Modern pharmacological studies have shown that Shengmai San has the effects of enhancing immunity and improving blood circulation, and Curcumae Longae Rhizoma(Jianghuang) has anti-inflammatory, anti-cancer, anti-oxidation and other functions. Shengmai San combined with Jianghuang is a new research direction in the study of anti-tumor of traditional Chinese medicines. The main treatment for nasopharyngeal carcinoma is radiation therapy, but radiation therapy can cause a variety of side effects, and it also changes the composition of the intestinal flora. In this study, the 16 s rDNA sequencing platform was used to perform macro-sequence sequencing of the intestinal flora samples of nude mice bearing the veins of Shengmai Jianghuang San, and then the results of intestinal flora data were analyzed to investigate the effect of Shengmai Jianghuang San on tumors. The results showed that Shengmai Jianghuang San combined with irradiation could enhance the therapeutic effect of tumor treatment. Radiation therapy would reduce the total number and diversity of intestinal flora in nude mice, and also change the structure of the flora. Shengmai Jianghuang San could protect the diversity of colonies, and also partially restore the colony imbalance caused by irradiation. This study provides a research idea for Shengmai Jianghuang San as a sensitizing adjuvant for radiotherapy of nasopharyngeal carcinoma.
Animals ; Drugs, Chinese Herbal ; pharmacology ; Gastrointestinal Microbiome ; drug effects ; Mice ; Mice, Nude ; Nasopharyngeal Carcinoma ; radiotherapy ; Radiation Tolerance ; Radiation-Sensitizing Agents ; pharmacology

Inevitable human exposure to ionizing radiation from man-made sources has been increased with the proceeding of human civilization and consequently public concerns focus on the possible risk to human health. Moreover, Fukushima nuclear power plant accidents after the 2011 East-Japan earthquake and tsunami has brought the great fear and anxiety for the exposure of radiation at low levels, even much lower levels similar to natural background. Health effects of low dose radiation less than 100 mSv have been debated whether they are beneficial or detrimental because sample sizes were not large enough to allow epidemiological detection of excess effects and there was lack of consistency among the available experimental data. We have reviewed an extensive literature on the low dose radiation effects in both radiation biology and epidemiology, and highlighted some of the controversies therein. This article could provide a reasonable view of utilizing radiation for human life and responding to the public questions about radiation risk. In addition, it suggests the necessity of integrated studies of radiobiology and epidemiology at the national level in order to collect more systematic and profound information about health effects of low dose radiation.
DNA Damage/drug effects ; Environmental Exposure ; Humans ; Leukemia/epidemiology/etiology ; Neoplasms, Radiation-Induced/epidemiology ; *Radiation Dosage ; Radiation Tolerance ; *Radiation, Ionizing ; Radioactive Hazard Release ; Risk

OBJECTIVETo study the radiosensitizing effect of resveratrol on hypopharyngeal carcinoma cell line FADU in vitro.

METHODSHypopharyngeal carcinoma cell line FADU was cultured in in vitro DMEM. Its inhibition on cell proliferation was detected using cytotoxicity test (MTT assay). The cell survival curve was drawn using clone formation to obtain sensitive enhancement ratio (SER). Changes of the cell cycle and cell apoptosis were analyzed using flow cytometry (FCM).

RESULTSResults of MTT showed the inhibition of resveratrol on FADU cells increased along with its concentrations (P < 0.05). Results of clone formation indicated the surviving fraction at 2 Gy (SF2) was 0.717 ± 0.062 in the irradiation group, and 0.426 ± 0.035 in the resveratrol plus irradiation group (with SER ranged 1.684 ± 0.178) with statistical difference (P = 0.007). Results of FCM showed that after radiation of 4 Gy radiation, cells at G2/M phase arrest increased, but cells at G1 decreased. After radiation of resveratrol for 24 h, cells at G1 decreased, but cells at G2/M phase and S phase arrest increased. When 4 Gy radiation combined resveratrol was used, cells at G2/M phase arrest significantly increased, but cells at G1 significantly decreased. The apoptosis rate was 1.94% ± 1.65% in the control group, 4.56% ± 0.92% in the irradiation group, 2.03% ± 1.46% in the resveratrol group, and 23.11% ± 7.22% in the resveratrol plus irradiation group. There was statistical difference between the resveratrol plus irradiation group and the rest 3 groups (P < 0.05).

CONCLUSIONResveratrol could enhance the radiosensitivity of hypopharyngeal carcinoma FADU cells in vitro possibly by inducing cell apoptosis and causing changes in the cell cycle distribution.

Apoptosis ; Carcinoma, Squamous Cell ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Head and Neck Neoplasms ; Humans ; Hypopharyngeal Neoplasms ; drug therapy ; Radiation Tolerance ; Radiation-Sensitizing Agents ; therapeutic use ; Stilbenes ; therapeutic use

OBJECTIVETo study the radiosensitizing effect of resveratrol on human hypo pharyngeal squamous cell carcinoma (FaDu) cells in nude mice.

METHODSForty-three nude mice bearing FaDu cell xenografts were randomized into control group, radiotherapy (12 Gy) group, resveratrol treatment (50 mg/kg) group, and radiotherapy plus resveratrol treatment group. After corresponding treatments, the tumor volume in the mice was measured every 3 days, and the microvessel density (MVD) in the tumor was evaluated with CD31 immunofluorescence histochemical staining.

RESULTSThe tumor volume and weight were the smallest in mice receiving radiotherapy plus resveratrol treatment (P<0.05) but comparable between those having resveratrol treatment alone and the control mice. Radiotherapy plus resveratrol treatment resulted in a tumor inhibition rate of 76.64% and a significantly decreased MVD in the tumor compared with the other 3 groups.

CONCLUSIONResveratrol can produce a radiosensitizing effect on human hypopharyngeal carcinoma in nude mice.

Animals ; Carcinoma, Squamous Cell ; drug therapy ; radiotherapy ; Cell Line, Tumor ; radiation effects ; Head and Neck Neoplasms ; drug therapy ; radiotherapy ; Humans ; Hypopharyngeal Neoplasms ; drug therapy ; radiotherapy ; Mice ; Mice, Nude ; Radiation Tolerance ; Radiation-Sensitizing Agents ; pharmacology ; Stilbenes ; pharmacology ; Transplantation, Heterologous ; Tumor Burden

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 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

OBJECTIVE: To study the radiation-sensitizing function and preliminary mechanism of paclitaxel in radiation-resistant nasopharyngeal carcinoma cells. METHOD: X-ray dose fractionated irradiation technology to build radiation-resistant subline of nasopharyngeal carcinoma; CNE-2S1 was treated with paclitaxel alone or combined with radiation therapy, while control group treated with radiation therapy; cell colony formation assay was used to observe sensitizing effect of paclitaxel on radiotherapy; flow cytometry analysis was used to analyze cell cycle distribution and apoptosis ratio of different treatment groups; immunoblotting was used to analyze SHP-1 expression levels of different treatment groups. RESULT: Nasopharyngeal carcinoma cells resistant to radiation was successfully established; cell colony formation assay showed that paclitaxel has obvious sensitizing effect on radiotherapy; FACS results showed that: CNE-2S1 treated by paclitaxel were arrested in G2M phase; paclitaxel and radiotherapy treatments significantly improved the CNE-2S1 apoptosis ratio; Western blot results showed that paclitaxel and combined radiotherapy can reduce the CNE-2S1 cells SHP-1 expression levels. CONCLUSION Paclitaxel enhanced radiation therapy for nasopharyngeal carcinoma cells resistant to radiation, and SHP-1 may be involved in this progress.
Apoptosis ; drug effects ; Carcinoma ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Humans ; Nasopharyngeal Carcinoma ; Nasopharyngeal Neoplasms ; pathology ; Paclitaxel ; pharmacology ; Protein Tyrosine Phosphatase, Non-Receptor Type 6 ; metabolism ; Radiation Tolerance ; drug effects

OBJECTIVE: To determine an approach enriching cancer stem cells from laryngeal cancer cell line. To investigate whether laryngeal cancer stem cells in chemoradiotherapy have the characteristic of resistance. METHOD: CD133+ cells and CD133- cells was detected and isolated from Hep-2 cell line by fluorescence activated cell sorting technology. The cytotoxicities of cisplatin and radiation were investigated by cell counting kit-8(CCK-8) assay. The apoptosis and cell cycle was analyzed with flow cytometry. RESULT: CD133+ cells accounted for a fraction of (2.43 +/- 0.77)% in Hep-2 cell line. CD133+ cells have a more obvious characteristics of cancer stem cells. Different cisplatin and radiation concentrations of for two cell have inhibition, in a certain concentration range and the dosage dependence. Cisplatin and radiation had synergistic inhibitory effects with CD133- cells on the growth of two cell. Moreover, cell cycle arrest at G0/G1 phase and more apoptosis was induced by synergistic combination. Different concentrations of cetuximab for Hep-2 cells have inhibition, in a certain concentration range and time and the dosage dependence. The half maxial inhibitory concentration (IC50) of cetuximab to Hep-2 cells on 24 h was 1 036.84 microg/L. Cisplatin and radiation had synergistic inhibitory effects with cetuximab on the growth of Hep-2 cell line. Moreover, cell cycle arrest at G0/G1 phase and more apoptosis was induced by synergistic combination. CONCLUSION Compared with CD133- cells, CD133+ cells subpopulation exhibited extraordinary cancer stem.
AC133 Antigen ; Antibodies, Monoclonal, Humanized ; pharmacology ; Antigens, CD ; analysis ; Antineoplastic Agents ; pharmacology ; Apoptosis ; Cell Cycle ; Cell Line, Tumor ; Cetuximab ; Chemoradiotherapy ; Cisplatin ; pharmacology ; Drug Resistance, Neoplasm ; Flow Cytometry ; Glycoproteins ; analysis ; Humans ; Laryngeal Neoplasms ; therapy ; Neoplastic Stem Cells ; drug effects ; radiation effects ; Peptides ; analysis ; Radiation Tolerance

Radiation and drug resistance remain the major challenges and causes of mortality in the treatment of locally advanced, recurrent and metastatic breast cancer. Dysregulation of phospholipase D (PLD) has been found in several human cancers and is associated with resistance to anticancer drugs. In the present study, we evaluated the effects of PLD inhibition on cell survival, cell death and DNA damage after exposure to ionizing radiation (IR). Combined IR treatment and PLD inhibition led to an increase in the radiation-induced apoptosis of MDA-MB-231 metastatic breast cancer cells. The selective inhibition of PLD1 and PLD2 led to a significant decrease in the IR-induced colony formation of breast cancer cells. Moreover, PLD inhibition suppressed the radiation-induced activation of extracellular signal-regulated kinase and enhanced the radiation-stimulated phosphorylation of the mitogen-activated protein kinases p38 and c-Jun N-terminal kinase. Furthermore, PLD inhibition, in combination with radiation, was very effective at inducing DNA damage, when compared with radiation alone. Taken together, these results suggest that PLD may be a useful target molecule for the enhancement of the radiotherapy effect.
Breast Neoplasms/*drug therapy/*enzymology/pathology ; Cell Death/drug effects/radiation effects ; Cell Line, Tumor ; Cell Proliferation/drug effects/radiation effects ; DNA Damage ; Enzyme Activation/drug effects/radiation effects ; Enzyme Inhibitors/*pharmacology/*therapeutic use ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Female ; Humans ; JNK Mitogen-Activated Protein Kinases/metabolism ; Phospholipase D/*antagonists & inhibitors/metabolism ; Radiation Tolerance/*drug effects ; Radiation, Ionizing ; p38 Mitogen-Activated Protein Kinases/metabolism

OBJECTIVETo investigate the effects of the ultra-filtration extract mixture from Hedysarum Polybotrys (UEMHP) on the radiosensitivity of HepG2 cells, and to explore its possible mechanisms.

METHODSThe proliferation inhibition effects of UEMHP on HepG2 cells was detected by CCK-8 assay. The colony formation assay was used for the survival fraction (SF) analysis. The distribution of the cell cycle and the apoptosis rate were detected using flow cytometry (FCM). The survivin mRNA expression level was detected using reverse transcription-PCR assay.

RESULTSThe inhibition of UEMHP on HepG2 cells was time-and dose-dependent at the concentration ranging between 5 -50 mg/L (P < 0.05). The parameters of the two curve for SF (P < 0.05) showed statistical difference between the irradiation group and the UEMHP irradiation group. UEMHP could inhibit the clone formation of HepG2 cells and enhance the radiosensitivity of HepG2 cells. The results of FCM showed that UEMHP could induce G2/M phase arrest. The apoptosis rate in the UEMHP irradiation group (21.42% +/- 3.74%) was higher than that in the control group (5.35% +/- 0.41%), the only UEMHP group (10.36% +/- 1.75%), or the irradiation group (10.58% +/- 2.01%) (P < 0.01). RT-PCR showed that the survivin mRNA expression level was lower in the UEMHP irradiation group (0.31 +/- 0.02) than in the control group (0.82 +/- 0.06) and the irradiation group (0.58 +/- 0.04) respectively, showing statistical difference (P < 0.01).

CONCLUSIONUEMHP can enhance the radiosensitivity of HepG2 cells, and its possible mechanisms might be correlated to down-regulating the survivin mRNA expression and promoting the apoptosis.

Apoptosis ; Cell Proliferation ; drug effects ; radiation effects ; Drugs, Chinese Herbal ; pharmacology ; Hep G2 Cells ; Humans ; Inhibitor of Apoptosis Proteins ; metabolism ; Radiation Tolerance ; drug effects