吸入氡对小鼠抗炎作用的研究进展

Norie Kanzaki, T. Kataoka, Reo Etani, K. Yamaoka
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引用次数: 3

摘要

在Misasa(日本)和Badgastein(奥地利)进行的氡疗法被发现对与疼痛有关的疾病有有益的效果。虽然一些临床研究已经报道了对疼痛相关疾病的疗效,但其机制仍未完全阐明。为了进一步明确其作用机制,我们开发了小动物氡暴露系统。本文就氡吸入对小鼠抗炎作用的研究进展作一综述。我们首先研究了吸入氡是否能抑制卡拉胶诱导的小鼠炎症。鼠笼氡浓度约为2000 Bq/ m3,与冈山大学医院Misasa医疗中心氡治疗水平相近。小鼠右后足经角叉菜胶处理可引起足部水肿,而吸入氡可抑制足部水肿。抗氧化剂如超氧化物歧化酶(SOD)和过氧化氢酶在氡处理小鼠显著高于假处理小鼠。由于卡拉胶诱导的炎症是由活性氧(ROS)介导的,吸入氡对足跖水肿的抑制可能是由于其抗氧化功能的激活。接下来,我们研究了吸入氡对小鼠葡聚糖硫酸钠(DSS)诱导的结肠炎的影响。结果表明,吸入氡可抑制dss所致结肠炎的损伤。此外,吸入氡可抑制肿瘤坏死因子-α (TNF-α)等炎症反应介质,增加SOD等抗氧化剂。接下来,我们研究了吸入氡对福尔马林引起的小鼠炎症性疼痛的影响。结果表明,吸入氡可抑制小鼠的舔食反应时间。被福尔马林诱导的炎症激活的TNF-α在氡处理的小鼠中比假处理的小鼠低。吸入氡后,小鼠体内SOD活性等抗氧化活性增加。这些发现表明,吸入氡通过激活抗氧化功能来抑制小鼠几种类型的炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Recent studies on anti-inflammatory effects of radon inhalation in mice
Radon therapy, which has been performed in Misasa (Japan) and Badgastein (Austria), was found to have a beneficial effect on pain-related diseases. Although several clinical studies of the curative effects on pain related diseases have been reported, the mechanism remains to be incompletely elucidated. In order to further clarify the mechanism, we developed radon exposure systems for small animals. In the present paper, we review several studies on the anti-inflammatory effects of radon inhalation in mice. We first examined whether radon inhalation inhibits carrageenan-induced inflammatory paw in mice. Radon concentration in mouse cage was approximately 2000 Bq/m 3 , which is similar to the level of radon therapy at Misasa Medical Center, Okayama University Hospital. Although carrageenan administration into right hind paw of mice induced paw edema, radon inhalation inhibited the edema. Antioxidants such as superoxide dismutase (SOD) and catalase were significantly higher in the radon-treated mice than in the sham-treated mice. Since the development of carrageenan-induced inflammation is mediated by reactive oxygen species (ROS), the inhibition of paw edema by radon inhalation is probably due to activation of antioxidant functions. We next examined the effects of radon inhalation on dextran sulfate sodium (DSS)-induced colitis in mice. Results showed that radon inhalation suppressed the damage caused by DSS-induced colitis. In addition, the mediators of inflammatory response such as tumor necrosis factor-alpha (TNF-α) were inhibited, and antioxidants such as SOD were increased by radon inhalation. Next, we examined the effects of radon inhalation on formalin-induced inflammatory pain in mice. Results showed that radon inhalation inhibited the licking response time. TNF-α, activated by formalin-induced inflammation, was lower in the radon-treated mice than in the sham-treated mice. Antioxidant activities such as SOD activity were increased in the mice that inhaled radon. These findings suggested that radon inhalation inhibits several types of inflammation in mice due to activation of antioxidant functions.
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