富氢水减轻丝线诱导的SD大鼠妊娠牙龈炎

目的： 探讨氢气对牙龈炎孕鼠牙龈局部损伤的保护作用及其可能的机制。方法： 取SD雌鼠，采用结扎法诱导牙龈炎后，与雄鼠合笼交配。将孕鼠随机分为对照组、造模组和氢水组。对照组和造模组孕鼠饮用纯水，氢水组给予饱和氢水，1天2次。于妊娠第16天处死孕鼠，ELISA法检测各实验组孕鼠牙龈中Prog、SOD、TNF-α的水平，免疫组织化学和Western 免疫印迹法检测牙龈中PR、NFκB和TNF-α的表达。采用SPSS13.0软件包对数据进行统计学分析。结果： 丝线结扎可诱导SD大鼠妊娠期牙龈炎，PR主要分布于各实验组牙龈上皮细胞的胞质中，孕激素（Prog）及其受体（PR）的水平在各实验组孕鼠牙龈局部无显著差异（P>0.05）。造模组大鼠牙龈内SOD含量显著降低，NFκB和TNF-α表达显著升高。与造模组相比，氢水组孕鼠牙龈炎症反应明显减轻，牙龈内NFκB和TNF-α的表达下调。结论： 孕激素及其受体可能在实验大鼠妊娠牙龈炎的发生与发展过程中发挥间接作用，氢气可能通过抑制氧化应激相关炎症反应，减轻实验大鼠的妊娠牙龈炎。

Hydrogen rich water attenuates pregnancy gingivitis induced by ligation in SD rats

PURPOSE: To investigate the effect of hydrogen rich water on experimental gingivitis in SD rats during pregnancy. METHODS: Female SD rats mated with male ones were chosen to induce experimental gingivitis after ligation for 2 weeks. The pregnant rats were randomly divided into control group, model group and HW group. In the control and model group, rats were given pure water, while animals in the HW group were given hydrogen-rich water twice a day. All pregnant animals were sacrificed on day 16 of pregnancy. The level of Prog, SOD and TNF-α in the gingiva of different groups were measured by ELISA, the expression of PR, NFκB and TNF-α were determined by immunohistochemistry and Western blot. SPSS 13.0 software package was used for data analysis. RESULTS: Pregnancy gingivitis of SD rats could be induced by thread ligation. PR was mainly distributed in the gingival epithelium, while there was no significant difference of Prog and PR in the gingiva among different groups(P>0.05). Furthermore, in the model group, lower SOD level as well as higher NFκB and TNF-α level were found in the gingiva. Compared with the model group, the inflammatory response of pregnancy gingivitis in HW group was significantly suppressed along with decreased NFκB and TNF-α. CONCLUSIONS: Progesterone and its receptor may play an indirect role in the process of pregnancy gingivitis of rats. Hydrogen rich water may be beneficial in suppressing pregnancy gingivitis progress by decreasing inflammatory response related to gingival oxidative stress.