The Chinese medicine nutrient diet intervention prevent against the neurologic damage induce by EMF irradiation in rat hippocampus / 中国应用生理学杂志

<p><b>OBJECTIVE</b>To 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.</p><p><b>METHODS</b>Eighty 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).</p><p><b>RESULTS</b>The 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).</p><p><b>CONCLUSION</b>The 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.</p>

The injury effects of microwave exposure on visual performance and retinal ganglion cells (RGCs) in rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the injury effects of microwave on the visual performance and the apoptosis of retinal ganglion cells (RGCs) in rats and the relationship between the impaired visual performance and RGCs apoptosis induced by microwave.</p><p><b>METHODS</b>The visual performance of rats was observed by Electroretinogram (ERG) and Flash visual evoked potentials (F-VEP). The apoptosis of RGCs in vivo and in vitro was detected by TUNEL assay and Hoechst staining.</p><p><b>RESULTS</b>Microwave exposure had no influence on ERG-a wave. The amplitude of ERG-b wave decreased significantly on the 3rd day and 7th day after microwave exposure (P < 0.01).The latency of ERG-b wave shortened significantly only at 3rd day after microwave exposure (P < 0.01). The latency of F-VEP extended markedly on the 3rd day after exposure (P < 0.05) and recovered on the 7th day after microwave exposure. The amplitude of F-VEP decreased significantly in exposure group, as compared with sham-exposure group, on the 3rd day and 7th day after microwave exposure (P < 0.05). After microwave exposure for 12 h, the apoptotic rate of RGCs in rat increased from 2.85% to 6.73%, and on the 7th day after exposure, the apoptotic rate of RGCs remained 8.93% (P < 0.05). The apoptotic rate of cultured RGCs increased from 8.42% to 13.91% at 6 hour (P < 0.05) and to 24.14% at 24 hour (P < 0.01) after microwave exposure (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Microwave exposure can injure the visual performance of rats, and the apoptosis of RGCs induced microwave may be one of the main pathological mechanisms.</p>

Relationship between activation of microglia and Jaks phosphorylation induced by microwave irradiation / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the relationship between microglial proinflammatory and electromagnetic radiation and unveil the role of microglia in microwave radiation induced central nervous system injury.</p><p><b>METHODS</b>N9 microglia cells cultured in vitro were exposed to microwave at 90 mW/cm2. Cell flow cytometry was used to observe the expression of CD11b at different time points after exposure; ELISA was used to detect the concentration of TNF-alpha in N9 cell culture supernatant; RT-PCR analysis confirmed iNOS mRNA expression in N9 microglia cells; and Nitrate Reductase Method was used to test NO amount in culture supernatant.</p><p><b>RESULTS</b>The CD11b positive microglial cells increased significantly at 3 h after microwave exposure (P < 0.05), continued to increase until 24 h and peaked at 6 h after exposure. The amount of TNF-alpha rose dramatically from 1 h to 24 h after exposure (P < 0.01) and peaked at 3 h [(762.1 +/- 61.5) pg/ml] after exposure (P < 0.01). The level of NO started to increase at 1 h [(4.48-0.59) micromol/L] and lasted for 24 h after exposure. The expression of iNOS mRNA increased significantly at 1 h (P < 0.05), and tripled the original expression at 6 h after exposure, hereafter, it decreased slightly, but all were higher than the control group within 24 h after exposure.</p><p><b>CONCLUSION</b>Microwave radiation could induce the activation of microglia cells. The activated microglia cells could induce microglial proinflammatory by producing large amounts of TNF-alpha, NO, etc.</p>

Effects of occupational microwave irradiation on heat shock protein 70 expressions in rat hippocampus / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the change of heat shock protein (HSP)70 expression after exposure to occupational microwave in rats hippocampus, and explore the role of HSP70 in the mechanism of bio-effect of microwave irradiation.</p><p><b>METHODS</b>The animal model was established by whole body exposures in 90, 5 W/cm(2) microwave irradiation field for 20 min in rats. Changes of the mRNA of hsp70 expressions in rat hippocampus at different time were studied by RT-PCR, and the protein change by Western blot.</p><p><b>RESULTS</b>The mRNA and protein expression of hsp70 in rat hippocampus increased after 90 W/cm(2) and 5 W/cm(2) microwave irradiation for 20 min. The anal temperature and the value of SAR increased significantly. These changes were positively correlated with power and irradiation time of microwave. The results indicated that microwave irradiation led to HSP70 syntheses effectively.</p><p><b>CONCLUSION</b>Microwave irradiation can obviously induce the thermal effect and activate HSP70, and initiate the endogenous protective mechanism of central nervous system.</p>

Effect of mitogen activated protein kinase signal transduction on apoptosis of PC12 cells induced by electromagnetic exposure / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe the effect of mitogen activated protein kinase (MAPK) signal transduction system on the apoptosis induced by electromagnetic exposure in PC12 cells.</p><p><b>METHODS</b>After 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.</p><p><b>RESULTS</b>U0126, 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.</p><p><b>CONCLUSION</b>The 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.</p>

Differential activation of mitogen-activated protein kinase in PC 12 cells apoptosis induced by electromagnetic irradiation / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the relationship between differential activation of mitogen-activated protein kinase (MAPK) signal transduction system and apoptosis in PC12 cells induced by electromagnetic irradiation.</p><p><b>METHODS</b>Cultured 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.</p><p><b>RESULTS</b>Electromagnetic 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.</p><p><b>CONCLUSION</b>The 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.</p>