11.19.07

Avon Anew Alternative Skin Care Product Review

Posted in AGE Breaker at 9:42 am by adamant

    Avon’s Anew Alternative Night Cream is a wonderful combination of modern science and ancient wisdom from the Far East. It combines high-tech tetrapeptides and alagebrium (HBR) with a unique blend of ancient Eastern herbs to reverse facial sag.

    The active ingredients, described in detail below, work to: break the cross links of advanced glycation endproducts (AGEs) which stiffen collagen fibers resulting in facial sag; protect the skin from inflammation caused by viruses, bacteria and fungi; improve circulation to speed repair and invigorate the skin; and control the body’s inflammatory response (as your own hormones did in younger days).

Alagebrium (HBR)

    Alagebrium is an AGE crosslink breaker. Glycation (the G in AGE) is the process by which glucose links with proteins and causes them to bind together, thus stiffening tissues and leading to the complications of diabetes and some of the physiologic problems associated with aging.

    There are no published studies yet that show topical application breaks AGE crosslinks, though the manufacturer, Alteon, has licensed Avon to use it for that very purpose.

    Several medical studies have shown that alagebrium taken internally significantly lowers high blood pressure by restoring flexibility to arteries.

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08.12.07

Research Abstract

Posted in AGE Research at 5:36 am by adamant

An advanced glycation endproduct cross-link breaker can reverse age-related increases in myocardial stiffness

[Abstract] Decreased elasticity of the cardiovascular system is one of the hallmarks of the normal aging process of mammals. A potential explanation for this decreased elasticity is that glucose can react nonenzymatically with long-lived proteins, such as collagen and lens crystallin, and link them together, producing advanced glycation endproducts (AGEs). Previous studies have shown that aminoguanidine, an AGE inhibitor, can prevent glucose cross-linking of proteins and the loss of elasticity associated with aging and diabetes. Recently, an AGE cross-link breaker (ALT-711) has been described, which we have evaluated in aged dogs. After 1 month of administration of ALT-711, a significant reduction (≈40%) in age-related left ventricular stiffness was observed [(57.1 ± 6.8 mmHgm²/ml posttreatment (1 mmHg = 133 Pa)]. This decrease was accompanied by improvement in cardiac function.

Breakers of advanced glycation end products restore large artery properties in experimental diabetes

[Abstract] Glucose and other reducing sugars react with proteins by a nonenzymatic, posttranslational modification process called nonenzymatic glycation. The formation of advanced glycation end products (AGEs) on connective tissue and matrix components accounts largely for the increase in collagen crosslinking that accompanies normal aging and which occurs at an accelerated rate in diabetes, leading to an increase in arterial stiffness. A new class of AGE crosslink “breakers” reacts with and cleaves these covalent, AGE-derived protein crosslinks. Treatment of rats with streptozotocin-induced diabetes with the AGE-breaker ALT-711 for 1-3 weeks reversed the diabetes-induced increase of large artery stiffness as measured by systemic arterial compliance, aortic impedance, and carotid artery compliance and distensibility. These findings will have considerable implications for the treatment of patients with diabetes-related complications and aging.

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06.04.07

非酶糖基化终末产物所致疾病的中药干预

Posted in AGE Breaker at 9:49 am by adamant

Diseases induced by advanced glycation end products and their treatments with Chinese materia medica

摘　要: 非酶糖基化终末产物(AGEs) 是蛋白质、脂质和核酸等大分子的游离氨基与还原性单糖的醛基反应所生成的稳定的共价化合物, 在体内的积累是导致糖尿病等多种疾病及其并发症的关键因素。AGEs 可直接或间接地对机体产生致病作用。目前AGEs 抑制剂特别是某些中药在治疗AGEs 引起的疾病方面研究进展迅速, 主要通过降低体内AGEs 水平、减少AGEs 交联、抗氧化、阻断与相关受体的结合等途径来干预A GEs 的合成、代谢和受体后效应。简述AGEs 的致病机制, 并探讨中药对AGEs 所致疾病的干预及其可能机制。

Key words: advanced glycation end products (AGEs) ; diabetic complications; Chinese materia medica

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Email: adamtangcn@gmail.com for full-text translation

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