中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
44期
7183-7187
,共5页
植入物%人工假体%表皮葡萄球菌%RNAⅢ抑制肽%黏附%HeLa细胞%群体感应%生物被膜%实验研究%国家自然科学基金
植入物%人工假體%錶皮葡萄毬菌%RNAⅢ抑製肽%黏附%HeLa細胞%群體感應%生物被膜%實驗研究%國傢自然科學基金
식입물%인공가체%표피포도구균%RNAⅢ억제태%점부%HeLa세포%군체감응%생물피막%실험연구%국가자연과학기금
背景:葡萄球菌导致的细菌感染和生物被膜形成可在骨科植入物或创口愈合时发生。受细菌群体感应机制调控,葡萄球菌RNAⅢ抑制肽可以干预葡萄球菌的群体感应系统,阻断葡萄球菌细胞间的信号传导通路,从而抑制葡萄球菌的生物被膜形成,防止葡萄球菌感染。<br> 目的:观察RNAⅢ抑制肽抑制表皮葡萄球菌对人宫颈癌上皮细胞黏附的效果。<br> 方法:体外培养人宫颈癌上皮细胞,实验分4组,空白组每孔加入DMSO的生理盐水,RNAⅢ抑制肽组加含RNAⅢ抑制肽的DMSO溶液,左氧组加入左氧氟沙星的水溶液,联合组用药剂量参照上述两组联合干预。通过组间对照的方法,对比研究表皮葡萄球菌在生理盐水、RNAⅢ抑制肽、左氧氟沙星及两药联合作用下对Hela细胞的黏附情况。<br> 结果与结论:空白组 Hela 细胞层表面有大量细菌黏附,而各用药组细菌黏附的数量均显著低于空白组(P<0.001),左氧组光点计数明显低于RNAⅢ抑制肽组(P<0.05),而联合组Hela细胞层表面黏附的细菌数量进一步降低(P<0.01)。结果证实,RNAⅢ抑制肽可以有效抑制表皮葡萄球菌对宿主细胞表面的黏附,并且与抗生素有协同作用。
揹景:葡萄毬菌導緻的細菌感染和生物被膜形成可在骨科植入物或創口愈閤時髮生。受細菌群體感應機製調控,葡萄毬菌RNAⅢ抑製肽可以榦預葡萄毬菌的群體感應繫統,阻斷葡萄毬菌細胞間的信號傳導通路,從而抑製葡萄毬菌的生物被膜形成,防止葡萄毬菌感染。<br> 目的:觀察RNAⅢ抑製肽抑製錶皮葡萄毬菌對人宮頸癌上皮細胞黏附的效果。<br> 方法:體外培養人宮頸癌上皮細胞,實驗分4組,空白組每孔加入DMSO的生理鹽水,RNAⅢ抑製肽組加含RNAⅢ抑製肽的DMSO溶液,左氧組加入左氧氟沙星的水溶液,聯閤組用藥劑量參照上述兩組聯閤榦預。通過組間對照的方法,對比研究錶皮葡萄毬菌在生理鹽水、RNAⅢ抑製肽、左氧氟沙星及兩藥聯閤作用下對Hela細胞的黏附情況。<br> 結果與結論:空白組 Hela 細胞層錶麵有大量細菌黏附,而各用藥組細菌黏附的數量均顯著低于空白組(P<0.001),左氧組光點計數明顯低于RNAⅢ抑製肽組(P<0.05),而聯閤組Hela細胞層錶麵黏附的細菌數量進一步降低(P<0.01)。結果證實,RNAⅢ抑製肽可以有效抑製錶皮葡萄毬菌對宿主細胞錶麵的黏附,併且與抗生素有協同作用。
배경:포도구균도치적세균감염화생물피막형성가재골과식입물혹창구유합시발생。수세균군체감응궤제조공,포도구균RNAⅢ억제태가이간예포도구균적군체감응계통,조단포도구균세포간적신호전도통로,종이억제포도구균적생물피막형성,방지포도구균감염。<br> 목적:관찰RNAⅢ억제태억제표피포도구균대인궁경암상피세포점부적효과。<br> 방법:체외배양인궁경암상피세포,실험분4조,공백조매공가입DMSO적생리염수,RNAⅢ억제태조가함RNAⅢ억제태적DMSO용액,좌양조가입좌양불사성적수용액,연합조용약제량삼조상술량조연합간예。통과조간대조적방법,대비연구표피포도구균재생리염수、RNAⅢ억제태、좌양불사성급량약연합작용하대Hela세포적점부정황。<br> 결과여결론:공백조 Hela 세포층표면유대량세균점부,이각용약조세균점부적수량균현저저우공백조(P<0.001),좌양조광점계수명현저우RNAⅢ억제태조(P<0.05),이연합조Hela세포층표면점부적세균수량진일보강저(P<0.01)。결과증실,RNAⅢ억제태가이유효억제표피포도구균대숙주세포표면적점부,병차여항생소유협동작용。
BACKGROUND:Staphylococcal infections and its biofilm formation can occur when orthopedic implants or wound is healing, and are regulated by bacterial population sensing mechanism. RNAIII inhibiting peptide intervenes the quorum-sensing system of staphylococcal and blocks the signal transduction among staphylococcal cells, and inhibits staphylococcal biofilm formation, and then prevents staphylococcal infections. <br> OBJECTIVE:To investigate the influence of RNAIII inhibiting peptide on the adhesion of staphylococcus epidermis to the Hela cells. <br> METHODS:The Hela cells were cultured in vitro. There were four groups in this study. In the blank group, saline with dimethyl sulfoxide was added in each wel . In the RNAIII inhibiting peptide group, dimethyl sulfoxide solution containing RNAIII inhibiting peptide was added. In the levofloxacin group, levofloxacin was added. In the combination group, the dose was in accordance with above methods. Using intergroup control method, the adhesion of staphylococcus epidermis to the Hela cells was compared under the effects of saline, RNAIII inhibiting peptide and levofloxacin and their combination. <br> RESULTS AND CONCLUSION:In the blank group, abundant bacterial adhered to Hela cells. The number of adhered bacteria was significantly lower in each medicine group than in the blank group (P<0.001). The spot count was significantly lower in the levofloxacin group than in the RNAIII inhibiting peptide group (P<0.05). In the combination group, the number of bacteria adhered to Hela cells was decreased (P<0.01). Results verified that RNAIII inhibiting peptide effectively suppressed the adhesion of staphylococcus epidermis to the host cells, and showed synergistic effects on antibiotics.