This study was conducted to investigate the effect of the antioxidative activity and develop the processed food of anthocyanin from purple sweet potatoes(PSP). Five-week-old male Sprague–Dawley rats were obtained from Daehan Biolink(Chungbuk, Korea). The animals were allowed to access to Purina rode...
This study was conducted to investigate the effect of the antioxidative activity and develop the processed food of anthocyanin from purple sweet potatoes(PSP). Five-week-old male Sprague–Dawley rats were obtained from Daehan Biolink(Chungbuk, Korea). The animals were allowed to access to Purina rodent chow(Seoul, Korea) and tap water, and they were maintained under specific pathogen-free conditions. They were acclimatized to the temperature (22 ± 2℃) and humidity(55 ± 5%) of controlled rooms with a 12-h light/dark cycle for at least 1 week prior to experimentation. The rats were divided into six groups of five animals. To study its ability to protect against t-BHP-induced hepatotoxicity, anthocyanin in saline was administered intragastrically at 10 ~ 200 mg/kg once a day for three consecutive days. Three hours after the final administration, animals were treated with t-BHP. Twenty-four hours after t-BHP administration, rats were anesthetized with CO2, blood was removed by cardiac puncture to determine serum ALT and AST activities, and animals were euthanized by cervical dislocation. After bleeding, livers were weighed and sliced; some slices were preserved in buffered formalin for histological examination. To induce hepatic fibrosis, DMN dissolved in sterile saline was administered as an intraperitoneal injection three times per week for 4 weeks. Anthocyanin (100 lL) was dissolved in saline and rats were intragastrically administered 50, 100, or 200 mg/kg of anthocyanin each day, six times per week for 4 weeks. Saline was administered to the control and the DMN-treated groups without drugs. The animals were sacrificed on 29th day. The results of this study were summarized as follows. Anthocyanin prevented death of t-BHP-induced cell death in HepG2 cells. Rupture of the plasma membrane during necrosis allows the release of such cytosolic proteins such as lactate dehydrogenase(LDH) into the culture medium. LDH release due to t-BHP treatment was also significantly reduced in cells pretreated with anthocyanin. To confirm that anthocyanin reduced t-BHP-induced oxidative stress in HepG2 cells, intracellular ROS production was assessed by monitoring H2DCFDA fluorescence. Rapid increases in intracellular oxidant levels were noted in cells after t-BHP treatment, but oxygen tension induced by t-BHP was concentration-dependently reduced by anthocyanin. As the oxidative stress of tissue generally involves the GSH system, we measured the level of GSH in HepG2 cells. Whereas the treatment of t-BHP significantly depleted GSH, pretreatment with anthocyanin significantly and concentration-dependently protected the GSH depletion induced by t-BHP. These results suggest that anthocyanin induces the expression of a gene(s) essential to ROS antagonism. To examine whether anthocyanin prevented caspases-like activities, cells were pretreated with anthocyanin for 12 h followed by 24-h t-BHP exposure ; DEVDase and LEHD-pNA activities were then measured. The level of t-BHP-induced DEVDase and LEHD-pNA activities were significantly reduced with anthocyanin treatment. The liver uses a variety of transaminases to synthesize and break down amino acids allowing for the inter-conversion of energy storage molecules. In this experiment, serum AST and ALT activities were assessed as biochemical markers of hepatic damage. The anthocyanin-treated group had significantly lower AST and ALT levels and significantly less DMN-induced lipid peroxidation in the liver than the DMN-induced liver injury group. The administration of DMN significantly depleted GSH, whereas treatment with anthocyanin significantly and dose-dependently protected the liver against this effect. In addition, there was lower GST activity in the liver homogenates of DMN-treated rats than in those of normal controls. The anthocyanin-treated group had significantly higher GST activity. Also, the hepatic GSH levels and GST activity were increased by treatment with anthocyanin alone (200 mg/kg). These results demonstrate that the protection afforded by anthocyanin against DMN-induced liver injury may be related to its ability to increase cellular GSH content and GST activity. To identify whether anthocyanin exerts its effects by regulating Nrf2 activity, we investigated Nrf2 mRNA and protein expression by semi-quantitative RT-PCR and Western blot analysis, respectively. The mRNA levels of Nrf2 were lower following DMN administration. However, oral administration of anthocyanin (100 and 200 mg/kg) reverses the suppression of Nrf2 mRNA levels by DMN treatment. In addition, the anthocyanin-treated group exhibited increased nuclear translocation of Nrf2 than the DMN-induced liver injury group. The mRNA levels of HO-1 were lower in the DMN-induced liver injury group than the control group, but significantly higher in the anthocyanin-treated group than the injury group. In addition, the mRNA levels of both NQO1 and GSTα in the anthocyanin-treated group were significantly higher than those of the DMN-induced liver injury group. To confirm these results, we examined the protein levels of HO-1, NQO1, and GSTα following anthocyanin treatment in the injury group. Anthocyanin induced the expression of various Nrf2-stimulated proteins and significantly augmented the expression of HO-1, NQO1, and GSTα compared to the injury group. To evaluate whether the preventive effects of anthocyanin on DMN-induced liver injury are related to its ability to regulate the activity of NF-κB, we assessed the nuclear translocation of NF-κB following anthocyanin treatment. Anthocyanin treatment attenuated NF-κB nuclear translocation in the injury group and inhibited the degradation of IκBα in a dose dependent manner. The pH and acidity during the rice wine fermentation using PSP and the residue of PSP extracts decreased significantly to 4.51 and 0.3% in early phase and showed 3.85 and 4.2% after 15 days, respectively. The sugar content was immediately 4.8 b
This study was conducted to investigate the effect of the antioxidative activity and develop the processed food of anthocyanin from purple sweet potatoes(PSP). Five-week-old male Sprague–Dawley rats were obtained from Daehan Biolink(Chungbuk, Korea). The animals were allowed to access to Purina rodent chow(Seoul, Korea) and tap water, and they were maintained under specific pathogen-free conditions. They were acclimatized to the temperature (22 ± 2℃) and humidity(55 ± 5%) of controlled rooms with a 12-h light/dark cycle for at least 1 week prior to experimentation. The rats were divided into six groups of five animals. To study its ability to protect against t-BHP-induced hepatotoxicity, anthocyanin in saline was administered intragastrically at 10 ~ 200 mg/kg once a day for three consecutive days. Three hours after the final administration, animals were treated with t-BHP. Twenty-four hours after t-BHP administration, rats were anesthetized with CO2, blood was removed by cardiac puncture to determine serum ALT and AST activities, and animals were euthanized by cervical dislocation. After bleeding, livers were weighed and sliced; some slices were preserved in buffered formalin for histological examination. To induce hepatic fibrosis, DMN dissolved in sterile saline was administered as an intraperitoneal injection three times per week for 4 weeks. Anthocyanin (100 lL) was dissolved in saline and rats were intragastrically administered 50, 100, or 200 mg/kg of anthocyanin each day, six times per week for 4 weeks. Saline was administered to the control and the DMN-treated groups without drugs. The animals were sacrificed on 29th day. The results of this study were summarized as follows. Anthocyanin prevented death of t-BHP-induced cell death in HepG2 cells. Rupture of the plasma membrane during necrosis allows the release of such cytosolic proteins such as lactate dehydrogenase(LDH) into the culture medium. LDH release due to t-BHP treatment was also significantly reduced in cells pretreated with anthocyanin. To confirm that anthocyanin reduced t-BHP-induced oxidative stress in HepG2 cells, intracellular ROS production was assessed by monitoring H2DCFDA fluorescence. Rapid increases in intracellular oxidant levels were noted in cells after t-BHP treatment, but oxygen tension induced by t-BHP was concentration-dependently reduced by anthocyanin. As the oxidative stress of tissue generally involves the GSH system, we measured the level of GSH in HepG2 cells. Whereas the treatment of t-BHP significantly depleted GSH, pretreatment with anthocyanin significantly and concentration-dependently protected the GSH depletion induced by t-BHP. These results suggest that anthocyanin induces the expression of a gene(s) essential to ROS antagonism. To examine whether anthocyanin prevented caspases-like activities, cells were pretreated with anthocyanin for 12 h followed by 24-h t-BHP exposure ; DEVDase and LEHD-pNA activities were then measured. The level of t-BHP-induced DEVDase and LEHD-pNA activities were significantly reduced with anthocyanin treatment. The liver uses a variety of transaminases to synthesize and break down amino acids allowing for the inter-conversion of energy storage molecules. In this experiment, serum AST and ALT activities were assessed as biochemical markers of hepatic damage. The anthocyanin-treated group had significantly lower AST and ALT levels and significantly less DMN-induced lipid peroxidation in the liver than the DMN-induced liver injury group. The administration of DMN significantly depleted GSH, whereas treatment with anthocyanin significantly and dose-dependently protected the liver against this effect. In addition, there was lower GST activity in the liver homogenates of DMN-treated rats than in those of normal controls. The anthocyanin-treated group had significantly higher GST activity. Also, the hepatic GSH levels and GST activity were increased by treatment with anthocyanin alone (200 mg/kg). These results demonstrate that the protection afforded by anthocyanin against DMN-induced liver injury may be related to its ability to increase cellular GSH content and GST activity. To identify whether anthocyanin exerts its effects by regulating Nrf2 activity, we investigated Nrf2 mRNA and protein expression by semi-quantitative RT-PCR and Western blot analysis, respectively. The mRNA levels of Nrf2 were lower following DMN administration. However, oral administration of anthocyanin (100 and 200 mg/kg) reverses the suppression of Nrf2 mRNA levels by DMN treatment. In addition, the anthocyanin-treated group exhibited increased nuclear translocation of Nrf2 than the DMN-induced liver injury group. The mRNA levels of HO-1 were lower in the DMN-induced liver injury group than the control group, but significantly higher in the anthocyanin-treated group than the injury group. In addition, the mRNA levels of both NQO1 and GSTα in the anthocyanin-treated group were significantly higher than those of the DMN-induced liver injury group. To confirm these results, we examined the protein levels of HO-1, NQO1, and GSTα following anthocyanin treatment in the injury group. Anthocyanin induced the expression of various Nrf2-stimulated proteins and significantly augmented the expression of HO-1, NQO1, and GSTα compared to the injury group. To evaluate whether the preventive effects of anthocyanin on DMN-induced liver injury are related to its ability to regulate the activity of NF-κB, we assessed the nuclear translocation of NF-κB following anthocyanin treatment. Anthocyanin treatment attenuated NF-κB nuclear translocation in the injury group and inhibited the degradation of IκBα in a dose dependent manner. The pH and acidity during the rice wine fermentation using PSP and the residue of PSP extracts decreased significantly to 4.51 and 0.3% in early phase and showed 3.85 and 4.2% after 15 days, respectively. The sugar content was immediately 4.8 b
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