目的：探讨自然光暴露对单眼远视离焦幼年恒河猴正常和准分子激光角膜切削术(PRK)损伤后角膜组织潜在的光损伤作用。

方法：选取12只2月龄恒河猴，行右眼PRK，矫正度数为-4.0D，制作单眼远视离焦近视动物模型。幼猴体质量和性别均衡配对后分为两组：人工照明组(AL组，n=6)和自然光组(NL组，n=6)。两组幼猴饲养于同一人工照明条件室内饲养环境，NL组幼猴每天9：00～11：00和15：00～17：00于室外随单笼接受自然光照射。PRK术后裂隙灯检查比较两组PRK眼角膜愈合及haze形成情况； PRK术后50d，每组各取4只幼猴双眼泪液，采用蛋白质芯片法检测泪液11种细胞因子含量。PRK术后180d取角膜组织，分别行病理组织学检查组织结构变化； 免疫组织化学法检测TGF-β1和α-SMA表达； TUNEL法检测细胞凋亡以及采用羟胺法和硫代巴比妥酸法分别测定角膜上皮细胞SOD和MDA含量。

结果：PRK术后NL组PRK眼出现一过性haze，术后40d两组haze分级评估有差异(P=0.015)。PRK术后50d，两组PRK眼泪液EGF和TGF-β1含量均有差异(P=0.045、0.038)，两组间对侧眼均无差异(P>0.05)； 且AL组、NL组组内泪液TGF-β1水平有差异(P=0.003、0.036)。术后180d，两组双眼角膜组织形态学一致； 角膜组织内各层偶见细胞凋亡染色，且无明显TGF-β1和α-SMA表达； 两组PRK眼和对侧眼角膜上皮细胞SOD活力和MDA含量均无差异(P>0.05)。

结论：自然光照射量可加剧幼猴PRK术后角膜组织修复反应，但远期未对角膜组织造成不可逆病理组织学改变，对正常的幼猴角膜组织无明显光损伤作用。

METHODS: Twelve infant rhesus monkeys(aged 2mo)were treated monocularly with PRK(-4.0D)and divided into two groups: AL group(n=6)and NL group(n=6). The monkeys in AL were reared under artificial lighting(indoor).The monkeys in NL were exposed to natural lighting(outdoor)for 4h per day(9:00-11:00 and 15:00-17:00), and to indoor lighting for the rest of the light phase. Corneal haziness after PRK was assessed biomicroscopically using the Fantes scale. At 50d post-PRK, tear fluids of both eyes from 8 monkeys in the two groups(4 animals each group)were collected and analyzed for 11 kinds of cytokines using protein microarray analysis. At 180d post-PRK. The corneas were obtained and evaluated by histopathological examination, immunohistochemistry with antibody to TGF-β1 and α-SMA, and TUNEL. The vitality of SOD and the level of MDA in corneas were detected with WST-1 and lipid peroxidation MDA assay kits, respectively.

RESULTS: The monkeys in AL group exhibited a lesser degree of haze than those in NL group at 40d following PRK(P=0.015). At 50d post-PRK, EGF and TGF-β1 levels in tears were different in PRK-treated eyes between the two groups(P=0.045, 0.038), and TGF-β1 were significantly different between both eyes in the same group(AL: P=0.003; NL: P=0.036). At 180d post-PRK, there were no differences in histological changes, the expression of TGF-β1 and α-SMA, and apoptosis cell staining of the corneal between the two groups. The vatility of SOD and the levels of MDA in corneal epithelium were not different between the two groups(P>0.05).

CONCLUSION: Exposure to natural light in our study could not induce light damage to the normal cornea of the infant rhesus monkeys, but it could aggravate the corneal tissue repair reaction transiently post-PRK.