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>

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>

Effect of microwave irradiation on neurocyte mitochondrial ultrastructure and mtTFA mRNA expression in rats cerebral cortex and hippocampus / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore molecular controlling mechanism of mitochondrial injury induced by different density of microwave irradiation.</p><p><b>METHODS</b>Rats 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.</p><p><b>RESULTS</b>After 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).</p><p><b>CONCLUSION</b>No 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.</p>