Objective To observe the protective effects of carnosic acid on retinal ganglion cells (RGCs) in acute ocular hypertension rats model.Methods Sixty male SPF SD rats (8-12 weeks) were randomly assigned to normal control group,carnosic-acid treated group and model control group with 20 rats for each group.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 minutes in the rats of the carnosic-acid treated group and model control group,and then the carnosic-acid (dissolving in DMSO) was intraperitoneally injected for consecutive 7 days in the carnosic-acid treated group,and only DMSO was injected in the same way in the model control group.The rates were sacrificed 2 weeks after experiment and retinal sections were prepared for histopathological and apoptotic retinal ganglion cells (RGCs) examination by hemotoxylin & eosin staining and TUNEL staining,and immunofluorescence was employed to examine the survival cell number of RGCs.This study protocol was approved by the Ethic Committee for Experimental Animal of Three Gorges University.Results The retinal morphology and structure were clear in the normal control group.The edema of retinal tissue,loosely arranged RGCs and swollen nucleus were seen in the model control 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 (2 363.17± 148.45),(1 308.67 ±106.02) and (1 614.17 ±96.39) / 0.235 mm2 in the normal control group,model control group and carnosic-acid treated group,respectively,with significant differences among the groups (F =339.284,81.583,122.68,all at P＜0.01).Compared with the normal control group,the RNFL thickness was thickened,the number of apoptotic RGCs was much more and the number of survived RGCs was decreased in the model control group,with significant differences (all at P＜0.01).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 normal control group,with significant differences (all at P＜0.01).Conclusions Carnosic-acid plays a protective effect on RGCs by inhibiting the cell apoptosis in acute ocular hypertension rats.