• Applied Biological Chemistry
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• v.51 no.3
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• pp.200-206
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• 2008

We investigated the effect of rice embryo and embryo jelly with black rice bran pigment on lipid metabolism and antioxidant activity. Thirty 4-week-old male Sprague-Dawley rats were fed high cholesterol diets supplemented with 15% rice embryo and 25% embryo jelly added black rice bran pigment, respectively, for 6 weeks. Plasma and hepatic lipid profile, lipid peroxidation, and the activity of antioxidant scavenger enzymes in liver were examined. Supplementation with rice embryo and embryo jelly had no effect on food intakes in high cholesterol-fed rats. The plasma triglyceride concentration was not significantly different among the groups. Supplementation with rice embryo and embryo jelly resulted in lower plasma and hepatic total cholesterol (TC) concentration and high-density lipoprotein-cholesterol (HDL-C)/TC ratio and atherogenic index compared to the control group, while the plasma HDL-C concentration tended to elevated. Rice embryo and embryo jelly tended to lower plasma and hepatic levels of thiobarbituric acid reactive substances than the control group. Moreover, hepatic antioxidant enzyme activities, including superoxide dismutase and glutathione peroxidase, were significantly higher in the rice embryo and embryo jelly groups. In conclusion, rice embryo and embryo jelly was very effective in improving the lipid metabolism and reducing oxidative stress by up-regulating the hepatic antioxidant enzymes in high cholesterol-fed rats.

• The Korean Journal of Pesticide Science
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• v.2 no.2
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• pp.75-82
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• 1998

This study was conducted to find out the biochemical or metabolic resistance mechanism of brown planthopper (BPH) to carbofuran. Differences between resistant ($LD_{50};\;20.3{\mu}g/g$) and susceptible strains($LD_{50};\;0.3{\mu}g/g$) were shown. The amounts of carbofuran metabolite, benzofuranol, and the origin, not developed by Thin Layer Chromatography, were much more in the susceptible strain. But the mother compound, carbofuran, was much more in the resistant strain. The tendencies of metabolism one and three hours after treatment were similar in both strains except for the amounts of metabolites described above. From the study, it is supposed that hydrolytic enzyme, esterase, changes its role from cleaving the esteric bond of carbofuran to making conjugates with carbofuran. This seems to be the main resistance mechanism of BPH to carbofuran. Oxidase and transferase may play little or no role in resistance mechanism. Oxidative and transferring enzymes gave no effects on the metabolism of carbofuran in the resistant strain compared with the susceptible strain.

• Korean Journal of Food Science and Technology
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• v.41 no.2
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• pp.191-195
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• 2009

We assessed the effect of surimi gel, which is prepared from the king oyster mushroom (pleurotus eryngii) and cuttlefish meat paste (KCP) on lipid metabolism and antioxidant activity in high-cholesterol-fed rats. Three groups of 3-week-old male Sprague-Dawley rats were fed on a diet containing 1 g cholesterol/kg for 6 weeks. We administered only a high-cholesterol diet to the control group, one group was fed on surimi gel containing cuttlefish paste and king oyster mushrooms, and another group was fed with general boiled fish meat paste (GFP), which is commonly sold in marketplaces. Plasma and hepatic lipid profiles were measured, and the antioxidant status of the liver was assessed. The plasma triglyceride concentration did not differ significantly among the groups. Supplementation with KCP resulted in lower plasma and hepatic cholesterol concentrations and atherogenic index as compared to the control group and GFP, whereas the plasma high-density lipoprotein-cholesterol concentration was elevated. Moreover, the KCP-supplemented animals evidenced greater bile acid excretion. The KCP groups evidenced significantly lower plasma and hepatic levels of thiobarbituric acidreactive substances as compared to the control group. Besides, hepatic antioxidant enzyme activities, including catalase and superoxide dismutase, were significantly higher in the KCP group. In conclusion, KCP was quite effective in improving the lipid metabolism and reducing oxidative stress by upregulating the hepatic antioxidant enzymes in high-cholesterol-fed rats.

• Animal Bioscience
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• v.34 no.6
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• pp.975-984
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• 2021

Objective: Inbreeding depression of reproduction is a major concern in the conservation of native chicken genetic resources. Here, based on the successful development of strongly inbred (Sinb) and weakly inbred (Winb) Langshan chickens, we aimed to evaluate inbreeding effects on reproductive traits and identify candidate genes involved in inbreeding depression of reproduction in Langshan chickens. Methods: A two-sample t-test was performed to estimate the differences in phenotypic values of reproductive traits between Sinb and Winb chicken groups. Three healthy chickens with reproductive trait values around the group mean values were selected from each of the groups. Differences in ovarian and hypothalamus transcriptomes between the two groups of chickens were analyzed by RNA sequencing (RNA-Seq). Results: The Sinb chicken group showed an obvious inbreeding depression in reproduction, especially for traits of age at the first egg and egg number at 300 days (p<0.01). Furthermore, 68 and 618 differentially expressed genes (DEGs) were obtained in the hypothalamus and ovary between the two chicken groups, respectively. In the hypothalamus, DEGs were mainly enriched in the pathways related to vitamin metabolism, signal transduction and development of the reproductive system, such as the riboflavin metabolism, Wnt signaling pathway, extracellular matrix-receptor interaction and focal adhesion pathways, including stimulated by retinoic acid 6, serpin family F member 1, secreted frizzled related protein 2, Wnt family member 6, and frizzled class receptor 4 genes. In the ovary, DEGs were significantly enriched in pathways associated with basic metabolism, including amino acid metabolism, oxidative phosphorylation, and glycosaminoglycan degradation. A series of key DEGs involved in folate biosynthesis (gamma-glutamyl hydrolase, guanosine triphosphate cyclohydrolase 1), oocyte meiosis and ovarian function (cytoplasmic polyadenylation element binding protein 1, structural maintenance of chromosomes 1B, and speedy/RINGO cell cycle regulator family member A), spermatogenesis and male fertility (prostaglandin D2 synthase 21 kDa), Mov10 RISC complex RNA helicase like 1, and deuterosome assembly protein 1) were identified, and these may play important roles in inbreeding depression in reproduction. Conclusion: The results improve our understanding of the regulatory mechanisms underlying inbreeding depression in chicken reproduction and provide a theoretical basis for the conservation of species resources.

• Journal of Ginseng Research
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• v.47 no.3
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• pp.376-384
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• 2023

Background: Hepatic lipid disorder impaired mitochondrial homeostasis and intracellular redox balance, triggering development of non-alcohol fatty liver disease (NAFLD), while effective therapeutic approach remains inadequate. Ginsenosides Rc has been reported to maintain glucose balance in adipose tissue, while its role in regulating lipid metabolism remain vacant. Thus, we investigated the function and mechanism of ginsenosides Rc in defending high fat diet (HFD)-induced NAFLD. Methods: Mice primary hepatocytes (MPHs) challenged with oleic acid & palmitic acid were used to test the effects of ginsenosides Rc on intracellular lipid metabolism. RNAseq and molecular docking study were performed to explore potential targets of ginsenosides Rc in defending lipid deposition. Wild type and liver specific sirtuin 6 (SIRT6, 50721) deficient mice on HFD for 12 weeks were subjected to different dose of ginsenosides Rc to determine the function and detailed mechanism in vivo. Results: We identified ginsenosides Rc as a novel SIRT6 activator via increasing its expression and deacetylase activity. Ginsenosides Rc defends OA&PA-induced lipid deposition in MPHs and protects mice against HFD-induced metabolic disorder in dosage dependent manner. Ginsenosides Rc (20mg/kg) injection improved glucose intolerance, insulin resistance, oxidative stress and inflammation response in HFD mice. Ginsenosides Rc treatment accelerates peroxisome proliferator activated receptor alpha (PPAR-α, 19013)-mediated fatty acid oxidation in vivo and in vitro. Hepatic specific SIRT6 deletion abolished ginsenoside Rc-derived protective effects against HFD-induced NAFLD. Conclusion: Ginsenosides Rc protects mice against HFD-induced hepatosteatosis by improving PPAR-α-mediated fatty acid oxidation and antioxidant capacity in a SIRT6 dependent manner, and providing a promising strategy for NAFLD.

• Nutrition Research and Practice
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• v.17 no.4
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• pp.682-697
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• 2023

BACKGROUND/OBJECTIVES: Tibetan tea is a kind of dark tea, due to the inherent complexity of natural products, the chemical composition and beneficial effects of Tibetan tea are not fully understood. The objective of this study was to unravel the composition of Tibetan tea using knowledge-guided multilayer network (KGMN) techniques and explore its potential antioxidant and hypolipidemic mechanisms in mice. MATERIALS/METHODS: The C57BL/6J mice were continuously gavaged with Tibetan tea extract (T group), green tea extract (G group) and ddH2O (H group) for 15 days. The activity of total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) in mice was detected. Transcriptome sequencing technology was used to investigate the molecular mechanisms underlying the antioxidant and lipid-lowering effects of Tibetan tea in mice. Furthermore, the expression levels of liver antioxidant and lipid metabolism related genes in various groups were detected by the real-time quantitative polymerase chain reaction (qPCR) method. RESULTS: The results showed that a total of 42 flavonoids are provisionally annotated in Tibetan tea using KGMN strategies. Tibetan tea significantly reduced body weight gain and increased T-AOC and SOD activities in mice compared with the H group. Based on the results of transcriptome and qPCR, it was confirmed that Tibetan tea could play a key role in antioxidant and lipid lowering by regulating oxidative stress and lipid metabolism related pathways such as insulin resistance, P53 signaling pathway, insulin signaling pathway, fatty acid elongation and fatty acid metabolism. CONCLUSIONS: This study was the first to use computational tools to deeply explore the composition of Tibetan tea and revealed its potential antioxidant and hypolipidemic mechanisms, and it provides new insights into the composition and bioactivity of Tibetan tea.

• Journal of Nutrition and Health
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• v.35 no.3
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• pp.296-302
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• 2002

This study was designed to investigate the effects of a butanol extract of pine needles (Pinus densiflora Sieb et Zucc) on lipid metabolism and oxidative stress in rats. Twenty-eight male Sprague-Dawley (SD) rats were divided into four groups over a 45 days study period: the control group on a basic diet, and three experimental groups on three different dietary levels of the butanol fraction, specifically 25 mg (BuOH-25), 50 mg (BuOH-50), and 100 mg (BuOH-100) butanol fraction/kg body weight/day, thereby 0.025%, 0.05%, 0.1% of butanol extract of pine needles was added to basic diet respectively. At the end of the experimental period, body weights and food intakes were food intakes were not different among the four groups. Total and LDL-cholesterol levels were markedly decreased in the BuOH-25, BuOH-50, and BuOH-100 groups, respectively, as follows: 12.8%, 19.1% and 21.6% reductions in total cholesterol; and 10.2%, 15.6% and 23.7% reductions in LDL-cholesterol. However, HDL-cholesterol levels were significantly increased (by approximately 20%) in the serum of the BuOH-100 group only, compared with the control and other experimental groups. Atherogenic indices were also markedly decreased in the three experimental groups, by 24.8%, 30.4% and 36.2%, for each of the BuOH-25, BuOH-50, and BuOH-100 groups, respectively, compared with the control group. The levels of the hydroxyl radical (·OH) and of lipid peroxide (LPO) in the serum of the three experimental groups were significantly reduced, by 9.8%, 19.7% and 21.2%; and by 13.3%, 13.3% and 16.7%, for the BuOH-25, BuOH-50, and BuOH-100 groups, respectively Significant increases in serum superoxide dismutase (SOD) were observed in the BuOH-50 and BuOH-100 groups; specifically, 12.1% in the BuOH-50 group and 23.3% in the BuOH-100 group, compared with the control group. Significant increases in catalase (CAT) avtivities, of 24.7% in the BuOH-50 group and 29.2% in the BuOH-100 group, were also observed, compared to the control group. These results suggest that a butanol extract of pine needles could inhibit chronic degenerative disease through improving lipid metabolism, and could also effectively modulate the aging process attenuating oxidative stress.

• Journal of Life Science
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• v.18 no.11
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• pp.1485-1492
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• 2008

Prostaglandin $A_2$ ($PGA_2$), one of cyclopentenone PGs, induced both apoptosis and heme oxygenase (HO)-1 expression in U2OS cells. $PGA_2$-induced apoptosis was not perturbed by either over-expression or knock-down of HO-1, whereas $H_2O_2$-induced cell death was inversely modulated by the expression level of HO-1. In addition, N-acetyl-L-cysteine (NAC), a thiol antioxidant, blocked both apoptosis and HO-1 expression induced by $PGA_2$. But, non-thiol antioxidants like butylated hydorxyanisole (BHA) and ascorbic acid did not block either apoptosis or HO-1-induction. Taken together, these results suggest that $PGA_2$ induces both apoptosis and HO-1 expression, which are critically related to the thiol- reactivity of $PGA_2$, but not oxidative stress, and HO-1 expression may be independent or functionally located downstream of apoptosis by $PGA_2$ without contribution to apoptosis progression.

• Journal of Life Science
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• v.31 no.5
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• pp.464-474
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• 2021

Inflammation induced by metabolic syndromes, cancers, injuries, and sepsis can alter cellular metabolism by reducing mitochondrial function via oxidative stress, thereby resulting in neuropathy and muscle atrophy. In this study, we investigated whether butyrate, a short chain fatty acid produced by gut microbiota, could prevent mitochondrial dysfunction and muscle atrophy induced by lipopolysaccharide (LPS) in the C2C12 cell line. LPS-activated MAPK signaling pathways increased the levels of the mitochondrial fission signal, p-DRP1 (Ser616), and the muscle atrophy marker, atrogin 1. Interestingly, butyrate significantly inhibited the phosphorylation of JNK and p38 and reduced the atrogin 1 level in LPS-treated C2C12 cells while increasing the phosphorylation of DRP1 (Ser637) and levels of mitofusin2, which are both mitochondrial fusion markers. Next, we investigated the effect of MAPK inhibitors, finding that butyrate had the same effect as JNK inhibition in C2C12 cells. Also, butyrate inhibited the LPS-induced expression of pyruvate dehydrogenase kinase 4 (PDK4), resulting in decreased PDHE1α phosphorylation and lactate production, suggesting that butyrate shifted glucose metabolism from aerobic glycolysis to oxidative phosphorylation. Finally, we found that these effects of butyrate on LPS-induced mitochondrial dysfunction were caused by its antioxidant effects. Thus, our findings demonstrate that butyrate prevents LPS-induced muscle atrophy by improving mitochondrial dynamics and metabolic stress via the inhibition of JNK phosphorylation. Consequently, butyrate could be used to improve LPS-induced mitochondrial dysfunction and myopathy in sepsis.

• Journal of Microbiology and Biotechnology
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• v.34 no.3
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• pp.606-621
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• 2024

This study evaluated the hepatoprotective effect of fermented Protaetia brevitarsis larvae (FPB) in ethanol-induced liver injury mice. As a result of amino acids in FPB, 18 types of amino acids including essential amino acids were identified. In the results of in vitro tests, FPB increased alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) activities. In addition, FPB treatment increased cell viability on ethanol- and H₂O₂-induced HepG2 cells. FPB ameliorated serum biomarkers related to hepatoxicity including glutamic oxaloacetic transaminase, glutamine pyruvic transaminase, total bilirubin, and lactate dehydrogenase and lipid metabolism including triglyceride, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol. Also, FPB controlled ethanol metabolism enzymes by regulating the protein expression levels of ADH, ALDH, and cytochrome P450 2E1 in liver tissue. FPB protected hepatic oxidative stress by improving malondialdehyde content, reduced glutathione, and superoxide dismutase levels. In addition, FPB reversed mitochondrial dysfunction by regulating reactive oxygen species production, mitochondrial membrane potential, and ATP levels. FPB protected ethanol-induced apoptosis, fatty liver, and hepatic inflammation through p-AMP-activated protein kinase and TLR-4/NF-κB signaling pathways. Furthermore, FPB prevented hepatic fibrosis by decreasing TGF-β1/Smad pathway. In summary, these results suggest that FPB might be a potential prophylactic agent for the treatment of alcoholic liver disease via preventing liver injury such as fatty liver, hepatic inflammation due to chronic ethanol-induced oxidative stress.