Lee, Eun Suk;Jee, Yun-jeong;Lee, Ji Yeon;Choi, Su Ji;Lee, Seung Eun;Kim, Hyung Don;Choi, Jehun;Kang, Min Hye;Kim, Dong Hwi;Jang, Gwi Yeong
The Korean Journal of Food And Nutrition
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v.33
no.6
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pp.645-654
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2020
Angelica gigas Nakai (A. gigas) easily changes its color during storage, and appropriate thermal treatment can improve storage stability through inactivation of enzymes such as polyphenol oxidase. Therefore, this study was performed to determine quality characteristics of dried A. gigas in response to high-temperature-short-time (HTST) treatment during storage. Dried A. gigas were treated at 120-180℃ for 10 min, the samples were stored at 4℃ and 50℃ for 10 weeks, and used for the analysis of qualities. Concerning the color values, the sample treated at 120℃ was similar to the control, and the color change was large when treated above 180℃. However, color difference (ΔE⁎ab) was lower in treated samples than in control. Browning index was similar for all the samples except for the sample treated at 180℃. Functional qualities (phenolics content, antioxidant activities, and level of major components) showed a slight difference according to storage periods in all samples without control, and nodakenin content was observed in control. The results of this study showed that HTST treatment improved storage stability such as stability of colors and browning index in dried A. gigas during storage, and the appropriate treatment temperature was 120℃ in terms of stability in color and browning index.
Type 2 diabetes is a serious chronic metabolic disease, and the goal of diabetes treatment is to keep blood glucose at a normal level and prevent complications from diabetes. Hyperglycemia is a key pathologic feature of type 2 diabetes that mainly results from insulin resistance and pancreatic β-cell dysfunction. Chronic exposure of β-cells to elevated glucose concentrations induces glucotoxicity. In this study, we examined whether an 80% ethanol extract of Oxya chinensis sinuosa Mishchenko (OEE) protected INS-1 pancreatic β-cells against glucotoxicity-induced apoptosis and oxidative stress. Pretreatment with a high concentration of glucose (high glucose = 30 mM) induced glucotoxicity and apoptosis of INS-1 pancreatic β cells. Treatment with OEE significantly increased cell viability. Treatment with 0.01-0.20 mg/ml OEE dose dependently decreased intracellular reactive oxygen species, lipid peroxidation, and nitric oxide levels and increased insulin secretion in high glucose-pretreated INS-1 β cells. OEE also significantly increased the activities of antioxidant enzymes in response to high-glucose-induced oxidative stress. Moreover, OEE treatment significantly reduced the expressions of pro-apoptotic proteins, including Bax, cytochrome C, caspase-3, and caspase-9, and increased anti-apoptotic Bcl-2 expression. Apoptotic cells were identified using Annexin-V/propidium iodide staining, which revealed that treatment with OEE significantly reduced high-glucose-induced apoptosis. These findings implicate OEE as a valuable functional food in protecting pancreatic β-cells against glucotoxicity-induced apoptosis and oxidative stress.
The anti-oxidant enzyme heme oxygenase-1 (HO-1) is known to exert anti-inflammatory effects. From a library of pyrazolo[3,4-d]pyrimidines, we identified a novel compound KKC080096 that upregulated HO-1 at the mRNA and protein levels in microglial BV-2 cells. KKC080096 exhibited anti-inflammatory effects via suppressing nitric oxide, interleukin1β (IL-1β), and iNOS production in lipopolysaccharide (LPS)-challenged cells. It inhibited the phosphorylation of IKK and MAP kinases (p38, JNK, ERK), which trigger inflammatory signaling, and whose activities are inhibited by HO-1. Further, KKC080096 upregulated anti-inflammatory marker (Arg1, YM1, CD206, IL-10, transforming growth factor-β [TGF-β]) expression. In 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridinetreated mice, KKC080096 lowered microglial activation, protected the nigral dopaminergic neurons, and nigral damage-associated motor deficits. Next, we elucidated the mechanisms by which KKC080096 upregulated HO-1. KKC080096 induced the phosphorylation of AMPK and its known upstream kinases LKB1 and CaMKKbeta, and pharmacological inhibition of AMPK activity reduced the effects of KKC080096 on HO-1 expression and LPS-induced NO generation, suggesting that KKC080096-induced HO-1 upregulation involves LKB1/AMPK and CaMKKbeta/AMPK pathway activation. Further, KKC080096 caused an increase in cellular Nrf2 level, bound to Keap1 (Nrf2 inhibitor protein) with high affinity, and blocked Keap1-Nrf2 interaction. This Nrf2 activation resulted in concurrent induction of HO-1 and other Nrf2-targeted antioxidant enzymes in BV-2 and in dopaminergic CATH.a cells. These results indicate that KKC080096 is a potential therapeutic for oxidative stress-and inflammation-related neurodegenerative disorders such as Parkinson's disease.
Objective: This work was conducted to investigate the effects of oxidative stress on meat quality, mitochondrial function, calcium metabolism and ferroptosis of broilers. Methods: In this study, a total of 144 one-day-old male Ross 308 chicks were divided into 3 groups (control group, saline group, and hydrogen peroxide [H2O2] group) with 6 replicates of 8 broilers each. The study lasted for 42 d. The broilers in the saline and H2O2 groups were intraperitoneally injected with 0.75% saline and 10.0% H2O2 on the 16th and 37th day of the experimental period respectively, the injection volumes were 1.0 mL/kg of broiler body weight. On the 42nd day of the experimental period, two chicks were randomly selected from each cage, a total of thirty-six chicks were stunned by electric shock and slaughtered to collect breast muscle samples. Results: The H2O2 exposure reduced pH value, increased drip loss and shear force of breast meat (p<0.05), impaired the ultrastructure and function of mitochondria. The H2O2 exposure damaged the antioxidant system in mitochondria, excessive reactive oxygen species carbonylation modified calcium channels on mitochondria, which impaired the activities of key enzymes on calcium channel, resulted in the increased calcium concentration in cytoplasm and mitochondria (p<0.05). In addition, the H2O2 exposure increased the iron content and lipid peroxidation (p<0.05), which induced ferroptosis. Conclusion: Oxidative stress could impair meat quality by causing mitochondrial dysfunction, resulting in calcium metabolism disorder and ferroptosis.
Mangiferin is a kind of natural xanthone glycosides and is known to have various pharmacological activities. However, since the beneficial efficacy of this compound has not been reported in retinal pigment epithelial (RPE) cells, this study aimed to evaluate whether mangiferin could protect human RPE ARPE-19 cells from oxidative injury mimicked by hydrogen peroxide (H2O2). The results showed that mangiferin attenuated H2O2-induced cell viability reduction and DNA damage, while inhibiting reactive oxygen species (ROS) production and preserving diminished glutathione (GSH). Mangiferin also antagonized H2O2-induced inhibition of the expression and activity of antioxidant enzymes such as manganese superoxide dismutase and GSH peroxidase, which was associated with inhibition of mitochondrial ROS production. In addition, mangiferin protected ARPE-19 cells from H2O2-induced apoptosis by increasing the Bcl-2/Bax ratio, decreasing caspase-3 activation, and blocking poly(ADP-ribose) polymerase cleavage. Moreover, mangiferin suppressed the release of cytochrome c into the cytosol, which was achieved by interfering with mitochondrial membrane disruption. Furthermore, mangiferin increased the expression and activity of heme oxygenase-1 (HO-1) and nuclear factor-erythroid-2 related factor 2 (Nrf2). However, the inhibition of ROS production, cytoprotective and anti-apoptotic effects of mangiferin were significantly attenuated by the HO-1 inhibitor, indicating that mangiferin promoted Nrf2-mediated HO-1 activity to prevent ARPE-19 cells from oxidative injury. The results of this study suggest that mangiferin, as an Nrf2 activator, has potent ROS scavenging activity and may have the potential to protect oxidative stress-mediated ocular diseases.
Su Jeong Kim;Hwang Bae Sohn;A Hyun Park;Jong Nam Lee;Su Hyoung Park;Jung Hwan Nam;Do Yeon Kim;Dong Chil Chang;Yul Ho Kim
Korean Journal of Plant Resources
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v.36
no.5
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pp.435-445
/
2023
The aim of this study was to explore the effects of vinegar extract from seed of common buckwheat (Fagopyrum esculentum Moench) and seed of tartary buckwheat (F. tataricum Gaertner) on acute ethanol-induced hangover in Sprague-Dawley rats. Vinegar extract from buckwheat is rich choline, quercetin and its glycoside, rutin known as flavonoid antioxidants. The test extract containing buckwheat was proven to alleviate hangovers through a significant reduction in the concentration of alcohol and acetaldehyde in the context of an alcohol-induced hangover model. Hepatic alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH) activities were significantly higher in buckwheat vinegar-treated rats than in ethanol-treated rats. Moreover, tartary buckwheat vinegar upregulated antioxidant enzyme such as superoxide dismutase and Catalase activities in liver tissues. These results suggest that buckwheat vinegar extract could alleviate ethanol-induced hangover symptoms by elevating activities related to hepatic ethanol-metabolizing enzymes against ethanol induced metabolites, and in particular, tartary buckwheat should be further developed to be a novel anti-hangover material.
Kim, Sun-Hwa;Hwang, In-Wook;Chung, Shin-Kyo;Seo, Young-Jin;Kim, Jong-Soo;Jeong, Yong-Jin;Kim, Mi-Yeon
Food Science and Preservation
/
v.22
no.5
/
pp.699-707
/
2015
To improve the utilization of the domestic plant Salvia miltiorrhiza Bunge (Danshen), this study investigated changes in the physicochemical qualities of Danshen extracts obtained from low-temperature extraction using the enzymes amylase, cellulase, pectinase, and protease. Changes in the yield, pH, sugar content, and chromaticity were investigated. The changes were found to be highest in the amylase-treated extract with the following values: yield, 58.3%; pH, 6.04; sugar content, $5.97^{\circ}Brix$. With regard to antioxidant properties, Danshen extracts treated with amylase showed the highest DPPH and ABTS scavenging activities of 84.25% and 74.11% at 55 ppm. The total phenolic compound content was highest in the group subjected to enzyme treatment at $60^{\circ}C$. The salvianolic acid B level of the Danshen extract was the highest in the amylase-treated group, with a value of 3,002.6 mg/100 g. Cryptotanshinone level was the highest in the amylase- and protease-treated group with a value of 3.8 mg/100 g. Tanshinone I was the highest in the protease-treated group, with a value of 14.2 mg/100 g. The results showed that the indicator components of Danshen were detected as stable in the extracts after using amylase for low-temperature extraction; therefore, it would be possible to use Danshen industrially as a functional ingredient through mass production. Furthermore, the enzyme-treatment extraction could be utilized for a variety of natural products.
The present study examined the effect of the dietary administration of a halophilic bacterium Bacillus sp. Mk22 on the growth improvement of black tiger shrimp, Penaeus monodon, and reduced shrimp infection by Vibrio parahaemolyticus and white spot syndrome virus (WSSV). The shrimp were fed 45 days using three experimental diets: no addition (control), commercial probiotic, and Bacillus sp. Mk22. The shrimp treated with the halophilic bacterium Mk22 showed a significant improvement of growth (7.1 ± 0.21 g), survival (94.3 ± 0.58%), weight gain (178 ± 4.93 g), and reduced feed conversion rate (0.8 ± 0.03 g) compared with the shrimp in the other groups. The shrimp treated with Bacillus sp. Mk22 also showed a lower Vibrio count (0.02 ± 0.01 × 102 CFU/ml) in the shrimp culture water compared with the other groups. The shrimp in the three groups were challenged with either Vibrio or WSSV. For the Vibrio infection, no mortality was observed from water infection or oral feeding infection in the commercial probiotic group and Mk 22 group. For the WSSV infection, a 68% survival rate from water infection and 20% survival rate from oral feeding infection was observed on day 45 in the Mk22 group, while 100% mortalities were recorded at a much earlier time in both the control and commercial probiotic groups. The antioxidant enzyme activities, indicators of oxidative stress, such as catalase and superoxide dismutase, significantly decreased in both the Vibrio and WSSV-infected Mk22 groups compared with the other groups, indicating that Bacillus sp. Mk22 was effective in reducing oxidative stress, possibly due to the reduced infection.
The phenolic contents which were extracted with water and 70% ethanol from O. undulatifolius were 7.7, 10.1 mg/g, respectively. The 1,1-diphenyl-2-picrylhydrazyl free radical scavenging activity of water and ethanol extracts were 78, 82% at $50{\mu}g/mL$ phenolics, respectively. The 2,2'-Azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) radical cation decolorization activity were 92, 76% at $100{\mu}g/mL$ phenolics. Antioxidant protection factor in water and ethanol extracts at $200{\mu}g/mL$ phenolics were 1.51 and 2.08 PF, respectively. Thiobarbituric acid reactive substance were 84% in water extracts and 99% in ethanol extracts at $50{\mu}g/mL$ phenolics, respectively. The inhibition activity on ${\alpha}-Glucosidase$ was 44% in ethanol extracts at $200{\mu}g/mL$ phenolics. The inhibition activity on ${\alpha}-amylase$ was 37-88% in water extracts at $50-200{\mu}g/mL$ phenolics. The tyrosinase inhibition activity as whitening effect were 82% in ethanol extracts. The elastase inhibition activity were 4, 61% in water and ethanol extracts, respectively. The collagenase inhibition activity of antiwrinkle effect showed an excellent wrinkle improvement effect as 39% in water extracts and 67% in ethanol extracts at $200{\mu}g/mL$ phenolics, respectively. The hyaluronidase inhibition activity as anti-inflammation effect of ethanol extracts was confirmed to 46% of inhibition at $200{\mu}g/mL$ phenolic. The astringent effect of water and ethanol extracts was confirmed to 13, 32% of effect at $200{\mu}g/mL$ phenolic, respectively.
Kim Tae-Hyung;Kim Kyung-Ju;Choe Mi-Kyung;Yeo In-Kyu
Journal of Aquaculture
/
v.19
no.2
/
pp.77-83
/
2006
This study was conducted to investigate changes of hemolymph count, antioxidant enzyme activities (catalase: CAT and superoxide dismutase: SOD) and Heat Shock Protein 70 (HSP70) mRNA in hemolymph, hepatopancreas and gill of abalone (Haliotis sieboldii) exposed to various water temperatures. Abalones were exposed to 10, 15, 20, 25 or $30^{\circ}C$ for 0, 6, 12, 24 or 48 hours. Survival rate of abalone was 100% at 10, 15, 20 and $25^{\circ}C$, but 0% at $30^{\circ}C$. Hemolymph counts increased at lower water temperatures (10 and $15^{\circ}C$) and decreased at $30^{\circ}C$. SOD activity decreased immediately after exposure to lower or higher water temperatures compared to the control ($20^{\circ}C$) with an exception at $30^{\circ}C$ where the activity increased. At lower temperatures, SOD activity rose high after 24 hours, but decreased again at 48 hours. At $25^{\circ}C$, it decreased compared to the control. CAT activity decreased immediately after exposure to 10 or $25^{\circ}C$ compared to the control, and then was recovered to the initial level after increment. At $15^{\circ}C$, CAT activity was high after 6 hours, and then was recovered to the initial level after increment. At $30^{\circ}C$, the activity decreased throughout the experiment. The HSP70 mRNA expression in gill increased at lower temperatures compared to the control ($20^{\circ}C$) and $25^{\circ}C$. In this study, rapid change of wale, temperature caused stress response in abalone which had been raised at $20^{\circ}C$. At molecular level, HSP70 was expressed rapidly, but antioxidant enzymes like SOD and CAT were expressed later than HSP70. At 15 and $25^{\circ}C$ of water temperatures, the HSP70, SOD and CAT expression were stable with time. However, at $30^{\circ}C$, all abalone died possibly because they could not develop resistance to high temperature.
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