方法：成年家兔43只，随机选取40只兔双眼行角膜基质层缝线建立兔角膜新生血管模型，造模成功后右眼(A组)未行特殊处理，左眼(B组)给予地塞米松局部注射，未造模3只兔双眼为正常对照，造模后裂隙灯动态观察新生血管的形态并计算其生长面积，并分别于造模后1，4，7，14，21d各处死8只兔，取角膜新生血管组织行HE染色观察其病理学特点，并检测角膜中IL-1β及TNF-α的表达情况。

结果：缝线后4d可见CNV长入，7～14d生长最为旺盛，HE染色见炎性细胞浸润，浅基质层大量新生血管生长，免疫组化染色提示，随缝线时间延长角膜IL-1β及TNF-α的表达逐渐增加； 而经地塞米松治疗后，CNV较前延迟长入，面积缩小，炎性细胞浸润减轻，且角膜中IL-1β及TNF-α的表达较单纯缝线眼明显降低，结果有统计学意义(P<0.05)。

结论：地塞米松可能通过早期抑制角膜组织中IL-1β及TNF-α表达而抑制新生血管的生长。

METHODS: For 43 healthy rabbits, 40 were randomly selected for establishing CNV model in corneal stroma. The right eyes(group A)were received no medicine and the left eyes(group B)were injected dexamethasone after successfully establishing the model. The no modeling 3 rabbits were normal control group. The morphologic change of corneal was observed with slit lamp microscope and the areas of CNV was calculated every day, then 8 rabbits were randomly chosen for sacrificing at 1, 4, 7, 14, 21d respectively. The pathological characteristics of CNV were observed after HE staining, and IL-1β and TNF-α expression was detected by immunohistochemistry.

RESULTS: CNV was grown at the 4d after suture, and the 7-14d was vigorous growth period. inflammatory cell infiltration appeared after HE staining, and CNV was located at the superficial stroma of cornea. Immunohistochemistry results showed that IL-1β and TNF-α expression was gradually increased with prolonged suture time. Compared with corneal stitch group, the rabbits cured by dexamethasone were found with less inflammatory cells infiltrating and neovescularization, moreover, the expression of IL-1β and TNF-α decreased. There were statistical significance between the two groups(P<0.05).

CONCLUSION: Dexamethasone can inhibit the CNV growth by controlling the inflammation of corneal and restraining IL-1β and TNF-α expression.