Rutin protects against trimethyltin-induced learning and memory impairment in BALB/c mice by antagonizing down-regulated synaptophysin expression / 南方医科大学学报

<p><b>OBJECTIVE</b>To explore the protective effects of rutin against learning and memory impairment induced by trimethyltin (TMT) and investigate the possible mechanism.</p><p><b>METHODS</b>Forty 6- to 9-week-old male BALB/c mice were randomized equally into saline group (control), TMT group, TMT+rutin group, and rutin group. Mouse models of learning and memory impairment were establish by acute TMT (2.25 mg/kg) exposure. In TMT+rutin and rutin treatment groups, the mice received intraperitioneal injection of rutin (10 mg/kg) for 1 week before TMT exposure. Twenty-four hours after TMT exposure, Morris water maze test was employed to test the escape latency of the mice, and the synaptophysin expression in the hippocampus and cortex were analyzed by Western blotting.</p><p><b>RESULTS</b>Compared that in TMT group, the escape latency of the mice in water maze test was significantly shorter in the other 3 groups (P<0.05); the escape latency in TMT +rutin group was similar with that in the control and rutin groups (P>0.05). Western blotting showed significantly decreased synaptophysin expression in the hippocampus and cortex in TMT group (P<0.05); synaptophysin expression in TMT +rutin group increased significantly compared with that in TMT group (P<0.05) but showed no statistical significance from that in rutin and control groups (P>0.05).</p><p><b>CONCLUSION</b>Rutin pretreatment offers protective effect against TMT-induced learning and memory impairment in mice possibly by antagonizing decreased synaptophysin in the hippocampus and cortex.</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>

Effect of microwave irradiation on expression of heat shock proteins family in primary cultured rat hippocampal neurons / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of microwave irradiation on the expression and regulation of heat shock proteins (HSPs) in primary cultured rat hippocampal neurons.</p><p><b>METHODS</b>Neurons were exposed to 90 mW/cm(2) microwave irradiation for 10 minutes. Western blot was used to determine the expression of HSP27, HSP70, HSP90 and heat shock factor 1 (HSF1) at 0, 3, 6, 12 and 24 hour respectively. Real-time RT-PCR was used to determine the mRNA expression of HSF1. DNA-binding activity of HSF1 was measured by electrophoretic mobility shift assay (EMSA).</p><p><b>RESULTS</b>The protein expression of HSP27 was significantly increased by 22%, 36%, 18% at 3, 6, 12 h, respectively (P < 0.05). The protein expression of HSP70 was significantly increased by 23%, 32%, 26% at 3, 6, 12 h, respectively (P < 0.05, P < 0.01). The protein expression of HSP90 was significantly increased by 27%, 33% at 6, 12 h, respectively (P < 0.05, P < 0.01). The DNA-binding activity of HSF1 was stimulated, however, no significant change of the expression of HSF1 was observed on both the mRNA and protein levels.</p><p><b>CONCLUSION</b>The transcriptional activity of HSF1 is activated by microwave irradiation, which promotes the expression of HSPs. Heat shock response which contributes to establish a cytoprotective state is induced by microwave irradiation in primary cultured rat hippocampal neurons.</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>