研究不同浓度西帕依固龈液对白细胞介素-1β(Interleukin-1β,IL-1β)刺激人牙龈成纤维细胞(Human Gingival Fibroblast,HGF)产生前列腺素E2(Prostaglandin E2,PGE2)水平的影响。采用健康人牙龈组织原代培养的HGF细胞,以1ng/mL的IL-1β作为刺激因子,将HGF细胞按5×104/mL的细胞密度接种到24孔培养板中,每孔200μL的细胞悬液。孵育24h贴壁后,弃原培养液,清洗2次后加药,分组为空白对照组(用含20mL/L的胎牛血清的DMEM培养液),IL-1β组(浓度为1ng/mL),IL-1β+西帕依固龈液组(西帕依固龈液终末浓度分别为12.5、25、50、100、200μg/mL),IL-1β+消炎痛(消炎痛浓度为100ng/mL)。用酶联免疫法测定PGE2含量,观察不同浓度的西帕依固龈液(分别为12.5、25、50、100、200μg/mL)对HGF培养上清中PGE2水平的影响。结果显示,5种不同浓度的西帕依固龈液均能显著抑制1ng/mL的IL-1β刺激后HGF产生PGE2,随着浓度的增加,抑制效果也增加,但5种浓度的西帕依固龈液抑制效果均低于100ng/mL的消炎痛。由此得出,HGF具有合成和分泌PGE2的功能,IL-1β能有效刺激HGF产生PGE2;西帕依固龈液对IL-1β刺激HGF合成和分泌PGE2具有显著抑制作用,其抑制作用在一定范围内呈浓度依赖性。
To observe the effects of Xipayi mouth rinse on the prostaglandin E2 (PGE2) production of Human Gingival Fibroblast (HGF) by stimulation of interleukin-1β (IL-1β), the HGF cells cultured by healthy human gingival tissue are used. With 1ng/mL IL-1β as a stimulating factor, HGF cells with 5×104/mL cell density were inoculated into a culture plate with 24 holes, each containing 200μL cell suspension. 24h after incubation and adhering to the wall, the original culture liquid was abandoned and the mouth was washed 2 times after adding the drugs, which were grouped into control group (with 20m/L fetal bovine serum medium DMEM), IL-1β group (beta concentration is 1ng/mL), IL-1β+Xipayi mouth rinse group (end concentrations of were 50, 100, 200g/mL, respectively ), IL-1β+indomethacin (100ng/mL of endcentration) group. The enzyme immunoassay method is used to check the PGE2 and observe the effects of different concentrations of Xipayi mouth rinse on PGE2 levels in the HGF supernatant. Results show that Xipayi mouth rinse at different concentrations suppresses the PGE2 production of HGF stimulated with 1ng/mL IL-1β significantly in a dose dependent manner. It is concluded that the human gingival fibroblast has the ability of synthesizing and secreting PGE2, and IL-1β is a potent stimulation for HGF cell to generate PGE2; and Xipayi mouth rinse can significantly inhibit the PGE2 production of HGF by stimulation of IL-1β.
