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Neuroprotective effects of ginsenosides

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EN
Ginseng, the root of the Panax species, is a well-known herbal medicine. Traditionally it has been used in Korea, China and Japan for thousands of years. Nowadays it has become a popular and worldwide known health drug. Current scientific studies demonstrate in vivo and in vitro its beneficial effects in a wide range of pathological conditions such as cardiovascular disease, cancer, immune deficiency and hepatotoxicity. Ginsenosides or ginseng saponins as the active ingredients have antioxidant, anti-inflammatory, anti-apoptotic and immunostimulant properties, which raised speculations that these compounds could positively affect neurodegenerative disorders and delay neuronal aging. Conclusive clinical data in humans are still missing. However, results from animal studies and neuronal cell culture experiments indicate that ginsenosides can counteract and attenuate factors promoting neuronal death as environmental toxins, excitotoxic action of glutamate and rises in intracellular calcium, excessive release of free radicals and apoptotic events. Thus, neuroprotective actions of ginsenosides could come about as a valuable option to slow down neurodegenerative diseases.
EN
Oxidative stress has been implicated in cognitive impairment in both experimental animals and humans. This implication has led to the notion that antioxidant defence mechanisms in the brain are not sufficient to prevent oxidative damage, and that dietary intake of a variety of antioxidants might be beneficial for preserving brain function. The present study, therefore, aimed to investigate the protective effect of melatonin against radiation-induced impairment in the learning ability of mice. Twenty days oral administration of melatonin (0.1 mg/kg b.w.), followed by an acute exposure to gamma-radiation (6 Gy), inhibited the radiation-induced decline in learning ability. Biochemical estimation of brain protein carbonyls, malondialdehide (MDA) and reduced glutathione (GSH) in these mice indicated that radiation-induced augmentation of protein oxidation and lipid peroxidation had been significantly ameliorated in melatonin treated, irradiated mice. Radiation-induced deficit of glutathione was also normalized by melatonin administration, as there was no statistical difference from normal at P<0.001. Results indicate the antioxidative as well as neuroprotective properties of melatonin against the radiation. These findings support results showing melatonin as a free radical scavenger.
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