| Objective:To investigate the therapeutic effects and anti-inflammation mechanism of retinoic acid in the rat cornea after alkali injury.Method:. A total of36SD female rats central corneas were injured by contacting eyes with filter paper saturated with1molL-1NaOH for30seconds, and randomly divided into treatment group (Group A) and control group (Group B). Group A was treated with0.3mgL-1RA and eye drops four times daily and Group B was treated with vehicle of eye drops, two groups were treated with0.5%levofloxacin eye drops four times daily each before and after injury for3days. The impression cytological analysis were conducted at1,4,7and14day after injury; each6rats were randomly sacrificed for analysis the inflammatory cells by HE staining in4,7and14days after injury; meanwhile the expression of IL-1a and NF-κB were determined by immunohistochemistry.Result:1.The goblet cells count were significant decreased in1,4and7days after injury (P<0.05), but there was no significant differences in14day (P>0.05) between two groups;The goblet cell count was significant greater in Group A than that the Group B (P<0.05) in4and.7days.2.The inflammatory reaction of Group A is lighter than that the Group B,and the inflammation cell count was significant differences in Group A and Group B in different phases after injury (P<0.05)3. The highest expression of IL-1α in two groups were in4day, compared with Group B, the expression of IL-la were significant decreased in4and7day after injury (P<0.05) in Group A, there was no significant difference in14day (P>0.05) between two groups.4. The highest expression of NF-κB were in7day in two groups, Compared with Group B, the expression of NF-κB in Group A were significant decreased in4and7day after injury (P<0.05), there was no significant difference in14day (P>0.05) between two groups.Conclusion:1. The retinoic acid can promote the conjunctival goblet cell proliferation, and then it plays a promoting healing effect in the rat corneal alkali burns.2. The retinoic acid maybe resist the inflammation by inhibiting the expression of interleukin-1alpha and nuclear factor kappa B. |
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