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1、Antiglycating potential of Zingiber officinalis and delay of diabetic cataract in ratsMegha Saraswat,1 Palla Suryanarayana,1 Paduru Yadagiri Reddy,1 Madhoosudan A. Patil,1 Nagalla Balakrishna,2 Geereddy Bhanuprakash Reddy11Biochemistry Division, National Institute of Nutrition, Hyderabad, India; 2St
2、atistics Division, National Institute of Nutrition, Hyderabad, IndiaPurpose: 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 ging
3、er (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
4、 (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, th
5、e 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
6、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 mainl
7、y 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.The statistical facts indicate that the world, particularly South-East Asia in
8、cluding India, is facing a growing diabetes epidemic of potentially devastating proportions 1,2. Prolonged exposure to chronic hyperglycemia, without proper management, can lead to various short-term and long-term secondary complications, which represent the main cause of morbidity and mortality in
9、diabetic patients. Cataract, characterized by the opacification of the eye lens that interferes with transmission of light onto the retina, is one of the earliest secondary complications of diabetes. Cataract is the leading cause of visual impairment across the world and studies indicate that the in
10、cidence of cataract is much higher in diabetic than in non-diaetic individuals 3,4.Considerable evidence suggests that the long-term pathological sequel of diabetes is a result of the accumulation of tissue macromolecules that have been progressively modified by non-enzymatic glycation 5-7. Glycatio
11、n is a non-enzymatic reaction between reducing sugar and free amino group of the protein (predominantly the -amino group of lysine and the guanidine group of arginine) forming an Amadori product 5-7. The latter then undergoes a series ofCorrespondence to: Dr. G. Bhanuprakash Reddy, National Institut
12、e of Nutrition, Jamai-Osmania, Tarnaka, Hyderabad - 500 604, India; Phone: 91-40-27008921; FAX: 91-40-27019074; email: complex reactions (oxidative and nonoxidative) resulting in the formation of advanced glycation end products (AGE). Non-enzymatic glycation of lens protein has been considered to be
13、 one of the major factors responsible for diabetic cataract 7-10, which alters protein conformation and stability, induces protein aggregation and cross-linking, and leads to protein insolubilization 11-14. Studies also show the formation of AGE not only plays a key role in the development of diabet
14、ic cataract but also in the several pathophysiologies associated with aging and diabetes such as arthritis, atherosclerosis, chronic renal insufficiency, Alzheimer disease, nephropathy, and neuropathy 5,15-17. This raises the possibility that inhibition of AGE formation may prevent the progression o
15、f diabetic complications including diabetic cataract. Aminoguanidine, a nucleophilic hydrazine compound, has been extensively studied for its AGE inhibition 5,18, 19. However, the trial was terminated due to various safety concerns 5,18. In case of cataract, aminoguanidine could delay the progressio
16、n of opacification of lens only in moderately diabetic rats 20. A wide variety of agents such as pyridoxamine, carnosine, carnitine, lipoic acid, taurine, OPB-9195, and phenyl thiazolium bromide have been investigated in several in vitro and in vivo studies 5,21-23 and some of these agents have been tested against cataract in animal model. However, except pyridoxamine, none haveMolecular Vision 2010; 16:1525-1537 Received 10 May 2010 | Accepted 3 August
