The prevention effect of aspirin on galactose cataract
- VernacularTitle:阿司匹林对半乳糖性白内障抑制作用的实验研究
- Author:
Jibing, YU
;
Hui, ZHOU
- Publication Type:Journal Article
- Keywords:
aspirin;
cataract;
superoxide dismutase;
glutathione peroxidase;
catalase;
ultrastructure;
oxygen damage
- From:Chinese Ophthalmic Research
2009;27(11):1015-1018
- CountryChina
- Language:Chinese
-
Abstract:
Objective Experimental research demonstrated that oxidative damage leads to formation of cataract in rats and its machanism is the decline of activities of superoxide dismutase(SOD), glutathione peroxidase(GSH-PX) and catalase(CAT) . Aaspirin can improve the antioxidative ability of lens. The purpose of this study was to observe the inhibition of aspirin on D-Galactose-induced cataractous lenses of rats. Methods Galactose cataract model was established in 40 cleaning Wistar rals by intraperitoneal injection of 20 mL/kg 80% D-Galactose for 10 days. The models were divided into model group (20 rats) and aspirin group(20 rats). 150 mg/kg of aspirin was administered immediately by gastrogavaging in aspirin group for 20 days. Other 20 normal Wistar rats were as control group. At day 3, 6, 10, 14, 20, the transparency of rat lenses was observed under the slit lamp microscopy. At day 5 after experiment, the ultrastructure of the lenses was examined and evaluated under the scanning electron microscopy. The activities of SOD, GSH-PX and CAT were detected by Coomassie Brilliant Blue color comparator, respectively. The use of experimental animal followed the Regulations for the Administration of Affair Concerning Experimental Animals by State Science and Technology Commission. Results All lenses were transparent in the rats of control group. The degree of lens opacity was more mild in asprin group compared with model group. 25. 00%, 41. 67%, 58. 33%, 83. 33% of lenses in aspirin group showed swelling at day 6, 10, 14, 20, respectively, but 65% lenses were opacity in model group on day 3 and 100% lenses were nuclear cataracts in 6 days. The structure of lenses was normal in control group, but the process number, fiber thickness and fiber density of lens were significantly increased in model group compared with control group (P ＜0. 05), and only process number was increased in asprin group. The activities of SOD, GSH-PX and CAT in lens of model group were obviously lower than in normal control group(P＜0. 05), but those in asprin group were significantly increased in comparison with model group(P ＜0. 05). Conclusion Aspirin could protect lenses of rats against oxidative damage by elevating activities of SOD, GSH-PX and CAT in lens and inhibiting the generation and development of galactose-induced cataract at early stage of cataract.
