Abstract:AIM:To observe whether progesterone has a protective effect on retinal neural cells by establishing the acute high intraocular pressure model and intervening with progesterone.
METHODS: Totally 140 Wistar rats were randomly divided into normal control group(group A)20, high intraocular pressure control group(group B)60 and high intraocular pressure progesterone treatment group(group C)60. The acute high intraocular pressure models were made by saline anterior chamber perfusion. Group C were treated with intraperitoneal injection of progesterone 4.0mg/Kg immediately after intraocular pressure restored, and after 6, 24h and every other day were treated with subcutaneous injection. Group B were injected with equivalent saline at the same time. At the 1, 3, 7d after ocular hypertension, the retinas of rats in each group were obtained respectively. Retinas pathological changes were observed in samples hemetoxylin and eosin staining. The protein expression of Caspase-3 was measured with immunohistochemistry and Western blot. Apoptosis in retinal nerve cells were tested with TUNEL technique. Statistical analysis was performed in each group.
RESULTS: The rats retina of group B and group C were edema, but the degree in group C was lower than that in group B. In relative quantitative detection of immunohistochemistry and Western blot, expression of Caspase-3 was lower than group B. Substantial expression of Caspase-3 protein lay in cell nucleus and cytoplasm. The level of Caspase-3 in group B was higher than in group C. The positive cells were mainly in inner nucleus layer and ganglion cell layer. The level on the first day after high intraocular pressure was the highest, then gradually decreased along with the passage of time. Apoptosis tested with TUNEL technique, positive cells could be observed in group B and group C, which in inner nucleus layer and ganglion cell layer. But the number in group B was significantly more than group C.
CONCLUSION: Progesterone has nerve protection functions on retinal acute high intraocular pressure injury in rats.