animals were irradiated daily with 0.01 Gy or 0.1 Gy from 1 to 4 days. The neuronal cell proliferation was evaluated using immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU), Ki-67 and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. Four consecutive daily irradiations with a 0.01 Gy/fraction increased the number of BrdU-positive and Ki-67-positive cells in a dose dependent manner, but this did not affect the number of TUNEL-positive cells. However, there was not a dose dependent relationship for the 0.1 Gy/fraction irradiation with the number of BrdU, Ki-67 and TUNEL positive cells. Our data support the explanation that the adaptive response, induced by low-dose radiation, in the hippocampus of rats is more likely a reflection of the perturbations of cell cycle progression.
Rats, Sprague-Dawley ; Rats ; Radiation Dosage ; Neurons/*cytology/*radiation effects ; Neuronal Plasticity/*radiation effects ; Male ; Dose-Response Relationship, Radiation ; Dentate Gyrus/*cytology/*radiation effects ; Cell Survival/radiation effects ; Cell Proliferation/*drug effects ; Animals ; Adaptation, Physiological/radiation effects

OBJECTIVETo investigate the effect of curcumin (Cur) on radiosensitivity of nasopharyngeal carcinoma cell CNE-2 and its mechanism.

METHODThe effect of curcumin on radiosensitivity was determined by the clone formation assay. The cell survival curve was fitted by Graph prism 6. 0. The changes in cell cycle were analyzed by flow cytometry (FCM). The differential expression of long non-coding RNA was detected by gene chip technology. Part of differentially expressed genes was verified by Real-time PCR.

RESULTAfter 10 micro mol L-1 Cur had worked for 24 h, its sensitization enhancement ratio was 1. 03, indicating that low concentration of curcumin could increase the radiosensitivity of nasopharyngeal carcinoma cells; FCM displayed a significant increase of G2 phase cells and significant decrease of S phase cells in the Cur combined radiation group. In the Cur group, the GUCY2GP, H2BFXP, LINC00623 IncRNA were significantly up-regulated and ZRANB2-AS2 LOC100506835, FLJ36000 IncRNA were significantly down-regulated.

CONCLUSIONCur has radiosensitizing effect on human nasopharyngeal carcinoma CNE-2 cells. Its mechanism may be related to the changes in the cell cycle distribution and the expression of long non-coding IncRNA.

Cell Cycle ; drug effects ; radiation effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Curcumin ; pharmacology ; Gene Expression Regulation, Neoplastic ; drug effects ; radiation effects ; Humans ; RNA, Long Noncoding ; genetics ; Radiation Tolerance ; drug effects

OBJECTIVETo study radiation-enhancing effects on human gastric cancer MKN28 cell line and underlying mechanisms of β-elemene.

METHODSInhibition of MKN28 cell proliferation at different concentrations of β-elemene was assessed using the methyl thiazolyl blue colorimetric method (MTT method), with calculation of IC50 value and choice of 20% of the IC50 as the experimental drug concentration. Irradiation group and β-elemene+irradiation group were established, and the cell survival fraction (SF) was calculated from flat panel colony forming analysis, and fitted by the 'multitarget click mathematical model'. Draw the survival curve and get the radiobiological parameters D0, Dq, SF2, N and SER. Flow cytometry (FCM) was used to detect changes in the cell cycle and cell apoptosis rates was detected by Annexin-V/PI assay.

RESULTSβ-elemene exerted inhibitory effects on proliferation of gastric cancer MKN28 cells, with an IC50 of 45.6 mg/L and we chose 8 mg/L as the experimental concentration. The cell survival fraction of MKN28 cells with irradiation decreased significantly after treated with β-elemene; D0, Dq decreased, SER = 1.3. After combined treatment of β-elemene+irradiation, the results of FCM showed that cells could be arrested in the G2/M phase and the cell apoptosis increased significantly.

CONCLUSIONSβ-elemene can enhance the radiosensitivity of gastric cancer MKN28 cell line. Mechanistically, β-elemene mainly influences the cell cycle distribution of MKN28 cells by inducing G2/M phase arrest, inhibits the repair of sublethal damage and induces cell apoptosis to enhance the killing effects of radioactive rays.

Apoptosis ; drug effects ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Humans ; Radiation Tolerance ; drug effects ; Sesquiterpenes ; pharmacology ; Stomach Neoplasms ; pathology

OBJECTIVETo explore the effect of NAD+ against radiation injury and its dose-effect relationship.

METHODSL02 liver cells cultured in RPMI 1640 medium containing 10% fetal calf serum were exposed to X-ray irradiation followed by immediate application of NAD+. The cellular viability was analyzed by MTT assay and the apoptotic cells were detected by TUNEL methods to observe the damages of L02 liver cells induced by X-ray exposure and analyze the dose-effect relationship of NAD+.

RESULTSThe viability of L02 liver cells was decreased with increasing dose of X-ray irradiation. The most obvious growth inhibition of L02 cells occurred 24 h after the irradiation. NAD+ significantly increased the cell survival rate after irradiation, and this effect was gradually increased within the concentration range of 100-1000 microg/ml; at higher concentrations, the survival rate of the irradiated L02 cells showed no significant increase.

CONCLUSIONNAD+ provides partial protection of the liver cells against radiation injury, and the effect is positively correlated to NAD+ concentration within a certain range.

Apoptosis ; drug effects ; radiation effects ; Cell Line ; Cell Survival ; drug effects ; radiation effects ; Dose-Response Relationship, Drug ; Hepatocytes ; cytology ; drug effects ; radiation effects ; Humans ; NAD ; administration & dosage ; pharmacology ; Radiation Injuries ; prevention & control

OBJECTIVETo explore the effects of Huqi Extractum (HQE) on the viability and apoptosis in mouse thymic lymphocytes against 60Co radiation.

METHODSThymic lymphocytes were isolated from 4 -8 weeks healthy male Kunming mice and primarily cultured. Then they were divided into the control group, the irradiation group, the low dose HQE group, the medium dose HQE group, and the high dose HQE group. Equal volume of serum free RPMI-1640 culture solution was added in the control group and the irradiation group, while equal volume of HQE solution (at the daily dose of 25, 50, and 100 mg/mL) was respectively added in the low, medium, and high dose HQE groups. Except the control group, those in the rest groups were exposed radiation at a single dose of 5 Gy gamma-ray. Changes of the thymic lymphocytes' viability were measured by MTT colorimetric assay at 12, 24, 36, and 48 h after radiation. The early apoptosis rate was detected using flow cytometry (FCM) after 10-h radiation. The apoptosis was detected using agarose gel electrophoresis to observe the DNA injury after 24-h radiation.

RESULTSThe viability level decreased more obviously in the irradiation group than in the control group at 24 -48 h after radiation (P < 0.01, P < 0.05). The average viability level was obviously higher in the low, medium, and high dose HQE groups than in the irradiation group (P < 0.05) in a dose dependent manner. The early apoptosis rate was obviously lower in the low, medium, and high dose HQE groups than in the irradiation group, with statistical difference shown in the high dose HQE group (P < 0.01). Typical DNA ladder fragments were found in the electrophoresis in all groups except the control group. But the DNA injury was comparatively milder in the low, medium, and high dose HQE groups, with more obvious effects shown in the high dose HQE group.

CONCLUSIONHQE showed protection for the viability of early thymic lymphocytes exposed to the 60CO radiation, and could lower the early apoptosis level.

Animals ; Apoptosis ; drug effects ; radiation effects ; Cell Survival ; drug effects ; radiation effects ; Cells, Cultured ; Drugs, Chinese Herbal ; pharmacology ; Gamma Rays ; adverse effects ; Male ; Mice ; Mice, Inbred Strains ; Thymocytes ; drug effects ; radiation effects

This study explored the role of radiation-induced autophagy in low-dose hyperradiosensitivity (HRS) in the human lung cancer cell line A549. A549 cells, either treated with an autophagic inhibitor 3-methyladenine (3-MA), or with a vehicle control, were irradiated at different low doses (≤0.5 Gy). The generation of autophagy was examined by laser scanning confocal microscopy. Western blotting was used to detect the expression of microtubule-associated protein l light chain 3B II (LC3B-II). Flow cytometry (FCM) and clonogenic assays were used to measure the fraction of surviving cells at the low irradiation doses. Our results showed that there was a greater inhibition of autophagic activity, but a higher degree of low-dose HRS in A549 cells treated with 3-MA than in control group. Our data demonstrated that radiation-induced autophagy is correlated with HRS in A549 cells, and is probably one of the mechanisms underlying HRS.
Adenine ; analogs & derivatives ; pharmacology ; Autophagy ; drug effects ; radiation effects ; Blotting, Western ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Dose-Response Relationship, Radiation ; Flow Cytometry ; Green Fluorescent Proteins ; genetics ; metabolism ; Humans ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Microscopy, Confocal ; Microscopy, Electron, Transmission ; Microtubule-Associated Proteins ; genetics ; metabolism ; Phagosomes ; drug effects ; radiation effects ; ultrastructure ; Radiation Tolerance ; drug effects ; radiation effects

AIMTo investigate the survival rate and the level of HaCaT cells damage with ultraviolet B (UVB) radiation at various doses, and observe the protective effects of ginsenoside Rg1 and Rb1 in vitro.

METHODSMTT assay was employed to analyze the cell survival rate after UVB radiation of 30, 60, 90 and 120 mJ x cm(-2). The damage of nucleolus and the protective effects of ginsenoside Rg1 and Rb1 were scanned by Hoechst 33258 staining and single cell gel electrophoresis assay (SCGE).

RESULTSIt was found that the cell survival rate decreased gradually and the damage of nucleolus aggravated as the radiation dose increased from 30 mJ x cm(-2) to 120 mJ x cm(-2). At the dose of 20 microg x mL(1-), obvious protective effect of ginsenoside Rg1 and Rb1 can be observed against UVB radiation-induced HaCaT cells growth inhibition and nucleolus damage.

CONCLUSIONUVB radiation inhibits HaCaT human keratinocytes growth and ginsenoside Rg1 and Rb1 can relief the damage.

Apoptosis ; drug effects ; radiation effects ; Cell Line ; Cell Survival ; drug effects ; radiation effects ; DNA Damage ; drug effects ; radiation effects ; Dose-Response Relationship, Radiation ; Ginsenosides ; isolation & purification ; pharmacology ; Humans ; Keratinocytes ; cytology ; drug effects ; radiation effects ; Panax ; chemistry ; Plants, Medicinal ; chemistry ; Protective Agents ; isolation & purification ; pharmacology ; Ultraviolet Rays ; adverse effects

OBJECTIVETo examine the changes of radiosensitivity of CNE1, a well differentiated squamous cell line of nasopharyngeal carcinoma (NPC), and CNE2, a poorly differentiated squamous cell line of NPC, after treatment with chemotherapeutic agents.

METHODSCNE1 and CNE2 cells with and without treated by adriamycin (ADM) were irradiated by X-ray and the radiosensitivity changes of ADM-treated cells were analyzed according to the cell survival curve generated by colony formation assay.

RESULT AND CONCLUSIONRadiosensitivity of CNE1 cells increased after ADM treatment, but that of CNE2 cells decreased, suggesting that different treatment regimens should be planned for advanced squamous cell NPC of different pathological types.

Antineoplastic Agents ; pharmacology ; Carcinoma, Squamous Cell ; pathology ; Cell Differentiation ; drug effects ; radiation effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Dose-Response Relationship, Radiation ; Doxorubicin ; pharmacology ; Humans ; Nasopharyngeal Neoplasms ; pathology ; X-Rays

OBJECTIVETo study the enhancing effect of isoflavonoid genistein in irradiation (IR) on prostate DU145 cancer cells.

METHODSProstate cancer cell line DU145 was used in this experiment. Clonogenic assay was applied to compare the survival fractions of DU145 cells after treatments with genistein alone and/or graded IR. DNA electrophoresis and TUNEL method were applied to detect cell apoptosis. Cell cycle was observed using flow cytometry and related protein expressions by immunoblotting.

RESULTClonogenic assay demonstrated that genistein, even at low to medium concentrations, enhanced the radiosensitivity of DU145 cells. After treatments with IR and/or genistein for 24 h, apoptosis was mainly seen with genistein at high concentration and was minimally dependent on IR. Apoptosis also occurred after treatments for 72 h with lower concentrations of genistein, especially when combined with IR. While IR or genistein led to a G2/M cell cycle arrest, combination of them could further increase DU145 cells at G2/M phase. This G2/M arrest was largely maintained at 72 h, and accompanied by increasing apoptosis and hyperdiploid cell populations. Cell-cycle related protein analysis disclosed biphasic changes in cyclin B1, less markedly increased cdc-2 and stably elevated p21(cip1) levels with increasing genistein concentrations.

CONCLUSIONGenistein could enhance the radiosensitivity of DU145 prostate cancer cells. The mechanisms might be involved in the increased apoptosis, prolonged cell cycle arrest and impaired damage repair induced by the combined treatment.

Apoptosis ; drug effects ; radiation effects ; CDC2 Protein Kinase ; analysis ; Cell Line, Tumor ; Cell Survival ; drug effects ; radiation effects ; Cyclin B ; analysis ; Cyclin B1 ; G2 Phase ; drug effects ; radiation effects ; Genistein ; pharmacology ; Humans ; Male ; Prostatic Neoplasms ; pathology ; radiotherapy ; Radiation-Sensitizing Agents ; pharmacology ; S Phase ; drug effects ; radiation effects

AIM: Radiation induces an important apoptosis response in irradiated organs. The objective of this study was to investigate the radioprotective effect of tetramethylpyrazine (TMP) on irradiated lymphocytes and discover the possible mechanism of protection. METHOD: Lymphocytes were pretreated for 12 h with TMP (25-200 μmol·L(-1)) and then exposed to 4 Gy radiation. Cell apoptosis and the signaling pathway were analyzed. RESULTS: Irradiation increased cell death, DNA fragmentation, activated caspase activation and cytochrome c translocation, downregulated B-cell lymphoma 2 (Bcl-2) and up-regulated Bcl-2-associated X protein (Bax). Pretreated with TMP significantly reversed this tendency. Several anti-apoptotic characteristics of TMP, including the ability to increase cell viability, inhibit caspase-9 activation, and upregulate Bcl-2 and down-regulate Bax in 4Gy-irradiated lymphocytes were determined. Signal pathway analysis showed TMP could translate nuclear factor-κB (NF-κB) from cytosol into the nucleus. CONCLUSION The results suggest that TMP had a radioprotective effect through the NF-κB pathway to inhibit apoptosis, and it may be an effective candidate for treating radiation diseases associated with cell apoptosis.
Apoptosis ; drug effects ; radiation effects ; Cell Line ; Cell Survival ; drug effects ; radiation effects ; DNA Fragmentation ; drug effects ; radiation effects ; Drugs, Chinese Herbal ; pharmacology ; Humans ; Lymphocytes ; cytology ; drug effects ; radiation effects ; NF-kappa B ; genetics ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Pyrazines ; pharmacology ; Radiation-Protective Agents ; pharmacology ; bcl-2-Associated X Protein ; genetics ; metabolism