| Objective To investigate the ocular application of peroxisome proliferators-activated receptor gamma (PPAR-γ) agonist pioglitazone on expression of NF-κB and TNF-αin alkali-burned corneal of rat.Methods After corneal alkali-burn models 48 Sprayue-Dawley rats were established, The rats were randomly divided into 3 groups, Group I for burned treatment group (I A:low-dose group,0.2g/L; I B:high-dose group,0.8g/L), PPAR-y agonist Pioglitazone of different concentrations were injected at the same way in Iâ… A,â… B groups respectively for once per day. Groupâ…¡for the treatment of the control group, Subconjunctival injection of dexamethasone for once per day.â… -â…¡groups of medication lasts 2 weeks. Normal saline was subconjunctivally injected after burning of cornea in control groupâ…¢. All of right eyes for the experimental eye, and left eyes as a negative control. The growth of CNV in 48 SD rats was observed by slit lamp microscope and the area of CNV was recorded. The expression of PPAR-γ,NF-κB and TNF-αwere detected by immunohistochemistry.Results PPAR-γwas not expressed in normal rat cornea. Corneal angiogenesis was observed after alkali-burned corneas of rats, and reached the peak after 4 to 7 days. The expression of PPAR-γwas positively correlated to CNV and the expressions of NF-κB and TNF-α. The corneal neovascularization area in group I B was significantly smaller than that in the control groupsâ…¡,â…¢(P<0.05). Compared with groupsâ…¡,â…¢, the occurence and the growth of CNV in groupâ… B were inhibited obviousily. But no difference betweenâ… A group andâ…¡group(P>0.05). On the 4 th, 7 th,14th day, the neovasctdarization area in theâ… B group were (5.42±0.25)mm2,(8.14±0.25)mm2,(9.67±0.42)mm2, respectively. The difference was highly significant(P<0.05). more expression of PPAR-γin theâ… B group,and the expressions of NF-κB and TNF-αwere statistically declined in varying degrees and at different times (P<0.05).Conclusion PPAR-γagonist Pioglitazone can reduce the inflammatory response of rats after alkali burn, and inhibit the growth of CNV. The mechanism may be related to activation of PPAR-γ, which reduced pro-inflammatory factor TNF-α, and inhibited of activation of NF-κB. |