Therapeutic potential of breakers of advanced glycation end product–protein crosslinks

Vasan, Sara; Foiles, Peter G.; Founds, Hank

doi:10.1016/j.abb.2003.08.016

Cited by 195 publications

(134 citation statements)

References 93 publications

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“…Reactions with nitric oxide in endothelial cells, free radicals lead to the loss of vasodilatation activity. During aging and in diabetic conditions long-lived proteins, collagen and elastin undergoes continual non-enzymatic crosslinking which is mediated by advanced glycation end products [16].…”

Section: Discussionmentioning

confidence: 99%

Study of Antioxidant Activity of Formononetin by in Vitro Method

Vishnuvathan

Lakshmi

Srividya

2017

Int J Pharm Pharm Sci

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Objective: Now the important field of research in phytomedicine is to search a new plant source as well as new phytoconstituents that have fewer side effects and low cost with the free radical scavenging activity. Methods:Different in vitro models such as DPPH, hydroxyl radical, hydrogen peroxide radical, nitric oxide radical and superoxide radical scavenging activity were performed using different concentrations of formononetin ranging from 0.1-50 μg/ml.Results: Formononetin showed only 84.39% inhibitory activity against DPPH radical and it was found to be 16 % less than the butylated hydroxytoluene with the IC 50 value of 4.65 μg/ml concentration. In scavenging hydroxyl radicals, formononetin inhibited only 67.63% with the IC50 value of 9.48 μg/ml concentration and it showed 12 % lesser inhibitory activity than standard alpha-tocopherol. Formononetin could able to scavenge maximum 73.53% of hydrogen peroxide radicals with the IC50 value of 4.75 μg/ml and its activity of scavenging hydrogen peroxide were found to be 10 % less than the standard ascorbic acid. Formononetin showed 94.33 % nitric oxide radical inhibitory activity with the IC50 value of 5.0 μg/ml and it showed 6% lesser activity when compared to standard quercetin. Formononetin showed 94.79 % activity against the scavenging of superoxide radical with the IC50 Conclusion: All these results suggested that, formononetin is a good natural antioxidant which is capable of scavenging almost all types of free radicals. So this could be used to treat various diseases like diabetes, atherosclerosis, cancers, the aging and cardiovascular disease which is being caused by free radicals.value of 4.27 μg/ml. Superoxide inhibitory activity of formononetin was 5.3 %less than the standard quercetin.

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Section: Discussionmentioning

confidence: 99%

Study of Antioxidant Activity of Formononetin by in Vitro Method

Vishnuvathan

Lakshmi

Srividya

2017

Int J Pharm Pharm Sci

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“…Finally, after dehydration, oxidation and rearrangement, the Amadori products yield stable and irreversible compounds known as AGEs (l " Fig. 1) [5,6]. Moreover, a variety of other pathways such as autoxidation of glucose, or ascorbate and lipid peroxidation, can also lead to AGE formation.…”

Section: The Mechanisms Of Inhibition Of Advanced Glycation End Produmentioning

confidence: 99%

The Mechanisms of Inhibition of Advanced Glycation End Products Formation through Polyphenols in Hyperglycemic Condition

et al. 2015

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Glycation, the non-enzymatic binding of glucose to free amino groups of an amino acid, yields irreversible heterogeneous compounds known as advanced glycation end products. Those products play a significant role in diabetic complications. In the present article we briefly discuss the contribution of advanced glycation end products to the pathogenesis of diabetic complications, such as atherosclerosis, diabetic retinopathy, nephropathy, neuropathy, and wound healing. Then we mention the various mechanisms by which polyphenols inhibit the formation of advanced glycation end products. Finally, recent supporting documents are presented to clarify the inhibitory effects of polyphenols on the formation of advanced glycation end products. Phytochemicals apply several antiglycation mechanisms, including glucose metabolism, amelioration of oxidative stress, scavenging of dicarbonyl species, and up/down-regulation of gene expression. To utilize polyphenols in order to remedy diabetic complications, we must explore, examine and clarify the action mechanisms of the components of polyphenols.

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“…Sorbinil is known to improve neurovascular dysfunctions (9,14). We also used alagebrium, which is an AGE breaker known to improve arterial elasticity in experimental animals (18,19) as well as in clinical studies (20,21) by its ability to reduce the accumulation of AGEs in diabetes (19,22).…”

mentioning

confidence: 99%

Aldose Reductase Pathway Inhibition Improved Vascular and C-Fiber Functions, Allowing for Pressure-Induced Vasodilation Restoration During Severe Diabetic Neuropathy

et al. 2006

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Pressure-induced vasodilation, a neurovascular mechanism relying on the interaction between mechanosensitive Cfibers and vessels, allows skin blood flow to increase in response to locally nonnociceptive applied pressure that in turn may protect against pressure ulcers. We expected that severe neuropathy would dramatically affect pressure-induced vasodilation in diabetic mice, and we aimed to determine whether pressure-induced vasodilation alteration could be reversed in 8-week diabetic mice. Control and diabetic mice received no treatment or sorbinil, an aldose reductase inhibitor, or alagebrium, an advanced glycation end product breaker, the last 2 weeks of diabetes. Laser Doppler flowmetry was used to evaluate pressureinduced vasodilation and endothelium-dependent vasodilation after iontophoretic delivery of acetylcholine (ACh). We assessed the nervous function with measurements of motor nerve conduction velocity (MNCV) as well as the C-fiber-mediated nociception threshold. Pressure-induced vasodilation, endothelial response, C-fiber threshold, and MNCV were all altered in 8-week diabetic mice. None of the treatments had a significant effect on MNCV. Although sorbinil and alagebrium both restored ACh-dependent vasodilation, sorbinil was the sole treatment to restore the C-fiber threshold as well as pressure-induced vasodilation development. Therefore, the inhibition of aldose reductase pathway by sorbinil improved vascular and C-fiber functions that allow pressure-induced vasodilation restoration that could limit neuropathic diabetic cutaneous pressure ulcers.

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Therapeutic potential of breakers of advanced glycation end product–protein crosslinks

Cited by 195 publications

References 93 publications

Study of Antioxidant Activity of Formononetin by in Vitro Method

Study of Antioxidant Activity of Formononetin by in Vitro Method

The Mechanisms of Inhibition of Advanced Glycation End Products Formation through Polyphenols in Hyperglycemic Condition

Aldose Reductase Pathway Inhibition Improved Vascular and C-Fiber Functions, Allowing for Pressure-Induced Vasodilation Restoration During Severe Diabetic Neuropathy

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