Powerful Herbal Medicine to Prevent Glycation
Combination of Medicinal Herbs KIOM-79 Reduces Advanced Glycation End Product Accumulation and the Expression of Inflammatory Factors in the Aorta of Zucker Diabetic Fatty Rats
Previous studies have reported that KIOM-79 shows a strong inhibitory effect on AGE formation and inhibited a proinflammatory state in a murine macrophage cell line. In the present study, we investigated the effect of KIOM-79 on AGE accumulation and vascular inflammation in the aorta of Zucker diabetic fatty (ZDF) rats, a commonly used model of type 2 diabetes.
Cardiovascular disease is one of the most common complications of diabetes. Chronic hyperglycemia accelerates the formation of advanced glycation end products (AGEs) and accumulation of AGEs in various tissues. AGE accumulation is an important feature in the development of diabetic macrovascular complications, such as atherosclerosis and cardiac dysfunction, and AGEs are believed to play a crucial role in the pathogenesis of diabetic vascular inflammation.
AGE inhibitors, such as LR-90 and aminoguanidine (AG), have anti-inflammatory properties and help protect against diabetic vascular damage. The inhibition of AGE formation, blockade of the AGE-RAGE interaction, and suppression of RAGE expression or its downstream pathways suggest novel therapeutic strategies for the treatment of the vascular complications of diabetes.
Traditional herbal medicines have been used for the treatment of diabetes or diabetic complications in Korea and Asian countries. The development of KIOM-79, which is a mixture of the 80% ethanol extract of parched Puerariae radix, gingered Magnoliae cortex, Glycyrrhizae rhizome, and Euphorbiae radix, was based on the basic known function of each herb used in traditional Korean medicine for a variety of medical purposes, including diabetes and diabetic complications.
In our previous studies, KIOM-79 has shown a stronger inhibitory effect on AGE formation than individual herbal medicines in vitro. KIOM-79 has also reduced accumulation of AGEs in the kidney and delayed the development of diabetic nephropathy in animal models for type 1 and 2 diabetes.
Taken together, we concluded that KIOM-79 inhibits AGE accumulation and reduces RAGE expression in the diabetic aorta. Decreased AGE/RAGE interaction decreases NF-?B activation, subsequently decreasing the expression of multiple inflammatory factors, including MCP-1, VEGF, VCAM-1, and iNOS. The present study shows that KIOM-79 may help in the prevention and delay of diabetes-induced vascular inflammation.