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靜磁場對脂多醣引發的過度免疫反應之影響

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靜磁場對脂多醣引發的過度免疫反應之影響 -對 BALB/cByJNarl 老鼠之體內實驗

The effect of static magnetic field on lipopolysaccharide induced excessive immune reaction

– in vivo investigations on BALB/cByJNarl mice

中文摘要

近年來由細菌引發發炎反應導致嚴重牙周病的患者逐年增加。研究已知革蘭氏陰 性菌細胞壁表面的脂多醣(lipopolysaccharide, LPS)是引發宿主過度免疫反應 (如細菌性敗血症或敗血性休克)的重要物質也是引發牙周病的重要物質,但依 此免疫反應作用機轉的治療以及藥物研究,始終沒有定論並且也沒有突破性的 發展。因此在臨床醫學上,似乎朝向非侵入性,也就是物理性的治療可作為一個

新的研究趨勢。本研究計畫探討BALB/cByJNarl 公鼠在靜磁場的作用下,是否

可降低由LPS 所引發的細胞的毒殺作用,而有較高的存活率。本實驗利用靜脈

注射的方式給予BALB/cByJNarl 公鼠 LPS 刺激,將這些經過內毒素刺激的老

鼠,以LPS 刺激的時間前後,分為預暴露磁場和後暴露磁場組,靜磁場強度為

4000 高斯。完全沒有受到磁場暴露的老鼠做為控制組。記錄各組的存活率來進

一步探討靜磁場對於發炎反應的關係。本研究結果顯示,當老鼠預暴露磁場2

小時後施予LPS,之後不再接受磁場暴露,存活率有上升的趨勢,其中完全沒

有接受磁場暴露的老鼠,其48 小時存活率為 16.67±8.08%,明顯地低於預 暴露2 小時的存活率 42.86±8.66% (p<0.05)。而不論是否有接受磁場暴露,

LPS 注射 48 小時後,所有組別的老鼠其存活率沒有明顯地變化。

根據實驗的結果,我們認為以靜磁場刺激並降低過度免疫反應(如敗血症或牙周 病)的程度具有深入研究價值。

英文摘要

Clinical observations found that patients suffered from bacterial-induced

inflammation which result in serious periodontal disease have gradually increased over the years. Lipopolysaccharide (LPS), found in the cell wall of bacteria, was the toxic substance responsible for the excessive immune reaction such as sepsis and septic shock, as well as the periodontal disease. However, drugs developed based on the above mechanism showed no

significant clinical breakthrough. Therefore, it seems to be a bias to find a non-

invasive and physical treatment in clinical research. This study aims to investigate the probability of increasing the survival rate of static magnetic field (SMF)-exposed mice challenged with LPS.

In this study, LPS was intravenous injected into BALB/cByJNarl male mice. The endotoxin-treated mice were divided into prevention (anticipatory SMF exposed) and

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treatment (SMF exposed after challenge of LPS) groups. Static magnetic field with a flux intensity of 4000 G was used as an endotoxicity inhibitor. Mice without SMF exposure were set as control group. The survival rates in each group of the samples were calculated for evaluating the endotoxin tolerance capability of SMF. Our results indicated that the survival rate of the tested mice was significantly increased due to SMF exposure in advance for 2 hours before LPS challenge. When the mice were challenged with LPS, the 48 hours survival rate is 16.67±8.08%, which is

significantly lower than the survival rate of the mice with 48 hours SMF pre- exposure, 42.86±8.66% (p<0.05). At 48 hours post LPS injection, all the survival mice recovered their health no matter the mice accepted SMF exposure or not.

Based on these results, we concluded that further advanced researches on static magnetic fields in inhibiting LPS-induced excessive immune reaction is valuable.

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