Source:http://linkedlifedata.com/resource/pubmed/id/18789666
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
2009-6-15
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pubmed:abstractText |
alpha-Crystallin, a molecular chaperone of the eye lens, plays an important role in maintaining the transparency of the lens by preventing the aggregation/inactivation of several proteins and enzymes in addition to its structural role. alpha-Crystallin is a long-lived protein and is susceptible to several posttranslational modifications during aging, more so in certain clinical conditions such as diabetes. Nonenzymatic glycation of lens proteins and decline in the chaperone-like function of alpha-crystallin have been reported in diabetic conditions. Therefore, inhibitors of nonenzymatic protein glycation appear to be a potential target to preserve the chaperone activity of alpha-crystallin and to combat cataract under hyperglycemic conditions. In this study, we investigated the antiglycating potential of cumin in vitro and its ability to modulate the chaperone-like activity of alpha-crystallin vis-à-vis the progression of diabetic cataract in vivo. Aqueous extract of cumin was tested for its antiglycating ability against fructose-induced glycation of goat lens total soluble protein (TSP), alpha-crystallin from goat lens and a nonlenticular protein bovine serum albumin (BSA). The antiglycating potential of cumin was also investigated by feeding streptozotocin (STZ)-induced diabetic rats with diet containing 0.5% cumin powder. The aqueous extract of cumin prevented in vitro glycation of TSP, alpha-crystallin and BSA. Slit lamp examination revealed that supplementation of cumin delayed progression and maturation of STZ-induced cataract in rats. Cumin was effective in preventing glycation of TSP and alpha-crystallin in diabetic lens. Interestingly, feeding of cumin to diabetic rats not only prevented loss of chaperone activity but also attenuated the structural changes of alpha-crystallin in lens. These results indicated that cumin has antiglycating properties that may be attributed to the modulation of chaperone activity of alpha-crystallin, thus delaying cataract in STZ-induced diabetic rats.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1873-4847
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
20
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
553-62
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pubmed:meshHeading |
pubmed-meshheading:18789666-Animals,
pubmed-meshheading:18789666-Cataract,
pubmed-meshheading:18789666-Cuminum,
pubmed-meshheading:18789666-Diabetes Mellitus, Experimental,
pubmed-meshheading:18789666-Disease Progression,
pubmed-meshheading:18789666-Glycosylation,
pubmed-meshheading:18789666-Male,
pubmed-meshheading:18789666-Molecular Chaperones,
pubmed-meshheading:18789666-Phytotherapy,
pubmed-meshheading:18789666-Plant Preparations,
pubmed-meshheading:18789666-Rats,
pubmed-meshheading:18789666-Rats, Wistar,
pubmed-meshheading:18789666-alpha-Crystallins
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pubmed:year |
2009
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pubmed:articleTitle |
Delay of diabetic cataract in rats by the antiglycating potential of cumin through modulation of alpha-crystallin chaperone activity.
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pubmed:affiliation |
National Institute of Nutrition, Hyderabad 500007, India.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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