Effect of carnosine, aminoguanidine, and aspirin drops on the prevention of cataracts in diabetic rats.
OBJECTIVE
To investigate the effect of carnosine (CA), aminoguanidine (AG), and aspirin (ASA) drops, all inhibitors of glycation, on the development of diabetic cataract in rat.


METHODS
Rats were made diabetic with streptozotocin, and based on the level of plasma glucose, they were assigned as non-diabetic rats (<14 mmol/l plasma glucose) and diabetic rats (>14 mmol/l plasma glucose). Animals in the treated groups received CA, AG, and ASA as drops to the left eyes starting from the day of streptozotocin injection. Progression of lens opacification was recorded using the slit lamp at regular time intervals. All the rats were killed after the week 13, and the levels of advanced glycation end products (AGE), glutathione reductase (GR), catalase (CAT), and glutathione (GSH) were determined.


RESULTS
Lens opacification progressed in a biphasic manner in the diabetic rats, an initial slow increase during the first eight weeks of diabetes followed by a steep increase in the next five weeks. Carnosine treatment delayed the progression of cataracts in diabetic rats, and the delay was statistically significant on the fourth week of diabetes (p<0.05, when compared with untreated moderately diabetic rats). A decrease in the antioxidant enzymes of CAT and the level of GSH was found in the lens of the untreated diabetic rats at 13 weeks after injection. Some protection was provided in the treated eyes. The level of glycation in the untreated diabetic rats was significantly higher than that in the normal rats (p<0.001). After treatment with CA, AG, and ASA, those diabetic rats had a lower level of glycated lens protein compared to the untreated diabetic rats (p<0.001).


CONCLUSIONS
These results thus suggest that the effect of CA, AG, and ASA is indeed inhibition of the formation of AGEs. However, the effect of CA, AG, and ASA is overwhelmed by the excessive accumulation of AGEs in the severely diabetic rats. CA compared with AG and ASA treatment can delay the progression of lens opacification in the diabetic rats only during the earlier stages. It also protects against the inactivation of enzymes.
Yan
Hong
H
Department of Ophthalmology, Tangdu Hospital, Fourth Military Medical University, Xi'an, China. yhongb@fmmu.edu.cn
Guo
Yong
Y
Zhang
Jie
J
Ding
Zhenghua
Z
Ha
Wenjing
W
Harding
J J
JJ
D000818:Animals; D001241:Aspirin / Q000494:pharmacology / Q000627:therapeutic use*; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002336:Carnosine / Q000494:pharmacology / Q000627:therapeutic use*; D002386:Cataract / Q000150:complications* / Q000473:pathology / Q000517:prevention & control*; D003315:Cornea / Q000187:drug effects / Q000473:pathology; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000473:pathology; D018450:Disease Progression; D005136:Eye Proteins / Q000378:metabolism; D006031:Glycosylation / Q000187:drug effects; D006146:Guanidines / Q000494:pharmacology / Q000627:therapeutic use*; D007908:Lens, Crystalline / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D008297:Male; D009883:Ophthalmic Solutions; D051381:Rats; D017207:Rats, Sprague-Dawley; D013194:Staining and Labeling; D013311:Streptozocin
D001786:Blood Glucose; D005136:Eye Proteins; D006146:Guanidines; D009883:Ophthalmic Solutions; D013311:Streptozocin; D002336:Carnosine; D001241:Aspirin; C004479:pimagedine