AIM: To evaluate the therapeutic effect of Nodinhibit-1 on alkali-burn-induced corneal neovascularization (CNV) and inflammation. The nucleotide-binding oligomerzation domain 1 (NOD1) is a potent angiogenic gene. METH...AIM: To evaluate the therapeutic effect of Nodinhibit-1 on alkali-burn-induced corneal neovascularization (CNV) and inflammation. The nucleotide-binding oligomerzation domain 1 (NOD1) is a potent angiogenic gene. METHODS: The alkali -burned rat corneas (32 right eyes) were treated with eye drops containing Nodinhibit-1 or phosphate buffered solution (PBS, pH 7.4) only, four times per day. CNV and inflammation were monitored using slit lamp microscopy, and the area of CNV was measured by formula. Vascular endothelial growth factor (VEGF) and pigment epithelium -derived factor (PEDF) was determined by Western blot analysis. The TUNEL assay was used to assess the corneal apoptosis cells. RESULTS: Alkali-burn-induced progressive CNV and inflammation in the cornea. After treatment for 7d and 14d, there were statistically significant differences in the CNV areas and inflammatory index on that between two group(P<0.05, respectively). Epithelial defect quantification showed a significant difference between the two groups at days 4 and 7 after the alkali burns (P<0.05). The apoptotic. cells on days 1, 4, and 7 between the two groups showed significant differences at all time points (P<0.05, respectively). Compared to that in control group, the protein level of VEGF expression was significantly reduced whereas the PEDF expression was increase in the Nodinhibit-1 groups on day 14(P<0.05, respectively). CONCLUSION: Topical application of 10.0 mu g/mL Nodinhibit -1 may have potential effect for the alkali burn -induced CNV and inflammation. The effect of Nodinhibit -1 on CNV may be by regulation the equilibrium of VEGF and PEDF in the wounded cornea.展开更多
基金Supported by the National Natural Science Foundation of China(No.81400372,No.81300729,No.81160118)Clinical Medicine Research Special-purpose Foundation of China(No.L2012052)+6 种基金Jiangxi Province Sailing Engineering(No.2014022)Shan Hai Foundation of China(No.2013SH008)Science Technology Foundation of Jiangxi Province(No.20151BBG70223)Youth Science Foundation of Jiangxi Province(No.20151BAB215016)Natural Science Foundation of Fujian Province(No.2015J05170)Education Department Youth Scientific Research Foundation(No.GJJ14170)Health Development Planning Commission Science Foundation of Jiangxi Province(No.20155154)
文摘AIM: To evaluate the therapeutic effect of Nodinhibit-1 on alkali-burn-induced corneal neovascularization (CNV) and inflammation. The nucleotide-binding oligomerzation domain 1 (NOD1) is a potent angiogenic gene. METHODS: The alkali -burned rat corneas (32 right eyes) were treated with eye drops containing Nodinhibit-1 or phosphate buffered solution (PBS, pH 7.4) only, four times per day. CNV and inflammation were monitored using slit lamp microscopy, and the area of CNV was measured by formula. Vascular endothelial growth factor (VEGF) and pigment epithelium -derived factor (PEDF) was determined by Western blot analysis. The TUNEL assay was used to assess the corneal apoptosis cells. RESULTS: Alkali-burn-induced progressive CNV and inflammation in the cornea. After treatment for 7d and 14d, there were statistically significant differences in the CNV areas and inflammatory index on that between two group(P<0.05, respectively). Epithelial defect quantification showed a significant difference between the two groups at days 4 and 7 after the alkali burns (P<0.05). The apoptotic. cells on days 1, 4, and 7 between the two groups showed significant differences at all time points (P<0.05, respectively). Compared to that in control group, the protein level of VEGF expression was significantly reduced whereas the PEDF expression was increase in the Nodinhibit-1 groups on day 14(P<0.05, respectively). CONCLUSION: Topical application of 10.0 mu g/mL Nodinhibit -1 may have potential effect for the alkali burn -induced CNV and inflammation. The effect of Nodinhibit -1 on CNV may be by regulation the equilibrium of VEGF and PEDF in the wounded cornea.
