Protective Effect of Que Zui Tea on d-Galactose-Induced Oxidative Stress Damage in Mice via Regulating SIRT1/Nrf2 Signaling Pathway.

Que Zui tea (QT) is an important herbal tea in the diet of the 'Yi' people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6'-O-caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1ß and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6'-O-caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway.

A Comparative Analysis of Chemical Constituents and Antioxidant Effects of Dendrobium fimbriatum Hook Fractions with Different Polarities.

The aim of this study was to investigate the chemical composition and antioxidant capacity of various polar fractions obtained from Dendrobium fimbriatum Hook (DH). First, a 90% ethanol-aqueous extract of DH (CF) was subjected to sequential fractionation using different organic solvents, resulting in the isolation of a methylene chloride fraction (DF), an ethyl acetate fraction (EF), an n-butanol fraction (BF), and a remaining water fraction (WF) after condensation. Additionally, the CF was also subjected to column chromatography via a D101 macroreticular resin column, eluted with ethanol-aqueous solution to yield six fractions (0%, 20%, 40%, 60%, 80%, and 100%). UPLC-Q-Exactive Orbitrap-MS/MS analysis identified a total of 47 chemical compounds from these polar fractions, including fatty acids, amino acids, phenolic acids, flavonoids, organic heterocyclic molecules, and aromatic compounds. Moreover, DF, EF, and the 60%, 80%, and 100% ethanol-aqueous fractions had higher total phenol content (TPC) and total flavonoid content (TFC) values and greater 2,2'-azinobis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt (ABTS-) and 1,1-diphenyl-2-picrylhydrazyl (DPPH)-scavenging abilities. In H2O2-induced HepG2 cells, the aforementioned fractions could increase the activities of antioxidative enzymes NAD(P)H: quinone oxidoreductase 1 (NQO1), superoxide dismutase (SOD), heme oxygenase-1 (HO-1) and catalase (CAT), stimulate glutathione (GSH) synthesis by increasing the activities of glutamic acid cysteine ligase (GCL) and glutathione synthetase (GS), regulate GSH metabolism by increasing glutathione peroxidase (GSH-Px) and glutathione reductase (GR) activities, and reduce levels of reactive oxygen species (ROS) and malondialdehyde (MDA). Furthermore, the antioxidative stress effect of the DH fractions was found to be positively correlated with the activation of nuclear factor-erythroid 2-related factor 2 (Nrf2) protein and the presence of antioxidative chemical constituents. In conclusion, this study highlights the efficacy of both liquid-liquid extraction and macroporous resin purification techniques in the enrichment of bioactive compounds from natural food resources. The comprehensive analysis of chemical constituents and antioxidant effects of different polar fractions from Dendrobium fimbriatum Hook contributes to the understanding of its potential application in functional foods and nutraceuticals.

Boosting photodetection performance of Cs2AgBiBr6 through A-site Rb substitution and interfacial engineering.

Bismuth-based double perovskite Cs2AgBiBr6 shows promise as a photodetection material. However, its detection performance and application are limited by high-exciton binding energy and poor carrier mobility. In this study, we address these limitations by delicately designing a solution-based method for incorporating A-site Rubidium (Rb) substitution into Cs2AgBiBr6 double perovskite films. The introduction of Rb resulted in a significant decrease in trap defect density and an improvement in film quality. The trap-filled limit voltage (VTFL) of pure and Rb-doped CABB film is determined to be 1.71 V and 0.48 V, respectively. Subsequently, by introducing an ultrathin atomic-layer-deposited (ALD) TiO2 films, the fabricated CABB photodetectors exhibit significantly improved photoresponse performance. The response speed and -3dB bandwidth are boosted from ∼93 ms to ∼350 µs and broadened from 1.4 kHz to 17 kHz, respectively. Density Functional Theory (DFT) calculations indicate Rb-substitution shortens the bond length and weaken exciton binding energy. Furthermore, we demonstrate a wireless near ultraviolet (UV) light communication system using CABB photodetectors as light receivers. Our findings provide an efficient approach to utilize A-site cation substitution as a tuning parameter for photodetection in high-exciton binding energy perovskite materials, thereby extending the potential applications of other functional perovskites.

Protective effect of hot-water and ethanol-aqueous extracts from Anneslea fragrans against acetaminophen-induced acute liver injury in mice.

Anneslea fragrans Wall. (AF) is an important medicinal and edible plant in China. The principal objectives of this study are to explore the hepatoprotective effect of ethanol-aqueous (AFE) and hot-water (AFW) extracts in vitro and in vivo. UPLC-ESI-MS/MS analysis showed that AFW and AFE are rich in dihydrochalcones. Both AFW and AFE significantly up-regulated the expressions of SOD, CAT and GSH, reduced the MDA content in acetaminophen (APAP)-induced HepG2 cells, and suppressed the expressions of NO, TNF-α, IL-1ß, and IL-6 in LPS-induced RAW246.7 cells. In APAP-induced mice, AFW and AFE administration significantly decreased the plasma levels of AST and ALT, and improved liver tissue damage, the collagen deposition and fibrosis formation. Moreover, AFW and AFE decreased the MDA and ROS accumulations via activating Nrf2 pathway to increase the hepatic GSH contents and activities of SOD, CAT, HO-1, and NQO-1, reduced the levels of NO, TNF-α, IL-1ß, and IL-6 by suppressing the JNK/p38/ERK/NF-κB pathways, and alleviated apoptosis via regulating Bcl-2, Bax, caspase-3/9 protein expressions. This study provides a new sight that AFW and AFE may have a potential natural resource for the treatment of liver injury.

E Se tea extract ameliorates CCl4 induced liver fibrosis via regulating Nrf2/NF-κB/TGF-ß1/Smad pathway.

BACKGROUND: Liver fibrosis is a crucial progress to deteriorate liver disease. E Se tea (ES) is an ethnic herbal tea in China that has various biological activities for human beings. However, the traditional application on the treatment of liver disease is not studied. PURPOSE: This study is firstly performed to explore the chemical constituents of ES extract together with its anti-hepatic fibrosis effect and potential mechanism on CCl4 treated mice. STUDY DESIGN AND METHODS: The chemical constituents of ethanol-aqueous extract from ES (ESE) were analyzed by UPLC-ESI-MS/MS. The anti-hepatic fibrosis effect of ESE was determined by measuring ALT and AST activities, antioxidative indexes, inflammatory cytokines and collagen protein levels on CCl4 treated mice. Moreover, H&E, Masson staining and immunohistochemical analysis were performed for evaluating the protective effect of ESE on histopathological changes of liver tissues. RESULTS: UHPLCHRESI-MS/MS analysis showed that the ESE was rich in flavonoids such as phlorizin, phloretin, quercetin and hyperoside. ESE could significantly reduce the plasma AST and ALT activities. The cytokines (IL-6, TNF-α, IL-1ß) expressions were inhibited after ESE administration via suppressing NF-κB pathway. In addition, ESE could decrease MDA accumulation for alleviating CCl4 induced liver oxidative stress via regulating Nrf2 pathway to promote the expressions of antioxidant enzymes (SOD, HO-1, CAT and NQO1). Moreover, ESE could inhibit the expressions of TGF-ß1, Smad2, α-SMA, and collagens Ⅰ and III proteins, thereby effectively alleviate the liver fibrosis. CONCLUSION: This study demonstrated that ESE could alleviate liver fibrosis through enhancing antioxidant and anti-inflammatory abilities by Nrf2/NF-κB pathway and reducing deposition of liver fibrosis via suppressing TGF-ß/Smad pathway.

Protective effect of Anneslea fragrans ethanolic extract against CCl4-induced liver injury by inhibiting inflammatory response, oxidative stress and apoptosis.

Anneslea Fragrans Wall. (AF) is a medicinal and edible plant distributed in China. Its leaves and barks are generally used for the treatments of diarrhea, fever, and liver diseases. While its ethnopharmacological application against liver diseases has not been fully studied. This study was aimed to evaluate the hepatoprotective effect of ethanolic extract from A. fragrans (AFE) on CCl4 induced liver injury in mice. The results showed that AFE could effectively reduce plasma activities of ALT and AST, increase antioxidant enzymes activities (SOD and CAT) and GSH level, and decrease MDA content in CCl4 induced mice. AFE effectively decreased the expressions of inflammatory cytokines (IL-1ß, IL-6, TNF-α, COX-2 and iNOS), cell apoptosis-related proteins (Bax, caspase-3 and caspase-9) and increased Bcl-2 protein expression via inhibiting MAPK/ERK pathway. Additionally, TUNEL staining, Masson and Sirius red staining, immunohistochemical analyses revealed that AFE could inhibit the CCl4-induced hepatic fibrosis formation via reducing depositions of α-SMA, collagen I and collagen III proteins. Conclusively, the present study demonstrated that AFE had an hepatoprotective effect by suppressing MAPK/ERK pathway to inhibit oxidative stress, inflammatory response and apoptosis in CCl4-induced liver injury mice, suggesting that AFE might be served as a hepatoprotective ingredient in the prevention and treatment of liver injury.

Effect of ultra-high pressure pretreatment on the phenolic profiles, antioxidative activity and cytoprotective capacity of different phenolic fractions from Que Zui tea.

This study aims to explore whether ultra-high pressure (UHP) pre-treatment strengthened the bioaccessibility and bioactivities of the free (QF), esterified (QE) and insoluble-bound phenolics (QIB) from Que Zui tea (QT). The results revealed that the extraction yields, the total phenolic (TPC) and total flavonoid contents (TFC) of three phenolic fractions from QT were markedly increased after ultra-high pressure (UHP) processing (p < 0.05). A total of 19 and 20 compounds were characterized and quantified in non- and UHP-treated QT, respectively, including the content of 6'-O-caffeoylarbutin (11775.68 and 13248.87 µg/g of dry extract) was highest in QF, the content of caffeic acid was highest in QE (2131.58 and 7362.99 µg/g of dry extract) and QIB (9151.89 and 10930.82 µg/g of dry extract). QF, QE and QIB from QT after UHP processing had better antioxidant, ROS scavenging, and anti-apoptosis effects. The possible mechanism of cytoprotective effect was related to Keap1-Nrf2 pathway.

L-Methionine inhibits 4-hydroxy-2-nonenal accumulation and suppresses inflammation in growing rats.

BACKGROUND/OBJECTIVES: 4-Hydroxy-2-nonenal (HNE) is a biomarker for oxidative stress to induce inflammation. Methionine is an essential sulfur-containing amino acid with antioxidative activity. On the other hand, the evidence on whether and how methionine can depress HNE-derived inflammation is lacking. In particular, the link between the regulation of the nuclear factor-κB (NF-κB) signaling pathway and methionine intake is unclear. This study examined the link between depression from HNE accumulation and the anti-inflammatory function of L-methionine in rats. MATERIALS/METHODS: Male Wistar rats (3-week-old, weighing 70-80 g) were administered different levels of L-methionine orally at 215.0, 268.8, 322.5, and 430.0 mg/kg body weight for two weeks. The control group was fed commercial pellets. The hepatic HNE contents and the protein expression and mRNA levels of the inflammatory mediators were measured. The interleukin-10 (IL-10) and glutathione S-transferase (GST) levels were also estimated. RESULTS: Compared to the control group, hepatic HNE levels were reduced significantly in all groups fed L-methionine, which were attributed to the stimulation of GST by L-methionine. With decreasing HNE levels, L-methionine inhibited the activation of NF-κB by up-regulating inhibitory κBα and depressing phosphoinositide 3 kinase/protein kinase B. The mRNA levels of the inflammatory mediators (cyclooxygenase-2, interleukin-1ß, interleukin-6, inducible nitric oxide synthase, tumor necrotic factor alpha) were decreased significantly by L-methionine. In contrast, the protein expression of these inflammatory mediators was effectively down regulated by L-methionine. The anti-inflammatory action of L-methionine was also reflected by the up-regulation of IL-10. CONCLUSIONS: This study revealed a link between the inhibition of HNE accumulation and the depression of inflammation in growing rats, which was attributed to L-methionine availability. The anti-inflammatory mechanism exerted by L-methionine was to inhibit NF-κB activation and to up-regulate GST.

Phylogenetic analysis and complete chloroplast genome of Salix wilhelmsiana M.B.

Salix wilhelmsiana M.B. Bieberstein 1819 is a perennial woody plant with high economic and ecological value. In this study, we annotated the chloroplast (cp) genome of Salix wilhelmsiana M.B. The results showed that the length of the complete cp genome is 155,577 bp, which is typically composed of two single-copy regions (large single-copy (LSC) of 84,439 bp and small single-copy (SSC) of 16,221 bp) and a pair of IR regions of 27,457 bp with a quadripartite structure. The genome contains 129 genes, including 84 protein-coding genes, 37 tRNA genes, and eight rRNA genes. The GC content was 36.70%. Phylogenetic analysis based on cp genome sequences of 19 species from the Salicaceae family revealed that S. wilhelmsiana M.B. is closely related to S. viminalis var. gmelinii.

The complete chloroplast genome sequence of Salix kochiana Trautv. and its phylogenetic analysis.

Salix kochiana Trautvetter 1837 is one of the highest value shrubs present in northern China with important economic and ecological benefits. This study revealed the structural characteristics and phylogenetic relationships of chloroplast genes in S. kochiana Trautv. The results showed that the length of the complete chloroplast genome was 155,657 bp, which was a typical circular double-stranded structure, including an 84,458 bp large single-copy region (LSC), a 16,221 bp small single-copy region (SSC) and a 27,489 bp pair of inverted repeat regions (IRA and IRB). The chloroplast genome contains 48,757 A bases, 28,017 G bases, 49,843 T bases, and 29,040 C bases, with a GC content of 36.66%. Through bioinformatics annotation, a total of 126 genes were found in the chloroplast genome, including 81 protein-coding genes, 37 tRNA genes, and eight rRNA genes. Phylogenetic analysis showed that S. kochiana Trautv. was closely related to S. triandroides.

Impact of Low-Temperature Storage on the Microstructure, Digestibility, and Absorption Capacity of Cooked Rice.

This study examined the effects of low-temperature storage on the microstructural, absorptive, and digestive properties of cooked rice. Cooked rice was refrigerated and stored at 4 °C for 0.5, 1, 3, 5, and 7 days, as well as frozen and preserved at -20, -40, and -80 °C for 0.5, 1, 3, 5, 7, 14, 21, and 28 days. The results indicated that the stored rice samples generally exhibited a higher absorption capacity for oil, cholesterol, and glucose than the freshly cooked rice. In addition, after storage, the digestibility of the cooked rice declined, namely, the rapidly digestible starch (RDS) content and estimated glycemic index (eGI) decreased, whereas the slowly digestible starch (SDS) and resistant starch (RS) content increased. Moreover, the increment of the storage temperatures or the extension of storage periods led to a lower amylolysis efficiency. Scanning electron microscopy (SEM) analysis indicated that storage temperature and duration could effectively modify the micromorphology of the stored rice samples and their digestion. Moreover, microstructural differences after storage and during simulated intestinal digestion could be correlated to the variations in the absorption capacity and digestibility. The findings from this study will be useful in providing alternative storage procedures to prepare rice products with improved nutritional qualities and functional properties.

Methionine strengthens anti-inflammation of rice protein via depressing NF-κB activation and stimulating Msr expression in rats fed cholesterol-enriched diets.

Oxidized low-density lipoprotein (ox-LDL) is an inducer of inflammation. To elucidate the link of depression of ox-LDL accumulation and anti-inflammatory function of rice protein (RP) whether dependent on methionine availability, growing and adult rats were fed RP and methionine-supplemented RP (RM) under cholesterol-enriched dietary condition. After two weeks feeding, RP and RMs exerted the anti-inflammatory effects through up-regulating IL-10, while RP and RMs significantly reduced ox-LDL levels and effectively suppressed the expressions of inflammatory mediators (COX-2, IL-1ß, IL-6, TNF-α, iNOS). The anti-inflammatory molecular mechanism was to inhibit NF-κB activation and to simulate methionine sulfoxide reductase expression. Results showed, under cholesterol-enriched dietary condition, the anti-inflammatory action can be induced by RP and enhanced by methionine in growing and adult rats. The present study reveals a link of the decreased ox-LDL accumulation with the anti-inflammatory function of RP, which is dependent on methionine availability and independent of dietary cholesterol.

l-Arginine prevents 4-hydroxy-2-nonenal accumulation and depresses inflammation via inhibiting NF-κB activation.

4-Hydroxy-2-nonenal (HNE) is an inducer of inflammation. The aim of this study was to elicit the link between the inhibition of HNE accumulation and the depression of inflammation whether dependent onl-arginine availability in growing rats. Male Wistar rats were fed with different levels of l-arginine at 250, 500, and 1000 mg/kg body weight for 14 days. The control group was fed with commercial pellets. After 14 days of oral administration, l-arginine significantly reduced hepatic accumulation of HNE and depressed inflammation in rats as compared with the control group. Compared to the control group, the anti-inflammatory action of l-arginine is reflected by upregulation of hepatic interleukin-10 (IL-10) and the suppression of hepatic cyclooxygenase-2, tumor necrotic factor α, IL-1ß, and IL-6 expressions in growing rats. With l-arginine administration, the activation of nuclear factor-κB (NF-κB) was efficaciously inhibited through the upregulation of inhibitory κBα, and the depression of phosphoinositide 3-kinase/protein kinase B (PI3K/Akt). In conclusion, this study demonstrated that l-arginine could reduce hepatic HNE levels and depress inflammation in growing rats, revealing a link between the inhibition of HNE accumulation with the depression of inflammation, which was attributed to the availability of l-arginine. A significant finding of this study was that the anti-inflammatory mechanism exerted by l-arginine was to inhibit NF-κB activation via downregulating PI3K/Akt.

Rice protein suppresses 4-hydroxy-2-nonenal-induced inflammation owing to methionine availability.

4-Hydroxy-2-nonenal (HNE) is one of the most important products of lipid peroxidation, which induces inflammation. To investigate the effects of rice protein (RP) on suppressing HNE-induced inflammation and the role of methionine in regulating the anti-inflammatory function of RP, Wistar rats (male, weighing 180-200 g) were either ad libitum fed a pellet diet with oral administration of methionine or ad libitum fed RP for 2 weeks. RP and methionine significantly reduced HNE levels and effectively suppressed the expressions of cyclooxygenase-2, tumor necrosis factor alpha, interleukin-1ß (IL-1ß) and IL-6, and inducible nitric oxide synthase. The anti-inflammatory action of RP was evident from the upregulation of IL-10 and glutathione S-transferase (GST), which played a role in the detoxification of HNE. The results show that the molecular mechanism responsible for the anti-inflammatory function of RP is the inhibition of nuclear factor kappa B (NF-κB) activation by the downregulation of protein kinase B/phosphoinositide 3 kinase. Further, this study demonstrates that Met availability contributes to the suppression of HNE-induced inflammation through upregulating IL-10 and GST in rats fed RP. Novelty: RP suppresses HNE-induced inflammation. Methionine plays a role in upregulating IL-10 and GST. Methionine availability regulates the inhibition of NF-κB by RP.

Rice protein stimulates endogenous antioxidant response attributed to methionine availability in growing rats.

Methionine sulfoxide reductase (Msr) and glutathione (GSH) are two endogenous antioxidant systems for depressing oxidative stress. The aim of this study is to investigate the role of methionine in involving the stimulation of endogenous antioxidant capacity of rice protein (RP). Seven-week-old male Wistar rats (body weight 180-200 g) were fed with commercial pellets (as control), methionine, and RP for 2 weeks. Compared with control, GSH synthesis and expressions of MsrA, MsrB2, and MsrB3 were stimulated by methionine and RP. After 2 weeks of feeding, Nrf2 was activated by RP and methionine, whereas the expressions of Keap1 and Cul3 were depressed. The ARE-driven antioxidant expressions (GCLC, GCLM, GS, HO-1, NQO1, CAT, SOD, GR, GST, GPx) were upregulated by methionine and RP. Results suggest that the endogenous antioxidant response induced by RP is primarily attributed to the methionine availability, in which the stimulation of Msr and GSH antioxidant system via Nrf2-ARE pathway. PRACTICAL APPLICATIONS: Rice protein is a major plant protein, which is rich in sulfur-containing amino acids and widely consumed in the world. This paper emphasizes that the amino acid plays a key role in inducing the antioxidant activity of rice protein. The present study provides an insight that the methionine availability of rice protein will be a useful target for health promoting by activating endogenous antioxidant response against ROS-induced oxidative damage.

Rice Protein Exerts Endogenous Antioxidant Capacity via Methionine Sulfoxide Reductase and the Nrf2 Antioxidant System Independent of Age.

The major aim of this study was to investigate the effect of rice protein (RP) on the activation of endogenous antioxidant defense in growing and adult rats. After 2 weeks, RP activated nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) by suppressing Kelch-like ECH-associated protein 1 (Keap1) and Cullin 3 (Cul3) in growing and adult rats. Compared with casein, the upregulation of antioxidant responsive element (ARE)-driven antioxidant expression levels (glutamate cysteine ligase catalytic subunit, glutamate cysteine ligase modulatory subunit, glutathione synthase, glutathione reductase, glutathione S-transferase, glutathione peroxidase, catalase, superoxide dismutase, heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1) were found in RP groups. Also, RP upregulated methionine sulfoxide reductase (MsrA, MsrB2, and MsrB3) expression levels in growing and adult rats. As a result, RP enhanced endogenous antioxidative capacities to reduce hepatic accumulations of malondialdehyde, protein carbonyl, and reactive oxygen species. This study demonstrates that RP exerts the endogenous antioxidant capacity in growing and adult rats, which is due to stimulating Msr antioxidant expression and activating Nrf2-ARE pathway. Results suggest that the antioxidant activity induced by RP is independent of age.

Rice Protein Exerts Anti-Inflammatory Effect in Growing and Adult Rats via Suppressing NF-κB Pathway.

To elucidate the effect of rice protein (RP) on the depression of inflammation, growing and adult rats were fed with caseins and RP for 2 weeks. Compared with casein, RP reduced hepatic accumulations of reactive oxygen species (ROS) and nitro oxide (NO), and plasma activities of alanine transaminase (ALT) and aspartate transaminase (AST) in growing and adult rats. Intake of RP led to increased mRNA levels, and protein expressions of phosphoinositide 3 kinase (PI3K), protein kinase B (Akt), nuclear factor-κB 1 (NF-αB1), reticuloendotheliosis viral oncogene homolog A (RelA), tumor necrotic factor α (TNF-α), interleukin-1ß (IL-1ß), interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and monocyte chemoattractant protein-1 (MCP-1) were decreased, whereas hepatic expressions of interleukin-10 (IL-10) and heme oxygenase 1 (HO-1) were increased by RP. The activation of NF-κB was suppressed by RP through upregulation of inhibitory κB α (IκBα), resulting in decreased translocation of nuclear factor-κB 1 (p50) and RelA (p65) to the nucleus in RP groups. The present study demonstrates that RP exerts an anti-inflammatory effect to inhibit ROS-derived inflammation through suppression of the NF-κB pathway in growing and adult rats. Results suggest that the anti-inflammatory capacity of RP is independent of age.

Rice protein reduces DNA damage by activating the p53 pathway and stimulating endogenous antioxidant response in growing and adult rats.

BACKGROUND: Reactive oxygen species (ROS) can cause DNA damage. Rice protein (RP) inhibits ROS accumulation. However, a link between the reduction of ROS-derived DNA damage and the intake of RP is far from clear. The main objective of this study is to elucidate the effects of RPs on the reduction of DNA damage in growing and adult rats. RESULTS: An intake of RP for 2 weeks significantly reduced the hepatic accumulation of ROS and 8-hydroxydeoxyguanosine (8-OHdG) in growing and adult rats, whereas the hepatic p53 content was markedly increased by RPs. After 2 weeks' feeding, the mRNA levels and protein expressions of p53, ataxia-telangiectasia mutated (ATM), and Checkpoint kinase 2 (Chk2) were up-regulated by RPs, whereas Murine Double Minute 2 (MDM2) expressions were markedly inhibited by RPs, resulting in more p53 being translocated into the nucleus. Nuclear factor erythroid 2 (NF-E2)-related factor 2 (Nrf2) was activated by RP by reducing Kelch-like ECH-associated protein 1 (Keap1), resulting in the up-regulation of antioxidant expressions of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) in RP groups. CONCLUSION: Rice protein can exert an endogenous antioxidant activity to reduce ROS-derived DNA damage by activating the Nrf2-Keap1 pathway. This study suggests that the activation of the ATM-Chk2-p53 pathway might be one of the mechanisms exerted by RP for reducing DNA damage in growing and adult rats. © 2019 Society of Chemical Industry.

l-Methionine activates Nrf2-ARE pathway to induce endogenous antioxidant activity for depressing ROS-derived oxidative stress in growing rats.

BACKGROUND: Methionine is an essential sulfur-containing amino acid. To elucidate the influence of l-methionine on activation of the nuclear factor erythroid 2-related factor 2-antioxidant responsive element (Nrf2-ARE) antioxidant pathway to stimulate the endogenous antioxidant activity for depressing reactive oxygen species (ROS)-derived oxidative stress, male Wistar rats were orally administered l-methionine daily for 14 days. RESULTS: With the intake of l-methionine, Nrf2 was activated by l-methionine through depressing Keap1 and Cul3, resulting in upregulation of ARE-driven antioxidant expression (glutamate cysteine ligase catalytic subunit, glutamate cysteine ligase modulatory subunit, glutathione synthase (GS), catalase (CAT), superoxide dismutase (SOD), heme oxygenase 1, NAD(P)H:quinone oxidoreductase 1, glutathione reductase (GR), glutathione S-transferase (GST), glutathione peroxidase (GPx)) with increasing l-methionine availability. Upon activation of Nrf2, glutathione synthesis was increased through upregulated expression of methionine adenosyltransferase, S-adenosylhomocysteine hydrolase, cystathionine ß-synthase, cystathionine γ-lyse, glutamate cysteine ligase (GCL) and GS, while hepatic expressions of methionine sulfoxide reductases (MsrA, MsrB2, MsrB3) and hepatic enzyme activities (CAT, SOD, GCL, GR, GST, GPx) were uniformly stimulated with increasing consumption of l-methionine. As a result, hepatic content of ROS and MDA were effectively reduced by l-methionine intake. CONCLUSION: The present study demonstrates that methionine availability plays a critical role in activation of the Nrf2-ARE pathway to induce an endogenous antioxidant response for depressing ROS-derived oxidative stress, which is primarily attributed to the stimulation of methionine sulfoxide reductase expression and glutathione synthesis. © 2019 Society of Chemical Industry.

Methionine Augments Antioxidant Activity of Rice Protein during Gastrointestinal Digestion.

To elucidate the influence of methionine, which is an essential sulfur-containing amino acid, on the antioxidant activity of rice protein (RP), methionine was added to RP (RM). The addition of methionine to RM0.5, RM1.0, RM1.5, RM2.0, and RM2.5 was 0.5-, 1.0-, 1.5-, 2.0-, and 2.5-fold of methionine of RP, respectively. Using the in vitro digestive system, the antioxidant capacities of scavenging free radicals (superoxide; nitric oxide; 2,2'-azinobis (3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt, ABTS), chelating metal (iron), and reducing power were investigated in the hydrolysates of RP and RMs. Upon pepsin-pancreatin digestion, the weakest antioxidant capacity was produced by RP. With the addition of methionine, RMs exhibited more excellent responses to free radical scavenging activities and reducing power than RP, whereas RMs did not produce the marked enhancements in iron chelating activity as compared to RP. The present study demonstrated that RMs differently exerted the free radical scavenging activities that emerged in the protein hydrolysates, in which the strongest scavenging capacities for ABTS, superoxide, and nitric oxide were RM1.5, RM2.0, and RM2.5, respectively. Results suggested that the availability of methionine is a critical factor to augment antioxidant ability of RP in the in vitro gastrointestinal tract.