この研究は、グルココルチコイド誘発性骨粗鬆症(GIOP)ラットを用いて、その骨形成および脂質代謝に対するパルス化電磁界(PEMF)の影響、さらにはGIOPラットにおける古典的Wnt信号伝達経路の重要な構成要素および標的を探索した。その結果、PEMFばく露終了から12週間後において、全身の骨密度(BMD)レベルが有意に上昇し、血清脂質レベルが有意に低下し、骨梁厚が増加した;このようなPEMFばく露の影響に古典的Wnt信号伝達経路が重要な役割を果たすことが示された、と報告している。
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The effects of exposure to a pulsed 50 Hz magnetic field on bone formation and lipid metabolism and the underlying signal pathways should be investigated in a rat osteoporosis model.
Glucocorticoid-induced osteoporosis should be investigated. Therefore, all rats, except for the control group (group 4, see below), were injected with dexamethasone sodium phosphate injection (2.5 mg/kg body weight) into their right haunch muscles twice a week, 12 weeks prior to (sham) exposure to the pulsed magnetic field.
Rats were divided into 4 groups (n=10 each): 1) exposure to the pulsed magnetic field, 2) sham exposure and daily oral calcium supplement (56.25 mg/kg body weight), 3) only sham exposure, 4) sham exposed control group.
ばく露 | パラメータ |
---|---|
ばく露1:
50 Hz
Modulation type:
pulsed
ばく露時間:
40 minutes/day for 12 weeks
|
|
周波数 | 50 Hz |
---|---|
タイプ |
|
波形 |
|
ばく露時間 | 40 minutes/day for 12 weeks |
Modulation type | pulsed |
---|---|
Pulse width | 200 µs |
ばく露の発生源/構造 |
|
---|---|
Sham exposure | A sham exposure was conducted. |
測定量 | 値 | 種別 | Method | Mass | 備考 |
---|---|---|---|---|---|
磁束密度 | 4 mT | - | - | - | - |
After exposure to the pulsed magnetic field for 12 weeks (group 1), the whole body bone mineral density was significantly increased, serum lipid levels were significantly decreased and trabecular bone (osseus tissue) in vertebra was significantly thicker compared to sham exposed GIOP rats (group 3).
The gene expressions and/or protein expressions of Wnt10b, LRP5, beta-catenin, OPG and Runx2 were significantly upregulated and Axin2, RANKL, PPAR-gamma, C/EBP-alpha, FABP4 and Dkk-1 were significantly downregulated in group 1 compared to group 3.
The authors conclude that exposure to a pulsed 50 Hz magnetic field might prevent bone loss and improve lipid metabolism disorders in osteoporosis model rats via the Wnt signaling pathway.
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