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Melon Glisodin: Detailed Information
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DATA- 1: Effect of GliSODin® (melon glisodin) on antioxidant enzyme activities in circulating blood
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DATA- 2: Antifibrotic activity of GliSODin® (melon glisodin) in liver fibrosis (liver cirrhosis model)
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DATA- 3: Effect of GliSODin® (melon glisodin) on intellectual disability
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DATA- 4: Effect of GliSODin® (melon glisodin) on age-related decline of cognitive ability
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DATA- 5: Protective effect against DNA damage caused by oxidative stress
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DATA- 6: Effect on skin inflammation caused by ultraviolet radiation
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DATA- 7: Effect of GliSODin® (melon glisodin) the changes in blood antioxidant enzyme and serum lactic acid levels caused by vigorous exercise
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DATA- 8: Suppression of allergic reaction
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DATA- 9: Effect on arthritis and synergy with glucosamine
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DATA-10: Prevention and improvement of atherosclerosis caused by the metabolic syndrome
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DATA-11: Support to weight-loss diet through prevention of mitochondrial dysfunction
DATA-1
Effect of GliSODin® (melon glisodin) on antioxidant enzyme activities in circulating blood <<University of Paris VI/National Hospital, Institut National de la Santé et de la Recherche Médicale (INSERM)>>
Summary
Groups of 6 to 8-weeks-old mice (body weight 25-30 g) were treated with forced feeding of 0.5, 1.0, and 5.0 mg GliSODin® (melon glisodin) daily for 28 days. Blood was sampled at 7-day intervals and tested for SOD activity in red blood cells.
Results
The groups treated at 1.0 and 5.0 mg/mouse showed significant increases in SOD activity. The differences from the level in the control group started to expand on the 14th day. CAT and GPx activities in red blood cells showed similar tendencies.
DATA-2
Antifibrotic activity of GliSODin® (melon glisodin) in liver fibrosis (liver cirrhosis model)
Summary
Chronic liver disease is caused by various agents such as hepatitis viruses, alcohol, infections, and parasites. Progression of chronic liver disease causes liver fibrosis. A remarkable study in rat models of liver cirrhosis demonstrated that GliSODin® (melon glisodin) was effective against fibrosis.
Study method
Rats with liver fibrosis induced by Schistosoma mansoni infection (liver cirrhosis model) were treated with oral GliSODin® (melon glisodin).
Results
The study demonstrated strong antifibrotic activity of GliSODin® (melon glisodin). This action was dose-dependent.
Oral administration of GliSODin® (melon glisodin) to rats with liver fibrosis induced by Schistosoma mansoni infection (liver cirrhosis model)
DATA-3
Effect of GliSODin® (melon glisodin) on intellectual disability
Summary
Radiation is a major factor that accelerates the generation of active oxygen species. The cytotoxicity of radiation is mediated by active oxygen species. In a study using a rat model of brain damage induced by radiation applied to the skull, the administration of GliSODin® (melon glisodin) to rats was shown to alleviate behavioral impairment in comparison with the control group. This result is considered to reflect the combined effect of the antioxidant activity and anti-stress property of GliSODin® (melon glisodin). It is therefore expected to reduce not only acute-phase symptoms but also late-onset complications. Further studies are awaited.
Results
GliSODin® (melon glisodin) alleviated intellectual disability induced by radiation. This suggests a possibility that the treatment may increase endogenous SOD and suppress radiation-mediated free radical generation.
Danger (electric shock) avoidance experiment using model rats with radiation-induced brain damage
DATA-4
Effect of GliSODin® (melon glisodin) on age-related decline of cognitive ability
Summary
This experiment comparing the learning ability of old and young rats suggested that GliSODin® (melon glisodin) improved the learning ability of old rats to the same level as that of young rats. The old rats in the control group that did not receive GliSODin® (melon glisodin) showed no improvement of learning ability.
Results
GliSODin® (melon glisodin) was found to improve the learning ability of old rats.
Experiment on the learning (cognitive) ability of young and old rats in water maze escape test
DATA-5
Protective effect against DNA damage caused by oxidative stress
Summary
Normal volunteers were treated with GliSODin® (melon glisodin) for 14 days and then exposed to oxidative stress in high-pressure oxygen environment. Blood was sampled before and after the exposure to oxidative stress, and DNA damage was evaluated using a comet assay. The elongation of tail moment (abscissa) in the graph represents the extent of damage.
While untreated subjects showed DNA damage due to oxidative stress, those treated with GliSODin® (melon glisodin) showed little DNA damage.
Results
This study confirmed the effectiveness in preventing DNA damage caused by exogenous oxidative stress. This report may open the way to the prevention and treatment of age-related conditions and other disorders.
DNA damage caused by oxidative stress
DATA-6
Effect on skin inflammation caused by ultraviolet radiation
Summary
Normal volunteers were treated with GliSODin® (melon glisodin) for 14 days and the minimal erythema dose (MED: the smallest amount of ultraviolet radiation that causes skin reddening) was measured before and after the treatment period. Ultraviolet erythema sensitivity was assessed based on the MED value.
GliSODin® (melon glisodin) treatment increased the MED. Treated subjects also showed quicker elimination of skin reddening than untreated subjects. In addition, treated subjects showed quicker increase in the number of capillary vessels in the erythematous sites, indicating better resilience.
Results
This clinical study provided objective numerical proof of the effectiveness in improving light-induced skin inflammation. The increase in the MED means the improvement of skin hypersensitivity to ultraviolet rays. This demonstrated the skin protection effect of GliSODin® (melon glisodin) against inflammatory skin problems.
Effect on skin inflammation caused by ultraviolet radiation
DATA-7
Effect of GliSODin® (melon glisodin) the changes in blood antioxidant enzyme and serum lactic acid levels caused by vigorous exercise
Summary
Normal volunteers were treated with GliSODin® (melon glisodin) for 4 weeks and high-intensity exercise tolerance tests were performed before and after treatment. Blood samples were collected before and after exercise and tested for the difference in lactic acid levels. Lactic acid generation due to exercise was decreased significantly by the use of GliSODin® (melon glisodin).
Results
GliSODin® (melon glisodin) can suppress lactic acid generation resulting form vigorous exercise.
Effect on the changes in blood antioxidant enzyme and blood lactic acid levels caused by vigorous exercise
DATA-8
Suppression of allergic reaction
Summary
Balb/c mice were sensitized to OVA (ovalbumin, used as the antigen) and the same mice were immunized with OVA again after 14 days. Thereafter, they were fed with GliSODin® (melon glisodin) for a week and then kept in an atmosphere with mist containing OVA. The changes in the numbers of immune cells and immune globulin levels in lung tissues and blood were compared between treatment and control groups. The mice treated with GliSODin® (melon glisodin) showed lower expression of various immune cells and IgE.
Results
GliSODin® (melon glisodin) was found to suppress excessive allergy reaction in tissues.
Suppression of allergic reaction
DATA-9
Effect on arthritis and synergy with glucosamine
Summary
Peritonitis mouse models were produced by intraperitoneal injection of LPS (a proinflammatory factor) to C57B16 mice. These mice were divided into groups, which were respectively fed with GliSODin® (melon glisodin), glucosamine, both of the above, and placebo for 28 days. After the feeding period, peritoneal macrophages were collected and tested for the ability of spontaneous production of cytokines and active oxygen species by immune cells in inflammation sites.
All active treatment groups showed significant decreases in TNF-α, NO, superoxide, and nitrogen peroxide. This effect was synergetic in the group treated with the combination of GliSODin® (melon glisodin) and glucosamine.
Results
GliSODin® (melon glisodin) suppressed the production of inflammatory cytokines. This result confirmed the beneficial effect on inflammation. The observed synergy in the combined use with glucosamine is a hopeful sign of usefulness in the treatment of arthritis.
Effect on arthritis and synergy with glucosamine
Prevention and improvement of atherosclerosis caused by the metabolic syndrome
DATA-10
Summary
Thirty-four subjects (23 men and 11 women) with risk factors of atherosclerosis, such as age, blood parameters, and genetic risks, were recruited. All subjects received dietary management and lifestyle guidance, and conditioned
during the 1-year preparation period.
The subjects were divided into 2 groups, which were treated with and without GliSODin® (melon glisodin) for 2 years.
Antioxidant indicators in blood and the thickening of carotid artery walls (IMT value) were measured.
Measured parameters
Blood SOD and Gpx: Indicators of the body’s antioxidant capacity.
Blood MDA (malondialdehyde): An indicator of lipid peroxidation in blood. Lipid peroxides produced by oxidative stress are a major causative factor of atherosclerosis.
Carotid artery intima-media thickness (IMT): This indicates the thickness of carotid artery walls. Thickening of arterial walls directly reflects the progression of atherosclerosis. Periodical examination of IMT therefore allows us to monitor the progression of atherosclerosis directly and accurately. In this study, subjects were recruited assuming that a thickness of 0.7 mm or more represented a risk.
Results
GliSODin® (melon glisodin) induced antioxidant enzymes (SOD and GPX) in the body and suppressed blood lipid peroxidation (MDA). Furthermore, reduction of arterial wall thickness (IMT) was confirmed as a result of the suppression of lipid peroxidation.
This strict large-scale study with long-term administration to humans proved the irrefutable efficacy of GliSODin® (melon glisodin). The use of this product is expected to prevent and improve atherosclerosis and other cardiovascular disorders caused by the metabolic syndrome.
DATA-11
Support to weight-loss diet through prevention of mitochondrial dysfunction
Summary
Mitochondria are organelles that are essential to energy metabolism, and are believed to be highly susceptible to damage from active oxygen species. In this study, mitochondria were collected from the skeletal muscles of mice that had been fed with food only or food + melon glisodin, and measured for active oxygen production. The mice fed with melon glisodin, in comparison with those without, showed lower active oxygen production form mitochondria.
Results
Melon glisodin is expected to prevent mitochondria damage and help improve energy metabolism.
