AIM： To investigate matrix metalloproteinases（MMPs）and tissue inhibitor of metalloproteinases（TIMPs）expression during the progress of fusarium solani（F.solani） keratitis in a rat model.· METHODS： A rat mo...AIM： To investigate matrix metalloproteinases（MMPs）and tissue inhibitor of metalloproteinases（TIMPs）expression during the progress of fusarium solani（F.solani） keratitis in a rat model.· METHODS： A rat model of F.solani keratitis was produced using corneal scarification and a hand-made contact lens. MMPs and TIMPs expressiond were explored in this rat model of F.solani keratitis using real-time polymerase chain reaction（PCR） and DIF.GM6001（400 μmol/m L） was used to treat infected corneas. The keratitis duration, amount and area of corneal neovascularization（CNV） were evaluated.·RESULTS： MMP-3 expression was 66.3 times higher in infected corneas compared to normal corneas. MMP-8,-9,and-13 expressions were significantly upregulated in the mid-period of the infection, with infected- to-normal ratios of 4.03, 39.86, and 5.94, respectively. MMP-2 and-7expressions increased in the late period, with the infected-to-normal ratios of 5.94 and 16.22, respectively.TIMP-1 expression was upregulated in the early period,and it was 43.17 times higher in infected compared to normal corneas, but TIMP-2,-3, and-4 expressions were mildly downregulated or unchanged. The results of DIF were consistent with the result of real-time PCR.GM6001, a MMPs inhibitor, decreased the duration of F.solani infection and the amount and area of CNV.·CONCLUSION： MMPs and TIMPs contributed into the progress of F.solani keratitis.展开更多
目的探讨基质金属蛋白酶（MMPs）MMP2、MMP9及其抑制物（TIMPs）TIMP-1在皮肤增生性瘢痕中的作用。方法取3-6个月、6-12个月皮肤增生性瘢痕，以正常皮肤组织为对照，ELISA方法测定其MMP2、MMP9以及TIMP-1的含量，采用SPSS统计软件，以...目的探讨基质金属蛋白酶（MMPs）MMP2、MMP9及其抑制物（TIMPs）TIMP-1在皮肤增生性瘢痕中的作用。方法取3-6个月、6-12个月皮肤增生性瘢痕，以正常皮肤组织为对照，ELISA方法测定其MMP2、MMP9以及TIMP-1的含量，采用SPSS统计软件，以成组设计的单因素方差分析，分析它们在不同时段瘢痕组织中变化的意义。结果（1）3-6月瘢痕组织和6-12月瘢痕组织的MMP2，均较正常皮肤显著增高（110.70±5.23ng／ml VS 54.59±3.01，P〈0.01；77.23±7.10ng／ml VS 54.59±3.01，P〈0.01），而3-6月瘢痕组织的MMP2较6-12月瘢痕组织的MMP2亦有显著增高（110.70±5.23 VS 77．23±7．10，P〈0．01）；3-6月瘢痕组织和6-12月瘢痕组织的MMP9之间（3.85±0.88 VS 3.61±0.43，P〉0.05）以及它们与正常皮肤组织的MMP9相比（3.85±0.88 VS 4.13±0.33，P〉0.05；3.61±0.43 VS 4.13±0.33，P〉0.05）均无显著性差异；（2）3-6月瘢痕组织和6-12月瘢痕组织的TIMP-1与正常皮肤组织相比有显著增高（4．74±0．35 VS 3．01±0．11，P〈0．01；5．12±0．34 VS 3.01±0．11，P〈0．01），6-12月瘢痕组织较3-6月瘢痕组织的TIMP-1有显著增高（5.12±0.34 VS 4.74±0．35，P〈0．05）；（3）3-6月瘢痕组织和6-12月瘢痕组织的MMP2与TIMP-1的比值与正常皮肤组织相比均有显著增高（23．38±1．01 VS 18．15±0．58，P〈0.01；15.10±1.45 VS 18．15±0．58，P〈0．01），3-6月瘢痕组织较6-12月瘢痕组织的MMP2与TIMP-1的比值有显著降低（23.38±1.01 VS 15.10±1.45，P〈0.01）。结论MMPs以及TIMPs参与了皮肤瘢痕的增生过程，MMP2、TIMP-1含量及其比值可作为瘢痕生长和预后的指标。展开更多
基金Supported by Tongji University,Shanghai,China(No.2012KJ042)
文摘AIM： To investigate matrix metalloproteinases（MMPs）and tissue inhibitor of metalloproteinases（TIMPs）expression during the progress of fusarium solani（F.solani） keratitis in a rat model.· METHODS： A rat model of F.solani keratitis was produced using corneal scarification and a hand-made contact lens. MMPs and TIMPs expressiond were explored in this rat model of F.solani keratitis using real-time polymerase chain reaction（PCR） and DIF.GM6001（400 μmol/m L） was used to treat infected corneas. The keratitis duration, amount and area of corneal neovascularization（CNV） were evaluated.·RESULTS： MMP-3 expression was 66.3 times higher in infected corneas compared to normal corneas. MMP-8,-9,and-13 expressions were significantly upregulated in the mid-period of the infection, with infected- to-normal ratios of 4.03, 39.86, and 5.94, respectively. MMP-2 and-7expressions increased in the late period, with the infected-to-normal ratios of 5.94 and 16.22, respectively.TIMP-1 expression was upregulated in the early period,and it was 43.17 times higher in infected compared to normal corneas, but TIMP-2,-3, and-4 expressions were mildly downregulated or unchanged. The results of DIF were consistent with the result of real-time PCR.GM6001, a MMPs inhibitor, decreased the duration of F.solani infection and the amount and area of CNV.·CONCLUSION： MMPs and TIMPs contributed into the progress of F.solani keratitis.
文摘目的探讨基质金属蛋白酶（MMPs）MMP2、MMP9及其抑制物（TIMPs）TIMP-1在皮肤增生性瘢痕中的作用。方法取3-6个月、6-12个月皮肤增生性瘢痕，以正常皮肤组织为对照，ELISA方法测定其MMP2、MMP9以及TIMP-1的含量，采用SPSS统计软件，以成组设计的单因素方差分析，分析它们在不同时段瘢痕组织中变化的意义。结果（1）3-6月瘢痕组织和6-12月瘢痕组织的MMP2，均较正常皮肤显著增高（110.70±5.23ng／ml VS 54.59±3.01，P〈0.01；77.23±7.10ng／ml VS 54.59±3.01，P〈0.01），而3-6月瘢痕组织的MMP2较6-12月瘢痕组织的MMP2亦有显著增高（110.70±5.23 VS 77．23±7．10，P〈0．01）；3-6月瘢痕组织和6-12月瘢痕组织的MMP9之间（3.85±0.88 VS 3.61±0.43，P〉0.05）以及它们与正常皮肤组织的MMP9相比（3.85±0.88 VS 4.13±0.33，P〉0.05；3.61±0.43 VS 4.13±0.33，P〉0.05）均无显著性差异；（2）3-6月瘢痕组织和6-12月瘢痕组织的TIMP-1与正常皮肤组织相比有显著增高（4．74±0．35 VS 3．01±0．11，P〈0．01；5．12±0．34 VS 3.01±0．11，P〈0．01），6-12月瘢痕组织较3-6月瘢痕组织的TIMP-1有显著增高（5.12±0.34 VS 4.74±0．35，P〈0．05）；（3）3-6月瘢痕组织和6-12月瘢痕组织的MMP2与TIMP-1的比值与正常皮肤组织相比均有显著增高（23．38±1．01 VS 18．15±0．58，P〈0.01；15.10±1.45 VS 18．15±0．58，P〈0．01），3-6月瘢痕组织较6-12月瘢痕组织的MMP2与TIMP-1的比值有显著降低（23.38±1.01 VS 15.10±1.45，P〈0.01）。结论MMPs以及TIMPs参与了皮肤瘢痕的增生过程，MMP2、TIMP-1含量及其比值可作为瘢痕生长和预后的指标。
