CAJ | 학술논문

目的：比较在牙龈卟啉单胞菌脂多糖（Pg-LPS）作用下，健康和高脂血症兔肺泡巨噬细胞（AM）膜表面清道夫受体-A（SR-A）的基因表达变化以及白细胞介素-10（IL-10）对其的调控作用。方法将健康新西兰兔12只随机分为2组，分别给予普通和高脂饲料喂养，6周后建立高脂血症模型，采用肺泡灌洗法分别获得健康和高脂组AM，将健康和高脂组AM随机分为对照组、加1μg/mLPg-LPS组、加1μg/mLPg-LPS＋0．1μg/mLIL-10组，24h后裂解细胞，荧光定量PCR法检测SR-A的基因表达。结果健康及高脂血症Pg-LPS组SR-A的表达均较对照组明显升高（P＜0．05），且高脂Pg-LPS组较健康Pg-LPS组升高更加显著（P＜0．05）；在加入IL-10后，健康组SR-A的表达高于单纯Pg-LPS组（P＜0．05），高脂组SR-A的表达则低于单纯Pg-LPS组（P＜0．05）。结论
목적：비교재아간계람단포균지다당（Pg-LPS）작용하，건강화고지혈증토폐포거서세포（AM）막표면청도부수체-A（SR-A）적기인표체변화이급백세포개소-10（IL-10）대기적조공작용。방법장건강신서란토12지수궤분위2조，분별급여보통화고지사료위양，6주후건립고지혈증모형，채용폐포관세법분별획득건강화고지조AM，장건강화고지조AM수궤분위대조조、가1μg/mLPg-LPS조、가1μg/mLPg-LPS＋0．1μg/mLIL-10조，24h후렬해세포，형광정량PCR법검측SR-A적기인표체。결과건강급고지혈증Pg-LPS조SR-A적표체균교대조조명현승고（P＜0．05），차고지Pg-LPS조교건강Pg-LPS조승고경가현저（P＜0．05）；재가입IL-10후，건강조SR-A적표체고우단순Pg-LPS조（P＜0．05），고지조SR-A적표체칙저우단순Pg-LPS조（P＜0．05）。결론
Objective To compare the expression of alveolar macrophages membrane receptor SR-A mRNA ,stimulated by Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) in healthy and hyper-lipidemic rabbit ,and detect the effect of interleukin10(IL-10) . Methods 12 healthy New Zealand rabbits were randomly divided into two groups ,and respectively gave them normal and high fat diets . After 6 weeks ,hyperlipidemia model was established . Alveolar macrophages (AM ) of both healthy and hyper-lipidemia groups were isolated by alveolar lavage and then further divided into three groups :control , 1 μg/mL Pg-LPS and 1 μg/mL Pg-LPS+0 .1 μg/mL IL-10 . After the treatment with Pg-LPS and IL-10 for 24 hours ,the mRNA expression levels of SR-A in all samples were detected by real-time fluorescence quantitative polymerase chain reaction (PCR) . Results Results of real-time PCR showed that the level of SR-A on both healthy and hyperlipidemic rabbit AM were significantly increased (P<0 .05) by Pg-LPS when compared with control group . Moreover ,the increasing of SR-A level in hyperlipidemic Pg-LPS group was more prominent than in healthy Pg-LPS group(P<0 .05) . Furthermore ,when compared with that in Pg-LPS group ,IL-10 induced higher SR-A expression in healthy group and lower SR-A expression in hyperlipidemic group (P<0 .05) . Conclusion Periodontal pathogen Pg-LPS might increase the risk of atherosclerosis by stimulating the expression of alveolar macrophages membrane receptor SR-A in hyper-lipidemia ,and this stimulation could be negatively regulated by IL-10 .