原发性青光眼合并2型糖尿病患者房水及血液中MMP-2及TIMP-2的表达

目的　探讨基质金属蛋白酶２（ｍａｔｒｉｘｍｅｔａｌｌｏｐｒｏｔｅｉｎａｓｅ-２，ＭＭＰ-２）及金属蛋白酶２组织抑制因子（ｔｉｓｓｕｅｉｎｈｉｂｉｔｏｒｏｆｍｅｔａｌｌｏｐｒｏｔｅｉｎａｓｅ-２，ＴＩＭＰ-２）与原发性青光眼合并２型糖尿病的关系。方法　研究对象分Ａ组、Ｂ组、Ｃ组、Ｄ组、Ｅ组、Ｆ组６组，每组３０眼。Ａ组为原发性开角型青光眼（ｐｒｉｍａｒｙｏｐｅｎａｎｇｌｅｇｌａｕｃｏｍａ，ＰＯＡＧ）组，Ｂ组为原发性闭角型青光眼（ｐｒｉｍａｒｙａｎｇｌｅｃｌｏ-ｓｕｒｅｇｌａｕｃｏｍａ，ＰＡＣＧ）组，Ｃ组为ＰＯＡＧ合并２型糖尿病组，Ｄ组为ＰＡＣＧ合并２型糖尿病组，Ｅ组为糖尿病性白内障组，Ｆ组为年龄相关性白内障组。采用酶联免疫吸附试验检测各组房水及血清中ＴＩＭＰ-２及ＭＭＰ-２的含量，并计算ＴＩＭＰ-２／ＭＭＰ-２值。结果　在６组研究对象的房水中，ＭＭＰ-２浓度在Ａ组为（２４．９２±６．６２）μｇ?Ｌ－１、Ｂ组为（３６．８０±１５．０７）μｇ?Ｌ－１、Ｄ组为（２８.４４±５．７８）μｇ?Ｌ－１，均较Ｆ组的（２２．８７±３.５４）μｇ?Ｌ－１显著升高（均为Ｐ＜０．０５）；同时房水中ＴＩＭＰ-２浓度在Ａ组为（４３.９２±１９．５７）μｇ?Ｌ－１、Ｂ组为（７６．１３±２７．６７）μｇ?Ｌ－１、Ｄ组为（６１．９２±６．５１）μｇ?Ｌ－１，也均较Ｆ组的（２２.４８±３．５６）μｇ?Ｌ－１显著升高（均为Ｐ＜０．０５）。Ａ、Ｂ、Ｃ、Ｄ组房水中ＴＩＭＰ-２／ＭＭＰ-２值较Ｅ组和Ｆ组显著提高，约为其２倍，但Ａ组、Ｂ组、Ｃ组、Ｄ组间ＴＩＭＰ-２／ＭＭＰ-２值无显著性差异。在６组研究对象的血清中，Ａ组ＭＭＰ-２和ＴＩＭＰ-２浓度最高，分别为（３９６．７５±４９．３０）μｇ?Ｌ－１和（３３７．６７±６２．７８）μｇ?Ｌ－１，其余各组间ＭＭＰ-２和ＴＩＭＰ-２浓度无显著性差异。６组研究对象血清中ＴＩＭＰ-２／ＭＭＰ-２值无明显差异。结论　原发性青光眼患者中ＴＩＭＰ-２／ＭＭＰ-２值均存在失衡，说明ＭＭＰ-２的活性变化及ＴＩＭＰ-２／ＭＭＰ-２值与ＰＯＡＧ和ＰＡＣＧ的发病密切相关，但２型糖尿病对原发性青光眼的病程进展无明显影响。

Expression of MMP-2 and TIMP-2 in blood and aqueous humour of patients with primary glaucoma and type 2 diabetes mellitus

Objective To explore the inherent connections of matrix metalloproteinase-2 ( MMP-2 ) and tissue inhibitor of metalloproteinase-2 ( TIMP-2) in patients with primary glaucoma and type 2 diabetes mellitus. Methods A total of 180 eyes were recruited and categorized int0 6 groups ( 30 eyes per group) ,including group A, B , C , D , E and F. Group A was primary open-angle glaucoma ( POAG) ,while group B to F were primary angle-closure glaucoma ( PACG) , POAG with type 2 diabetes mellitus, POCG with type 2 diabetes mellitus . diabetic cataract, and age-related cataract , respectively. Peripheral blood and aqueous humor samples were collected from patients of each group. Blood samples were collected on the day of surgery and aqueous humor samples were collected during glaucoma surgery. The content of TIMP-2 and MMP-2 was measured by enzyme linked immunosorbent assay-sandwich technique ( ELISA) and the ratios of TIMP-2 and MMP-2 were calculated. Results In aqueous humor of all groups, concentration of MMP-2 in group A was ( 24. 92 +6. 62 ) Vg . L ’l , group B was ( 36. 80 + 15 . 07 ) Vg . L -l and group D was ( 28. 44 + 5. 78) Vg . L ’l , which were sigruficantly higher than that in group F ( 22. 87 + 3. 54) Vg . L-l ( all P < 0. 05 ). And concentration of TIMP-2 in group A was (43. 92 + 19. 57) Vg . L’l , group B was (76. 13 + 27. 67) pg . L’l , group D was (61. 92 +6. 51) vg . L-l ,which were also higher than that in group F ( 22. 48 + 3. 56) Vg . L -l ( all P < 0. 05 ) . Ratio of TIMP-2/MMP-2 in all patients with glaucoma in groups A,B,C ,D was about twice of that in non-glaucoma patients groups. In peripheral blood of all groups, group A exhibited the highest concentration of MMP-2 (396. 75 +49. 30) Vg . L-l and TIMP-2 ( 337. 67 + 62. 78) Vg . L-l among all groups. There was no significant difference in concentration of MMP-2 and TIMP-2 in other groups , and ratio of TIMP-2/MMP-2 in all groups almost the same. Conclrision The concentration of MMP-2.TIMP-2 and ratio of TIMP-2/MMP-2 are closely related to primary glaucoma.however type 2 diabetes is redundant for the progression of primary glaucoma.