OBJECTIVETo explore molecular controlling mechanism of mitochondrial injury induced by different density of microwave irradiation.

METHODSRats were exposed to microwave irradiation for 1 hour at average power density of 3 mW/cm(2) or 30 mW/cm(2). After microwave irradiation, the changes of pathological ultrastructure of rat cerebral cortex and hippocampus were observed by electron microscope, and mitochondrial transcription factor A (mtTFA) mRNA expression level were determined by RT-PCR.

RESULTSAfter 3 mW/cm(2) microwave irradiation for 0, 3, 24 h, mitochondrial ultrastructure and mtTFA mRNA expression level didn't significantly change in rat cerebral cortex and hippocampus. After 30 mW/cm(2) microwave irradiation for 0, 3, 24 h, mitochondrial ultrastructure obviously changed, mtTFA mRNA expression in rat hippocampus significantly increased by 67.00%, 80.00%, 30.00% respectively, and in rat cerebral cortex by 133.00%, 86.00%, 233.00% respectively. There were significant differences between the corresponding groups of hippocampus and cerebral cortex (P < 0.01).

CONCLUSIONNo obvious change in mitochondria was found after 3 mW/cm(2) microwave irradiation, but it was found after 30 mW/cm(2) microwave irradiation. Mitochondria injury in cerebral cortex was more severe than that in hippocampus. mtTFA mRNA may have certain regulation in mitochondrial energy metabolism.

Animals ; Cerebral Cortex ; metabolism ; radiation effects ; DNA-Binding Proteins ; genetics ; Hippocampus ; metabolism ; radiation effects ; Male ; Microscopy, Electron ; Microwaves ; adverse effects ; Mitochondria ; metabolism ; radiation effects ; ultrastructure ; Mitochondrial Proteins ; genetics ; Nuclear Proteins ; genetics ; RNA ; genetics ; metabolism ; RNA, Messenger ; genetics ; metabolism ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factors ; genetics

OBJECTIVETo observe the neurologic damage in rat hippocampus after electromagnetic field (EMF) acute or chronic irradiation and research the protective effects of Chinese medicine diet (CMD) which comprised ferulic acid, ginsenoside, astragalus polysaccharide and rhodiola sachalinensis.

METHODSEighty rats were divided into ten groups (n = 8): normal diet with shame irradiation group (NS), normal diet with chronic irradiation group (NCI), three groups of normal diet with acute irradiation after 3 h, 24 h, 72 h (NAI), Chinese medicine diet with shame irradiation group (CS), Chinese medicine diet with chronic irradiation group (CCI), three groups of Chinese medicine diet with acute irradiation after 3 h, 24 h, 72 h (CAI). The chronic EMF irradiation were performed by electromagnetic wave at 15 W/cm2 for 20 min everyday for 8 weeks continuously. The acute EMF irradiation were performed by electromagnetic wave at 65 W/cm2 for 20 min after feeding with CMD for 8 weeks. The learning and memory were evaluated by Morris water maze before/after electromagnetic wave irradiation. The apoptotic cells in hippocampus was detected by Tunel staining. The peroxidation damage of EMF and the protective effect of CMD intervention were assayed by measuring superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and reactive oxygen species (ROS).

RESULTSThe acute and chronic EMF irradiation disturbed the ability of learning and memory significantly (P < 0.05), CMD intervention markedly antagonized this effect. The apoptotic cells in hippocampus increased evidently after EMF irradiation (P < 0.05), but CMD intervention reduced the apoptotic cells. The acute and chronic EMF irradiation induced the oxidative stress by down-regulating SOD activity, GSH-Px activity, ROS inhibiting and up-regulating the content of MDA obviously (P < 0.05), and CMD intervention reduced peroxidation damage significantly (P < 0.05).

CONCLUSIONThe acute and chronic EMF irradiation could initiate neurologic damage in hippocampus. CMD intervention has protective effect on the impaired learning and memory, the neuron apoptosis, the peroxidation damage induced by EMF irradiation. CMD intervention plays a significant protective role in antagonizing neurologic damage in the later stage of acute irradiation and chronic irradiation.

Animals ; Apoptosis ; Drugs, Chinese Herbal ; therapeutic use ; Electromagnetic Fields ; adverse effects ; Female ; Hippocampus ; radiation effects ; Male ; Oxidation-Reduction ; Oxidative Stress ; Phytotherapy ; Radiation Injuries, Experimental ; drug therapy ; Rats ; Reactive Oxygen Species

Objective To determine kinetics of TNF-α and miR-146a (microRNA-146a)expressions in lipopolysaccharide (LPS)-induced NR8383 alveolar macrophages (AM) at different intervals and their relationships in order to explore regulatory effect and mechanism of miR-146a on alveolar macrophages inflammatory responses.Methods NR8383 alveolar macrophages were seeded in a 6-well plate,and stimulated with 1 μg/ml of LPS for 0 h,3 h,6 h and 12 h separately after 90 min.Cells were harvested and supernatant were collected 0 h,3 h,6 h and 12 h after incubation.The expressions of miR146a and TNF-α mRNA in cells were detected by real-time qPCR and the levels of TNF-α protein in the supematant of cells were assayed by enzyme-linked immunosorbent assay ( ELISA ).Pearson correlation analysis was used to analyze the correlation between miR-146a and TNF-α mRNA.Results ①The level of TNF-α protein in the supernatant of cell was significantly increased 3 h after LPS challenge ( 359.80 ±57.54) pg/ml (P ＜0.01 ),and peaked 12 h later (729.22 ±50.40) pg/ml (P＜0.01 ) ; ②the expression of TNF-α mRNA peaked 3 h after LPS challenge (67.48 ±24.52) fold,P ＜0.01 ),and then decreased gradually; ③the expression of miR-146a mRNA increased continuously until 6 h or 12 h after LPS challenge 6 h:(5.33 ±0.81) fold,12 h:(8.21 ±1.19) fold,(P＜0.01),and it showed an upward tendency;④ the expression of miR-146a mRNA was negatively correlated with TNF-α mRNA ( r =-0.895,P ＜0.01).Conclusions The miR-146a mRNA showed a negative correlation with TNF-α mRNA present in lipopolysaccharide-stimulated alveolar macrophages,suggesting miR-146a mRNA involved in regulating the inflammatory response of alveolar macrophages.

OBJECTIVETo observe the effect of mitogen activated protein kinase (MAPK) signal transduction system on the apoptosis induced by electromagnetic exposure in PC12 cells.

METHODSAfter pretreated by SB203580 alone or together with U0126, PC12 cells were exposed to 65 mW/cm(2) electromagnetic wave for 20 min. The phosphorylations of ERK1/2, JNK and P38 MAPK were tested by Western-blot at 3 h and 24 h after electromagnetic exposure. The apoptosis of PC12 cells were detected by Annexin-V-FITC flow cytometry.

RESULTSU0126, but not SB203580 could inhibit the activation of ERK1/2 induced by electromagnetic exposure. U0126 and SB203580 had no effects on the activation of JNK. SB203580 could inhibit the activation of P38 MAPK significantly. But U0126 had no such effect on the activation of P38 MAPK. After pretreated by SB203580 alone or together with U0126, the apoptosis of PC12 cells decreased. But the pretreatment by U0126 alone had no influence on the apoptosis of PC12 cells.

CONCLUSIONThe P38 MAPK signal transduction modulate the apoptosis of PC12 cells induced by electromagnetic exposure. ERK signal transduction has no effect on the apoptosis of PC12 cells. JNK signal transduction may promote the apoptosis of PC12 cells in the early stage after electromagnetic exposure.

Animals ; Apoptosis ; radiation effects ; Electromagnetic Radiation ; Mitogen-Activated Protein Kinases ; metabolism ; PC12 Cells ; Phosphorylation ; Rats ; Signal Transduction

OBJECTIVETo explore the relationship between differential activation of mitogen-activated protein kinase (MAPK) signal transduction system and apoptosis in PC12 cells induced by electromagnetic irradiation.

METHODSCultured PC12 cells were exposed to 65 mW/cm(2) electromagnetic wave for 20 min. The PC12 cells apoptosis was detected by flow cytometry 0, 3, 12, 24 h after electromagnetic irradiation. The phosphorylations of ERK1/2, JNK and P38 MAPK were tested by Western-blot.

RESULTSElectromagnetic irradiation induced apoptosis in PC12 cells soon after irradiation. The apoptotic rate of PC12 cells increased to about 23.5% at 3 h. But compared with that at 3 h, there was no significant difference in the apoptotic rate at 12 h (P > 0.05). The apoptotic rate of PC12 cells increased sharply again at 24 h. After exposure to electromagnetic irradiation, the phosphorylations of ERK1/2 and JNK increased significantly. The increased phosphorylation of ERK1/2 lasted for 3 hours, but of JNK lasted for 12 hours, and 24 hours after irradiation. The phosphorylation of both ERK1/2 and JNK were significantly lower than that of control. The phosphorylation of P38 MAPK was always higher after electromagnetic irradiation, and there were two phosphorylation peaks at 3 h and 24 h.

CONCLUSIONThe electromagnetic irradiation can induce the activation of MAPK signal transduction system, and ERK1/2, JNK, P38 MAPK showed differential activation. The differential activation of MAPKs may play an important role in the apoptosis of PC12 cells induced by electromagnetic irradiation.

Animals ; Apoptosis ; radiation effects ; Blotting, Western ; Flow Cytometry ; MAP Kinase Kinase 4 ; metabolism ; physiology ; Mitogen-Activated Protein Kinase 3 ; metabolism ; physiology ; Mitogen-Activated Protein Kinases ; metabolism ; physiology ; PC12 Cells ; Phosphorylation ; Rats ; Signal Transduction ; radiation effects ; p38 Mitogen-Activated Protein Kinases ; metabolism ; physiology

OBJECTIVE: The primary objective of this study was to examine the validity and reliability of a semi-quantitative food frequency questionnaire (FFQ) among Chinese children aged 12-17 years. METHODS: A semi-quantitative 72-food item FFQ was developed for children aged 12-17 years. The reliability and validity of this FFQ were evaluated against 24-h dietary recalls (24 h DRs) to measure the consumption of foods and nutrients. We administered two FFQs and three DRs to children (N = 160) over a period of 1 month to evaluate the reliability and validity. Reliability was examined by quartile agreement and intraclass correlation coefficients (ICCs), and validity was examined by quartile agreement, Bland-Altman plots and correlation with DRs. RESULTS: For reliability, the ICCs between the two FFQs ranged from 0.21 to 0.76 for foods and nutrients, and the quartile agreement ranged from 70.0% to 95.0% in the same or adjacent quartiles. Spearman's correlation coefficients of foods and nutrients between the second FFQ and the 24 h DRs ranged from -0.04 to 0.59. The Bland-Altman plots demonstrated good agreement across the range of intakes among nutrients. The quartile agreement ranged from 50.0% to 100.0%, with infrequent misclassification. CONCLUSION The FFQ assessment of dietary intakes demonstrated acceptable relative validity and high reproducibility for Chinese children aged 12-17 years.
Adolescent ; Child ; Diet Records ; Female ; Humans ; Male ; Reproducibility of Results ; Surveys and Questionnaires