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[GM6001治疗碱烧伤后角膜溶解的实验研究]

[Experimental study on the treatment of corneal melting after alkali burn with GM 6001].

作者信息

Liu Haixia, Zhang Wenhua, Pan Zhiqiang, Wu Yuying

机构信息

Beijing Tong Ren Ophthalmic Center, Capital University of Medical Sciences, Beijing 100730, China.

出版信息

Zhonghua Yan Ke Za Zhi. 2002 Sep;38(9):539-42.

PMID:12410973
Abstract

OBJECTIVE

To eva1uate the effect of synthetic inhibitors of matrix metalloproteinases (GM 6001) on the prevention of melting of rabbit corneas after alkali burn.

METHODS

Severe and moderate rabbit alkali burns were made by different concentrations of NaOH. Corneas with severe or moderate alkali injuries were topically treated with 400 mg/L or 200 mg/L GM 6001 for 30 days. Vehicle was used as control. All corneas were evaluated for melting, opacity and other pathological changes.

RESULTS

After severe alkali burns, all of the 8 corneas of the control group melted in 13 +/- 5 days, and 2 corneas perforated. Only did 2 corneas melt in 19 +/- 4 days after burn and not perforate in 400 mg/L GM 6001 group. The rates of corneal melting and perforation in 400 mg/L GM 6001 group were lower than that of the control (P < 0.05), and the initial time of melting was later than that of the control (P < 0.0l). After moderate alkali burn, all of the 6 corneas of control melted in 14 +/- 6 days, and 1 cornea perforated. Only did 2 of 200 mg/L GM 6001 treated corneas melt in 19 +/- 4 days without perforation after burn. The rate of corneal melting and the degree of corneal opacity were lower in 200 mg/L GM 6001 treated than that of the control, the difference being significant (P < 0.0l). Histologic section of GM 6001 treated corneas revealed much less collagen fiber destruction and inflammatory cell infiltration than that of the control.

CONCLUSION

GM 6001 not only can prevent and delay the corneal melting after alkali burn, but also can reduce the destruction of corneal collagen fibers and infiltration of inflammatory cells in the corneal tissue.

摘要

目的

评估基质金属蛋白酶合成抑制剂(GM 6001)对预防兔碱烧伤后角膜溶解的作用。

方法

用不同浓度的NaOH造成兔的重度和中度碱烧伤。对重度或中度碱损伤的角膜局部给予400 mg/L或200 mg/L GM 6001治疗30天。以赋形剂作为对照。评估所有角膜的溶解、混浊及其他病理变化。

结果

重度碱烧伤后,对照组的8只角膜均在13±5天内溶解,2只角膜穿孔。在400 mg/L GM 6001组,仅2只角膜在烧伤后19±4天溶解且未穿孔。400 mg/L GM 6001组角膜溶解和穿孔的发生率低于对照组(P<0.05),溶解的初始时间晚于对照组(P<0.01)。中度碱烧伤后,对照组的6只角膜均在14±6天内溶解,1只角膜穿孔。在200 mg/L GM 6001治疗的角膜中,仅2只在烧伤后19±4天溶解且未穿孔。200 mg/L GM 6001治疗组角膜溶解率和角膜混浊程度低于对照组,差异有统计学意义(P<0.01)。GM 6001治疗的角膜组织学切片显示,与对照组相比,胶原纤维破坏和炎性细胞浸润明显减少。

结论

GM 6001不仅能预防和延缓碱烧伤后角膜溶解,还能减少角膜组织中胶原纤维的破坏和炎性细胞的浸润。

相似文献

1
[Experimental study on the treatment of corneal melting after alkali burn with GM 6001].[GM6001治疗碱烧伤后角膜溶解的实验研究]
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Treatment of alkali-injured rabbit corneas with a synthetic inhibitor of matrix metalloproteinases.用基质金属蛋白酶的合成抑制剂治疗碱损伤的兔角膜。
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Recombinant tissue inhibitor of metalloproteinases type 1 suppresses alkali-burn-induced corneal ulceration in rabbits.重组1型金属蛋白酶组织抑制剂可抑制兔碱烧伤诱导的角膜溃疡形成。
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