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suck abstract from ncbi


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pmid26120273
      Mol+Vis 2015 ; 21 (ä): 688-98
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  • Fasudil hydrochloride, a potent ROCK inhibitor, inhibits corneal neovascularization after alkali burns in mice #MMPMID26120273
  • Zeng P ; Pi RB ; Li P ; Chen RX ; Lin LM ; He H ; Zhou SY
  • Mol Vis 2015[]; 21 (ä): 688-98 PMID26120273 show ga
  • PURPOSE: To investigate the effects and mechanisms of fasudil hydrochloride (fasudil) on and in alkali burn-induced corneal neovascularization (CNV) in mice. METHODS: To observe the effect of fasudil, mice with alkali-burned corneas were treated with either fasudil eye drops or phosphate-buffered saline (PBS) four times per day for 14 consecutive days. After injury, CNV and corneal epithelial defects were measured. The production of reactive oxygen species (ROS) and heme oxygenase-1(HO-1) was measured. The infiltration of polymorphonuclear neutrophils (PMNs) and the mRNA expressions of CNV-related genes were analyzed on day 14. RESULTS: The incidence of CNV was significantly lower after treatment with 100 ?M and 300 ?M fasudil than with PBS, especially with 100 ?M fasudil. Meanwhile, the incidences of corneal epithelial defects was lower (n=15, all p<0.01). After treatment with 100 ?M fasudil, the intensity of DHE ?uorescence was reduced in the corneal epithelium and stroma than with PBS treatment (n=5, all p<0.01), and the number of filtrated PMNs decreased. There were significant differences between the expressions of VEGF, TNF-a, MMP-8, and MMP-9 in the 100 ?M fasudil group and the PBS group (n=8, all p<0.05). The production of HO-1 protein in the 100 ?M fasudil group was 1.52±0.34 times more than in the PBS group (n=5 sample, p<0.05). CONCLUSIONS: 100 ?M fasudil eye drops administered four times daily can significantly inhibit alkali burn-induced CNV and promote the healing of corneal epithelial defects in mice. These effects are attributed to a decrease in inflammatory cell infiltration, reduction of ROS, and upregulation of HO-1 protein after fasudil treatment.
  • |1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/*analogs & derivatives/pharmacology [MESH]
  • |Alkalies/toxicity [MESH]
  • |Animals [MESH]
  • |Burns, Chemical/*drug therapy/*enzymology/pathology [MESH]
  • |Corneal Neovascularization/etiology/pathology/*prevention & control [MESH]
  • |Disease Models, Animal [MESH]
  • |Eye Burns/*drug therapy/*enzymology/pathology [MESH]
  • |Female [MESH]
  • |Heme Oxygenase-1/metabolism [MESH]
  • |Membrane Proteins/metabolism [MESH]
  • |Mice [MESH]
  • |Mice, Inbred BALB C [MESH]
  • |Protein Kinase Inhibitors/pharmacology [MESH]
  • |RNA, Messenger/genetics/metabolism [MESH]
  • |Reactive Oxygen Species/metabolism [MESH]
  • |Wound Healing/drug effects [MESH]


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