一氧化碳释放分子对大鼠实验性牙周炎的影响

目的 研究一氧化碳释放分子（CORM）对大鼠实验性牙周炎的影响。方法 将42只健康雄性Wistar大鼠分为正常组（ NL组）、牙周炎组（ LO组）和一氧化碳干预组（ CO组）。NL组不作任何处理；CO及LO组采用牙周丝线结扎法建立牙周炎实验模型；建模当天起 CO组经腹腔注射 CORM-2，每天 10 mg•kg-1，连续 10 d，LO组注射等体积生理盐水。分别于结扎 3、7、10 d后自心脏抽取静脉血，用酶联免疫吸附测定法检测血清中肿瘤坏死因子 -α（TNF-α）和白细胞介素 -1β（IL-1β）的质量浓度。10 d后在体视显微镜下测量牙槽骨的吸收高度，并于光镜下观察牙周组织炎症细胞的浸润情况。结果 丝线结扎10 d后，LO、CO组牙槽骨的吸收高度均明显大于NL组，而CO组明显小于 LO组（ P<0.05）； LO、CO组炎症细胞浸润指数明显高于 NL组，而 CO组明显低于 LO组（ P<0.05）。在同一观察时期内， LO组TNF-α及IL-1β质量浓度均明显高于其他两组，而 CO组虽高于 NL组，但明显低于 LO组（ P<0.05）。结论 CORM-2能有效抑制大鼠实验性牙周炎的炎症细胞浸润和牙槽骨吸收。

Effect of carbon monoxide releasing molecule on experimental periodontitis in rats

 Objective  To evaluate the effects of carbon monoxide releasing molecule-2 (CORM-2) on experimental perio-dontitis inrats. Methods  Forty-two Wistarratswere divided into three groups.Ratsin the normal group (NL group)did not undergo any procedure, whereas the other rats were ligatured and treated with saline solution (NaCl 0.9%) (LO group) or treated with CORM-2 (10 mg• kg-1 per day) (CO group). A 3-0 silk suture was placed around the mandibular first molars. Rats were sacrificed after 3, 7, and 10 d. Blood samples were collected from all animals for tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) analysis. Changes in alveolar bone levels were measured clinically, and periodontal tissues were histopathologically examinedto assess the infiltration of inflammatory cells. Results  Ligature placement increased alveolar bone loss and inflammatory cell infiltration in periodontal tissue. Alveolar bone loss in CO group was significantly higher than that in NL group, but was lower than that in LO group (P<0.05). The ratio of inflammatory cell infiltration in LO group was significantly higher than that in CO and NL groups, and that in CO group was lower than in LO group (P<0.05). Serum levels of TNF-α and IL-1β in the LO group were significantly higher than those in the CO and NL groups, and those in CO group were lower than in LO group (P<0.05). Conclusion  Systemic administration of CORM-2 reduced periodontal inflam-mation andalveolar bone loss in experimental periodontitis in rats.