Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in rats.
OBJECTIVE
Advanced glycation end products (AGE) are associated in the development of several pathophysiologies including diabetic cataract. Earlier we have reported that some common dietary agents have antiglycating activity and ginger (Zingiber officinalis) was one of the few prominent agents that effectively prevented AGE formation in vitro. In this study we investigated the potential of ginger to prevent diabetic cataract in rats.


METHODS
Diabetes was induced in Wistar-NIN rats by intraperitoneal injection of streptozotocin (35 mg/kg bodyweight) and the control rats received vehicle alone. While a set of diabetic animals received AIN-93 diet, another set received either 0.5 or 3% ginger in their diet for a period of two months. Cataract progression was monitored by slit-lamp biomicroscope. At the end of two months, the animals were sacrificed to evaluate non-enzymatic glycation and osmotic stress in the eye lens.


RESULTS
Slit-lamp examination revealed that feeding of ginger not only delayed the onset but also the progression of cataract in rats. Molecular analyses indicated that feeding of ginger significantly inhibited the formation of various AGE products including carboxymethyl lysine in the eye lens. In addition, ginger also countered hyperglycemia-induced osmotic stress in the lens.


CONCLUSIONS
The results indicated that ginger was effective against the development of diabetic cataract in rats mainly through its antiglycating potential and to a lesser extent by inhibition of the polyol pathway. Thus, ingredients of dietary sources, such as ginger, may be explored for the prevention or delay of diabetic complications.
Saraswat
Megha
M
Biochemistry Division, National Institute of Nutrition, Hyderabad, India.
Suryanarayana
Palla
P
Reddy
Paduru Yadagiri
PY
Patil
Madhoosudan A
MA
Balakrishna
Nagalla
N
Reddy
Geereddy Bhanuprakash
GB
D000449:Aldehyde Reductase / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000187:drug effects; D002386:Cataract / Q000097:blood / Q000150:complications* / Q000473:pathology / Q000517:prevention & control*; D048909:Diabetes Complications / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D018450:Disease Progression; D005136:Eye Proteins / Q000378:metabolism; D005247:Feeding Behavior / Q000187:drug effects; D020939:Zingiber officinale / Q000737:chemistry*; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors* / Q000378:metabolism; D006031:Glycosylation / Q000187:drug effects; D007328:Insulin / Q000097:blood; D007064:L-Iditol 2-Dehydrogenase / Q000378:metabolism; D007908:Lens, Crystalline / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D008297:Male; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology*; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D012995:Solubility / Q000187:drug effects
D001786:Blood Glucose; D005136:Eye Proteins; D017127:Glycation End Products, Advanced; D007328:Insulin; D010936:Plant Extracts; D007064:L-Iditol 2-Dehydrogenase; D000449:Aldehyde Reductase
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