牙龈卟啉单胞菌对血管内膜粘附因子和金属蛋白酶的影响(英文)

目的:观察牙龈卟啉单胞菌(Pg,为牙周病的主要致病菌)对血管内膜粘附因子和金属蛋白酶的影响。方法:大鼠120只,按数字表随机分为空白对照组、Pg低剂量组(2ml)与Pg高剂量组(5ml),各40只,后两组每3d分别接受相应剂量Pg肌注,且均不进行抗生素干预,历时12周。取其静脉血,检测三组血液中的细胞间粘附分子-1(ICAM-1)、血管细胞粘附分子-1(VCAM-1)、基质金属蛋白酶(MMP)-3及MMP-9的水平。结果:与空白对照组相比,Pg低剂量组与高剂量组大鼠静脉血中ICAM-1[(175.79±14.30)ng/ml比(182.62±15.07)ng/ml、(189.39±14.93)ng/ml]、VCAM-1[(256.49±37.17)ng/ml比(271.58±32.85)ng/ml、(286.66±30.66)ng/ml]、MMP-3[(3.23±0.69)ng/ml比(3.61±0.82)ng/ml、(3.97±0.83)ng/ml]及MMP-9[(1.30±0.39)mg/L比(1.48±0.39)mg/L、(1.67±0.45)mg/L]含量显著增加(P0.05或0.01),且与Pg低剂量组相比,Pg高剂量组上述因子含量显著增加(P0.05)。结论:牙龈卟啉单胞菌可引起大鼠血清中血管内膜粘附因子和金属蛋白酶含量的显著增加,可加剧冠心病的病理演变。

Influence of Porphyromonas gingivalis on vascular intima adhesion factors and metalloproteinases

Objective：To observe influence of porphyromonas gingivalis （Pg,a main pathogenic bacterium of perio-dontal disease）on vascular intima adhesion factors and metalloproteinases.Methods：A total of 120 rats Were ran-domly and equally divided into blank control group,Pg loW dose group （Pg 2ml）and Pg high dose group （Pg 5ml） according to number table.The latter tWo groups respectively received intramuscular injection of corresponding dose Pg every three days Without antibiotic intervention for 1 2 Weeks.Then their venous blood Was taken to measure lev-els of intercellular adhesion molecule-1 （ICAM-1 ）,vascular cell adhesion molecule-1 （VCAM-1 ）,matrix metallo-proteinase （MMP）-3 and MMP-9 in three groups.Results：Compared With blank control group,there Were sig-nificant increase in contents of ICAM-1 [（175.79±14.30）ng/ml vs.（182.62±15.07）ng/ml,（189.39±14.93） ng/ml]、VCAM-1 [（256.49±37.17）ng/ml vs.（271.58±32.85）ng/ml ,（286.66±30.66）ng/ml]、MMP-3 [（3.23±0.69）ng/ml vs.（3.61±0.82）ng/ml,（3.97±0.83）ng/ml]and MMP-9 [（1.30±0.39）mg/L vs. （1.48±0.39）mg/L,1.67±0.45）mg/L]（P＆lt;0.05,or ＆lt;0.01）,Compared With Pg loW dose group,there Were significant increase in levels of above indexes in Pg high dose group （P＆lt;0.0 5 ）.Conclusion：Porphyromonas gingi-valis can significantly increase serum contents of vascular intima adhesion factors and metalloproteinases,aggravat-ing pathological development of coronary heart disease.