Protective effect of heat-processed American ginseng against diabetic renal damage in rats.
ABSTRACT We investigated the effects of American ginseng (AG) and heat-processed American ginseng (H-AG) on diabetic renal damage using streptozotocin (STZ)-induced diabetic rats in this study. The diabetic rats showed a loss of body weight gain, and increases in kidney weight, food intake, water intake, and urine volume, whereas the oral administration of H-AG at a dose of 100 mg/kg of body weight per day for 20 days attenuated these diabetes-induced physiological abnormalities. Among the renal function parameters, the elevated urinary protein levels in diabetic control rats were significantly decreased by the AG or H-AG administrations, and the decreased creatinine clearance level was significantly increased in H-AG-administered rats. In addition, the markedly high serum levels of glucose and glycosylated protein in diabetic control rats were significantly decreased by the administration of H-AG, implying that H-AG might prevent the pathogenesis of diabetic complications caused by impaired glucose metabolism and glycosylation of serum proteins. Although no significant ameliorations were shown in overexpressed protein expressions related to diabetic oxidative stress by the AG or H-AG administrations, the accumulation of N (epsilon)-(carboxymethyl)lysine and receptors for advanced glycation endproduct (AGE) expressions were significantly reduced by the administration of H-AG. On the basis of these results, we found that AG and H-AG inhibit AGE accumulation in diabetic rat kidney by their hypoglycemic and renal function ameliorating effects, and this effect was stronger in the H-AG-administered group than in the AG-administered group. These findings indicate that H-AG may have beneficial effect on pathological conditions associated with diabetic nephropathy.
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ABSTRACT: Early diabetic nephropathy is characterized by glomerular hyperpermeability as a result of impaired glomerular filtration structure caused by hyperglycemia, glycated proteins or irreversible advanced glycosylation endproducts (AGE). To investigate the effect of ginseng total saponin (GTS) on the pathologic changes of podocyte ZO (zonula occludens)-1 protein and podocyte permeability induced by diabetic conditions, we cultured mouse podocytes under: 1) normal glucose (5 mM, = control); 2) high glucose (HG, 30 mM); 3) AGE-added; or 4) HG plus AGE-added conditions and treated with GTS. HG and AGE increased the dextran filtration of monolayered podocytes at early stage (2-8 hr) in permeability assay. In confocal imaging, ZO-1 colocalized with actin filaments and β-catenin at cell contact areas, forming intercellular filtration gaps. However, these diabetic conditions suppressed ZO-1 immunostainings and disrupted the linearity of ZO-1. In Western blotting, diabetic conditions also decreased cellular ZO-1 protein levels at 6 hr and 24 hr. GTS improved such quantitative and qualitative changes. These findings imply that HG and AGE have an influence on the redistribution and amount of ZO-1 protein of podocytes thereby causing hyperpermeability at early stage, which can be reversed by GTS.Journal of Korean medical science 10/2011; 26(10):1316-21. · 0.84 Impact Factor
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ABSTRACT: The existence of a complex relationship between soil microbes and ginsenoside contents in their host plants has been reported by previous studies. Here, we analyzed the interaction between the root pathogens and the ginsenoside content in the roots of American ginseng. Two fungal pathogen species were isolated from diseased American ginseng roots, and identified as Fusarium oxysporum (isolate C1) and Fusarium solani (isolate F19) by molecular sequencing analysis. To determine the effect of Fusarium-mediated infection of American ginseng roots, the contents of three ginsenosides, ginsenosides Rb1, ginsenosides Re and ginsenosides Rg1, were monitored over a time course of 120h post infection using high performance liquid chromatography (HPLC). We found that the level of Rb1 was rapidly upregulated upon fungal infection, whereas the contents of Re or Rg1 were not altered significantly. Furthermore, the presence of Rb1, but not Re or Rg1, significantly inhibited conidium germination of both Fusarium species. Thus, Rb1 is likely the disease-resistance compound produced by American ginseng roots in response to the pathogenic fungi. Our study is the first to report the three ginsenosides with different chemical structure respond differently to soilborne pathogen infection. KeywordsGinsenosides–American ginseng–Root pathogen–Chemical response– Fusarium solani – Fusarium oxysporumPlant and Soil 04/2012; 339(1):317-327. · 2.64 Impact Factor
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ABSTRACT: As incidence of diabetes is increasing worldwide, besides it is associated with complications, the present study aimed to investigate the effect of a traditional botanical, ginseng on diabetes induced alterations in kidney functions. Thirty male rats were used in the study by randomly allocating them into three groups, each of ten rats, namely the control group, diabetes group (D), and diabetes+ ginseng group (DG). The latter two groups were rendered diabetic by I/P injection of streptozotocin (50 mg/kg). Daily ginseng extract was administered orally (100 mg/kg BW), one week post streptozotocin (STZ) injection. Ninety days post STZ injection; rats were sacrificed, where serum and kidneys were obtained for determination of metabolic profile, serum electrolytes, kidney function tests, renal tissue enzymes, and renal antioxidant status, together with histopathology. The obtained results revealed a modest improvement in metabolic profile due to ginseng extract administration. However, the kidney functions were greatly improved as evidenced by amelioration of urea nitrogen, creatinine, total protein concentrations and serum electrolytes. Also an increase was noted in renal tissue enzymes and antioxidants with a decrease in malondialdehyde and renal pathology. In conclusion, ginseng extract may be of supportive treatment to combat diabetes complications.Journal of Agricultural Science. 07/2011; 3.