Department of Ophthalmology, Yichang Central People's Hospital, The First College of Clinical Medical Science, China Three Gorges University, Yichang, 443003, People's Republic of China.
Int Ophthalmol. 2020 Jul;40(7):1869-1878. doi: 10.1007/s10792-020-01359-8. Epub 2020 Apr 10.
To observe the protective effects of carnosic acid on rat retinal ganglion cells (RGCs) among acute ocular hypertension rats.
Sixty male SPF (specific-pathogen-free) SD rats (10 weeks) were randomly assigned to untreated group, carnosic-acid-treated group and hypertensive group with 20 rats for each. The acute ocular hypertension animal model was induced by the perfusion of normal saline solution into anterior chamber of eyes to elevate the intraocular pressure (IOP) to 110 mmHg for 60 min in the rats of the carnosic-acid-treated group and hypertensive group. Then, the carnosic acid dissolving in dimethyl sulfoxide (DMSO) was intraperitoneally injected for consecutive 7 days in the carnosic-acid-treated group, and only DMSO was used in the same way in the hypertensive group. The rats were killed 2 weeks after experiment, and retinal sections were prepared for histopathological and apoptotic retinal ganglion cells (RGCs) examination by hemotoxylin and eosin staining and TUNEL staining. Use immunofluorescence employed to examine the survival of RGCs. This study protocol was approved by the Ethic Committee for Experimental Animal of Three Gorges University.
The retinal morphology and structure were clear in the untreated group. The edema of retinal tissue, loosely arranged RGCs and swollen nucleus were seen in the hypertensive group. In the carnosic-acid-treated group, the retinal morphology and structure were regular. The retinal nerve fiber layer (RNFL) thickness was (32.96 ± 1.63), (58.96 ± 1.57) and (50.11 ± 2.37) μm, and the apoptotic cell number was (6.92 ± 2.96), (29.85 ± 6.40) and (14.69 ± 2.98)/field, and the survived cell number was (2363.17 ± 148.45), (1308.67 ± 106.02) and (1614.17 ± 96.39)/0.235 mm in the untreated group, hypertensive group and carnosic-acid-treated group, respectively, showing significant differences among groups (F = 339.284, 81.583, 122.68, all at P < 0.01). Compared with the untreated group, the RNFL thickness was thickened, the number of apoptotic RGCs was much more, and the number of survived RGCs was decreased in the hypertensive group. In the carnosic-acid-treated group, the RNFL thickness was thinner, the number of apoptotic RGCs was reduced, and the number of survived RGCs was increased in comparison with the untreated group (all at P < 0.01).
Carnosic acid plays a protective effect on RGCs by inhibiting the cell apoptosis in acute ocular hypertension rats.
观察迷迭香酸对急性高眼压大鼠视网膜神经节细胞（RGCs）的保护作用。
60 只雄性 SPF（无特定病原体）SD 大鼠（10 周龄）被随机分为未处理组、迷迭香酸处理组和高眼压组，每组 20 只。在迷迭香酸处理组和高眼压组大鼠的前房中灌注生理盐水以将眼内压升高至 110mmHg，持续 60min，诱导急性高眼压动物模型。然后，在迷迭香酸处理组中连续 7 天腹膜内注射溶于二甲亚砜（DMSO）的迷迭香酸，而在高眼压组中以同样的方式使用 DMSO。实验结束后 2 周处死大鼠，通过苏木精和伊红染色和 TUNEL 染色制备视网膜切片，进行组织病理学和凋亡的 RGC 检查。免疫荧光法用于检查 RGC 的存活情况。本研究方案得到了三峡大学实验动物伦理委员会的批准。
未处理组的视网膜形态和结构清晰。高眼压组的视网膜组织水肿，RGC 排列松散，细胞核肿胀。在迷迭香酸处理组中，视网膜形态和结构规则。视网膜神经纤维层（RNFL）厚度分别为（32.96±1.63）、（58.96±1.57）和（50.11±2.37）μm，凋亡细胞数分别为（6.92±2.96）、（29.85±6.40）和（14.69±2.98）/视野，存活细胞数分别为（2363.17±148.45）、（1308.67±106.02）和（1614.17±96.39）/0.235mm，在未处理组、高眼压组和迷迭香酸处理组之间差异均有统计学意义（F值分别为 339.284、81.583、122.68，均 P<0.01）。与未处理组相比，高眼压组的 RNFL 厚度增厚，凋亡的 RGC 数量更多，存活的 RGC 数量减少。在迷迭香酸处理组中，与未处理组相比，RNFL 厚度变薄，凋亡的 RGC 数量减少，存活的 RGC 数量增加（均 P<0.01）。
迷迭香酸通过抑制急性高眼压大鼠的细胞凋亡对 RGC 发挥保护作用。
