Chen L L, Yan J
Department of Stomatology, the Second Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310009, China.
Acta Pharmacol Sin. 2001 Jul;22(7):614-8.
To study the effects of Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) on inducing interleukin-1 (IL-1), tumor necrosis factor (TNF), prostaglandin E (PGE), and activating osteoclasts, in order to understand mechanism of osteoclast activation.
Pg-LPS was prepared by phenol-water method. IL-1, TNF, and PGE induced by Pg-LPS were isolated by chromatography. Ca2+ concentration was detected by atomic absorption spectrophotometry. Acid phosphatase and carbonic anhydrase in periodontal membranes were examined by histochemistry.
Pg-LPS was able to stimulate peripheral blood mononuclear cells (PBMC) or the cells from human periodontal tissue secreting IL-1, TNF, and PGE. The outputs of these cytokines were increased in pace with the enhancement of Pg-LPS at the dose range of 0.5 - 5.0 mg/L. All of the three cytokines showed activities of accelerating Ca2+ release from rat calvarial bones, and the activity of PGE was the strongest. The amounts of both the acid phosphatase and carbonic anhydrase in the periodontal membranes of Pg-LPS injected rats were obviously increased (P < 0.01). In the periodontal membranes of Pg-LPS injected rats, the amount of activated osteoclasts were obviously increased in pace with Pg-LPS injection times (P < 0.01). However, the activating rates of osteoclasts were stable to approximately 65 % because of the increase of inactivated osteoclasts.
Pg-LPS possessed strong activities to induce human PBMC and the cells from human periodontal tissue to produce IL-1, TNF, and PGE in a dose-dependent m anner within a certain concentration range of the LPS. Pg-LPS could efficiently activate osteoclasts, and the mechanism of osteoclast activation was probably associated with the increase of acid phosphatase and carbonic anhydrase.
研究牙龈卟啉单胞菌脂多糖(Pg-LPS)对诱导白细胞介素-1(IL-1)、肿瘤坏死因子(TNF)、前列腺素E(PGE)以及激活破骨细胞的作用,以了解破骨细胞激活机制。
采用酚水法制备Pg-LPS。通过色谱法分离Pg-LPS诱导产生的IL-1、TNF和PGE。用原子吸收分光光度法检测钙离子浓度。采用组织化学法检测牙周膜中的酸性磷酸酶和碳酸酐酶。
Pg-LPS能够刺激外周血单个核细胞(PBMC)或人牙周组织细胞分泌IL-1、TNF和PGE。在0.5 - 5.0 mg/L剂量范围内,随着Pg-LPS浓度的增加,这些细胞因子的分泌量也随之增加。这三种细胞因子均具有促进大鼠颅骨释放钙离子的活性,其中PGE的活性最强。注射Pg-LPS的大鼠牙周膜中酸性磷酸酶和碳酸酐酶的含量均明显增加(P < 0.01)。在注射Pg-LPS的大鼠牙周膜中,随着Pg-LPS注射次数的增加,活化破骨细胞的数量明显增加(P < 0.01)。然而,由于失活破骨细胞的增加,破骨细胞的激活率稳定在约65%。
在一定浓度范围内,Pg-LPS具有较强的活性,能够以剂量依赖的方式诱导人PBMC和人牙周组织细胞产生IL-1、TNF和PGE。Pg-LPS能够有效激活破骨细胞,破骨细胞激活机制可能与酸性磷酸酶和碳酸酐酶的增加有关。