医学信息
醫學信息
의학신식
MEDICAL INFORMATION
2014年
12期
653-654
,共2页
王艳春(综述)%税艳青(审校)
王豔春(綜述)%稅豔青(審校)
왕염춘(종술)%세염청(심교)
龈紫龈单胞菌%牙龈上皮细胞%P2X7受体%AKT/IP3信号%凋亡
齦紫齦單胞菌%牙齦上皮細胞%P2X7受體%AKT/IP3信號%凋亡
간자간단포균%아간상피세포%P2X7수체%AKT/IP3신호%조망
Porphyromonas gingivalis%HGEC%P2X7receptor%AKT/IP3singal%Apoptosis
龈紫龈单胞菌(Porphyromonas gingivalis,Pg)为黑色杆状G+耐氧厌氧菌(aerotolerant anaerobes),可定殖、感染于口腔组织,并通过牙龈蛋白酶降解胞外基质及细胞骨架蛋白,实现对宿主细胞的入侵和胞内自我复制。研究发现,Pg定殖、感染后可促进宿主细胞活性氧簇(reactive oxygen species, ROS)释放、介导炎症细胞因子分泌,并在感染部位通过多通路调节宿主细胞凋亡,引发牙周疾病。实验证实,Pg可调节牙周组织的中成纤维细胞,上皮细胞,淋巴细胞的凋亡活动。 Pg诱导的细胞凋亡调节是多因素共同作用的结果,本文主要从P2X7嘌呤受体及AKT/IP3信号对Pg调控牙龈上皮细胞(human gingival epithelial cel s、HGEC)凋亡的作用研究进展做一简要综述。
齦紫齦單胞菌(Porphyromonas gingivalis,Pg)為黑色桿狀G+耐氧厭氧菌(aerotolerant anaerobes),可定殖、感染于口腔組織,併通過牙齦蛋白酶降解胞外基質及細胞骨架蛋白,實現對宿主細胞的入侵和胞內自我複製。研究髮現,Pg定殖、感染後可促進宿主細胞活性氧簇(reactive oxygen species, ROS)釋放、介導炎癥細胞因子分泌,併在感染部位通過多通路調節宿主細胞凋亡,引髮牙週疾病。實驗證實,Pg可調節牙週組織的中成纖維細胞,上皮細胞,淋巴細胞的凋亡活動。 Pg誘導的細胞凋亡調節是多因素共同作用的結果,本文主要從P2X7嘌呤受體及AKT/IP3信號對Pg調控牙齦上皮細胞(human gingival epithelial cel s、HGEC)凋亡的作用研究進展做一簡要綜述。
간자간단포균(Porphyromonas gingivalis,Pg)위흑색간상G+내양염양균(aerotolerant anaerobes),가정식、감염우구강조직,병통과아간단백매강해포외기질급세포골가단백,실현대숙주세포적입침화포내자아복제。연구발현,Pg정식、감염후가촉진숙주세포활성양족(reactive oxygen species, ROS)석방、개도염증세포인자분비,병재감염부위통과다통로조절숙주세포조망,인발아주질병。실험증실,Pg가조절아주조직적중성섬유세포,상피세포,림파세포적조망활동。 Pg유도적세포조망조절시다인소공동작용적결과,본문주요종P2X7표령수체급AKT/IP3신호대Pg조공아간상피세포(human gingival epithelial cel s、HGEC)조망적작용연구진전주일간요종술。
Porphyromonas gingivalis, a black-pigmented, Gram-negative anaerobe, is an important etiologic agent of periodontal disease. it has been shown that this organism has the ability to invade,survive and copy itselves within eukaryotic cells through degrading extracellular matrices and cleaving actin. The harsh inflammatory condition of the periodontal pocket implies that this organism has properties that wil facilitate its ability to respond and adapt to oxidative stress./ inflammatory condition. In vitro studies show that P. gingivalis can modulate apoptosis in the fol owing celltypes: epithelial cells, fibroblasts,endothelial cells and lymphocytes and apoptosis has been proposed as a mechanism to explain the extensive tissue destruction in chronic periodontitis lesions. Pg induces gingival epithelial cellApoptosis that is triggered through various factors and multiple pathway. I wil discuss the role of the purinergic receptor P2X7,AKT/IP3 singal in the apoptosis modification of gingival epithelial cellthat is involved in regulation of Pg in this view.