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      Ginsenosides Protect Apical Transporters of Cultured Proximal Tubule Cells from Dysfunctions Induced by H 2O 2

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          Oxidative stress has been implicated as a primary cause of renal failure in certain renal diseases. Indeed, renal proximal tubule is a very sensitive site to oxidative stress and retains functionally fully characterized transporters. It has been reported that ginsenosides have a beneficial effect on diverse diseases including oxidative stress. However, the protective effect of ginsenosides on oxidative stress has not been elucidated in renal proximal tubule cells. Thus, we examined the effect of ginsenosides on oxidative stress-induced alteration of apical transporters and its related mechanism in renal proximal tubule cells. In the present study, hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) (>10<sup>–5</sup> M) inhibited α-methyl- D-glucopyranoside uptake in a dose-dependent manner (p < 0.05). It also inhibited Pi and Na<sup>+</sup> uptake. At a concentration of 20 µg/ml, total ginsenosides significantly reduced H<sub>2</sub>O<sub>2</sub>-induced inhibition of apical transporters. In contrast, protopanaxadiol (PD) and protopanaxatriol (PT) saponins exhibited a less preventive effect than total ginsenosides (p < 0.05). Furthermore, we examined its action mechanism. H<sub>2</sub>O<sub>2</sub> increased lipid peroxide formation, arachidonic acid (AA) release, and Ca<sup>2+</sup> uptake. These effects on H<sub>2</sub>O<sub>2</sub> were significantly prevented by total ginsenosides and PD or PT sanponins. However, total ginsenosides appear to be more protective than PD and PT saponins (p < 0.05). In conclusion, ginsenosides prevented H<sub>2</sub>O<sub>2</sub>-induced inhibition of apical transporters via a decrease in oxidative stress, AA release, and Ca<sup>2+</sup> uptake in primary cultured renal proximal tubule cells.

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          Most cited references 12

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          Panax ginseng pharmacology: a nitric oxide link?

          Panax ginseng is used in traditional Chinese medicine to enhance stamina and capacity to cope with fatigue and physical stress. Major active components are the ginsenosides, which are mainly triterpenoid dammarane derivatives. The mechanisms of ginseng actions remain unclear, although there is an extensive literature that deals with effects on the CNS (memory, learning, and behavior), neuroendocrine function, carbohydrate and lipid metabolism, immune function, and the cardiovascular system. Reports are often contradictory, perhaps because the ginsenoside content of ginseng root or root extracts can differ, depending on the method of extraction, subsequent treatment, or even the season of its collection. Therefore, use of standardized, authentic ginseng root both in research and by the public is to be advocated. Several recent studies have suggested that the antioxidant and organ-protective actions of ginseng are linked to enhanced nitric oxide (NO) synthesis in endothelium of lung, heart, and kidney and in the corpus cavernosum. Enhanced NO synthesis thus could contribute to ginseng-associated vasodilatation and perhaps also to an aphrodisiac action of the root. Ginseng is sold in the U.S. as a food additive and thus need not meet specific safety and efficacy requirements of the Food and Drug Administration. Currently, such sales amount to over $300 million annually. As public use of ginseng continues to grow, it is important for this industry and Federal regulatory authorities to encourage efforts to study the efficacy of ginseng in humans by means of appropriately designed double-blind clinical studies.
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            Neurotrophic and neuroprotective actions of ginsenosides Rb(1) and Rg(1).

            The ginsenosides have many pharmacological actions, including various actions on the nervous system. Our previous studies have demonstrated that two ginsenosides, Rb(1) and Rg(1) improve performance in a passive avoidance-learning paradigm and enhance cholinergic metabolism. The present study was designed to examine the cellular neurotrophic and neuroprotective actions of two pure ginsenosides in two model systems. PC12 cells were grown in the absence or presence of nerve growth factor (NGF) as a positive control, and different concentrations of Rb(1) or Rg(1). To assess neurotrophic properties, neurite outgrowth was quantified for representative fields of cells. After 8 days in culture, both ginsenosides enhanced neurite outgrowth in the presence of a sub-optimal dose of (2 ng/ml) NGF, but did not significantly stimulate neurite outgrowth in the absence of NGF. However, after 18 days in culture, both ginsenosides increased neurite outgrowth in the absence of NGF. SN-K-SH cells were grown in the absence or presence of MPTP or beta-amyloid to assess neuroprotection. Rb(1) and Rg(1) both reversed MPTP-induced cell death. beta-Amyloid-induced cell death was not reversed by either ginsenoside, but Rg(1) produced a modest enhancement of cell death in this model. These results suggest that these two ginsenosides have neurotrophic and selective neuroprotective actions that may contribute to the purported enhancement of cognitive function.
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              Pathogenesis of diabetic nephropathy: the role of oxidative stress and protein kinase C.

              Hyperglycemia, a well recognized pathogenetic factor of long-term complications in diabetes mellitus, not only generates more reactive oxygen species but also attenuates antioxidative mechanisms through glycation of the scavenging enzymes. Therefore, oxidative stress has been considered to be a common pathogenetic factor of the diabetic complications including nephropathy. A causal relationship between oxidative stress and diabetic nephropathy has been established by observations that (1) lipid peroxides and 8-hydroxydeoxyguanosine, indices of oxidative tissue injury, were increased in the kidneys of diabetic rats with albuminuria; (2) high glucose directly increases oxidative stress in glomerular mesangial cells, a target cell of diabetic nephropathy; (3) oxidative stress induces mRNA expression of TGF-beta1 and fibronectin which are the genes implicated in diabetic glomerular injury, and (4) inhibition of oxidative stress ameliorates all the manifestations associated with diabetic nephropathy. Proposed mechanisms involved in oxidative stress associated with hyperglycemia are glucose autooxidation, the formation of advanced glycosylation end products, and metabolic stress resulting from hyperglycemia. Since the inhibition of protein kinase C (PKC) effectively blocks not only phorbol ester-induced but also high glucose- and H2O2-induced fibronectin production, the activation of PKC under diabetic conditions may also have a modulatory role in oxidative stress-induced renal injury in diabetes mellitus.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                28 November 2002
                : 25
                : 5
                : 308-314
                aDepartment of Veterinary Physiology, College of Veterinary Medicine, Biotechnology Research Institute, Chonnam National University, Kwangju, and bCollege of Veterinary Medicine, Chonbuk National University, Jeonju, Korea
                66795 Kidney Blood Press Res 2002;25:308–314
                © 2002 S. Karger AG, Basel

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                Page count
                Figures: 5, References: 29, Pages: 7
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/66795
                Original Paper

                Cardiovascular Medicine, Nephrology

                Kidney, Oxidative stress, Ginsenosides, Apical transporters


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