The Inhibitory Effect Of Triamcinolone Acetonide (TA) On Retinal Neovascularization In Oxygen-Induced Retinopathy Of Prematurity In The Mouse

Retinopathy of prematurity is a disease which badly affect the life ofpremature babies. This disease was first reported by TERRY in 1942.It iscommonly caused by premature,low birth weight,oxygen therapy afterbirth.The pathogenesis of ROP is not very clear still, but recent researchindicate that retinal neovascularization may play the dominant effect.Theretinal blood vessel starts to grow in embryo sixteenth week.Until theembryo thirty-second week, the developing retinal blood vessel extend tothe nasal side .when the embryo become mature the retinal blood vesselextend to the temporal side.The retinal vessel of prematurity is notdeveloped which is the basic pathophysiological characteristics of ROP.when the prematurity exposed to higher-than-in normal oxygenconcentration , the developing capillary buds are dropout. When the baby istaken to the normal oxygen concentration . This pathologic vesselexaggerates the normal angiogenic process, and large retinalneovascularizations produce. These vessels are pathologic vessels whichlose normal density and shape and lead to proliferation retinopathy evenretinal detachment. Vascular endothelial growth factor(VEGF)and otherangiogenic factors are upregulated. As more and more studies focus oninhibiting neovascularization, we establish an animal model of Oxygen-Induced Retinopathy of prematurity to explore the inhibitory effect oftriamcinolone acetonide (TA) on retinal neovascularization. Methods:sixty 7-day-old C57BL/6J mice were devided into fourgroups that include large-dosage group ,small-dosage group, high andnormal oxygen control groups. Forty-five mice were putted into theenvironment with 75% oxygen for 5 days to establish models of vascularproliferation retinopathy. In large-dosage group (fifteen mice) one eyereceived injection of intravitreal Triamcinolone Acetonide 5μl, and oneeye of small-dosage group(fifteen mice) received injection of intravitrealTriamcinolone Acetonide 2.5μl, and the same volume of balanced saltsolution (BSS) was injected into the other eye of the mice both in these twogroups as a control. To observe the changes of retinal vessels of mice byink perfusion.The inhibitory effect of Triamcinolone Acetonide on retinalneovascularization was evaluated by counting the endotheliocyte nuclei ofnew vessels which extended from retina to vitreous in the tissue-slice ofHE staining. Results: There were large retinal neovascularization in the highconcentration oxygen group compared with in the normal air conditiongroup, and the density and shape of retinal neovascularization weredisordered. This result indicated that the animal model of Oxygen-InducedRetinopathy of prematurity was successful. Comparing with highconcentration oxygen group, regular distributions and reduced density ofretinal neovascularization were observed in the TA treatment group. Thenumber of the endotheliocyte nuclei of new vessels extending from retinato vitreous was less in the TA treatment group than in high concentrationoxygen group (P<0.001). The difference of the number of new bloodvessels endotheliocyte nuclei in two treatment groups was not significant(P>0.05). No retinal toxicity or inflammation response was found in thetissue-slice after injection of intravitreal Triamcinolone Acetonide. Conclusion: Retinal neovascularization can be inhibitted byintravitreal injection of Triamcinolone Acetonide. But the mechanism ofthe effect is demanded to further investigate.