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High fructose has been reported to drive glomerular podocyte oxidative stress and then induce podocyte foot process effacement in vivo, which could be partly regarded as podocyte hypermotility in vitro. Atractylodin possesses anti-oxidative effect. The aim of this study was to explore whether atractylodin prevented against fructose-induced podocyte hypermotility via anti-oxidative property. In fructose-exposed conditionally immortalized human podocytes, we found that atractylodin inhibited podocyte hypermotility, and up-regulated slit diaphragm proteins podocin and nephrin, and cytoskeleton protein CD2-associated protein (CD2AP), α-Actinin-4 and synaptopodin expression, which were consistent with its anti-oxidative activity evidenced by up-regulation of catalase (CAT) and superoxide dismutase (SOD) 1 expression, and reduction of reactive oxygen species (ROS) production. Atractylodin also significantly suppressed expression of transient receptor potential channels 6 (TRPC6) and phosphorylated Ca 2+ /calmodulin-dependent protein kinase IV (CaMK4) in cultured podocytes with fructose exposure. Additionally, in fructose-exposed podocytes, CaMK4 siRNA up-regulated synaptopodin and reduced podocyte hypermotility, whereas, silencing of TRPC6 by siRNA decreased p-CaMK4 expression, inhibited podocyte hypermotility, showing TRPC6/p-CaMK4 signaling activation in podocyte hypermotility under fructose condition. Just like atractylodin, antioxidant N-acetyl-L-cysteine (NAC) could inhibit TRPC6/p-CaMK4 signaling activation to reduce fructose-induced podocytes hypermotility. These results first demonstrated that the anti-oxidative property of atractylodin may contribute to the suppression of podocyte hypermotility via inhibiting TRPC6/p-CaMK4 signaling and restoring synaptopodin expression abnormality., (Copyright © 2021. Published by Elsevier B.V.)

Excessive fructose intake is a risk factor for liver oxidative stress injury. Magnesium isoglycyrrhizinate as a hepatoprotective agent is used to treat liver diseases in clinic. However, its antioxidant effects and the underlying potential mechanisms are still not clearly understood. In this study, magnesium isoglycyrrhizinate was found to alleviate liver oxidative stress and inflammatory injury in fructose-fed rats. Magnesium isoglycyrrhizinate suppressed hepatic reactive oxygen species overproduction (0.97 ± 0.04 a.u. versus 1.34 ± 0.07 a.u.) in fructose-fed rats by down-regulating mRNA and protein levels of nicotinamide adenine dinucleotide phosphate oxidase (NOX) 1, NOX2 and NOX4, resulting in reduction of interleukin-1β (IL-1β) levels (1.13 ± 0.09 a.u. versus 1.97 ± 0.12 a.u.). Similarly, magnesium isoglycyrrhizinate reduced reactive oxygen species overproduction (1.07 ± 0.02 a.u. versus 1.35 ± 0.06 a.u.) and IL-1β levels (1.14 ± 0.09 a.u. versus 1.66 ± 0.07 a.u.) in fructose-exposed HepG2 cells. Furthermore, data from treatment of reactive oxygen species inhibitor N-acetyl-L-cysteine or NOXs inhibitor diphenyleneiodonium in fructose-exposed HepG2 cells showed that fructose enhanced NOX1, NOX2 and NOX4 expression to increase reactive oxygen species generation, causing oxidative stress and inflammation, more importantly, these disturbances were significantly attenuated by magnesium isoglycyrrhizinate. The molecular mechanisms underpinning these effects suggest that magnesium isoglycyrrhizinate may inhibit NOX1, NOX2 and NOX4 expression to reduce reactive oxygen species generation, subsequently prevent liver oxidative stress injury under high fructose condition. Thus, the blockade of NOX1, NOX2 and NOX4 expression by magnesium isoglycyrrhizinate may be the potential therapeutic approach for improving fructose-induced liver injury in clinic., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Proteins were extracted from Se-enriched peanut leaves, an agro-byproduct, and the foliar application of sodium selenite was indicated to be an effective method to incorporate Se into leaf selenoproteins with 75-80% incorporation rates. After trypsin digestion, the most abundant proteins from Se-enriched peanut leaf (PSPL) were identified as pathogenesis-related class 10 proteins, Ara h 8 allergen and its isoforms, using LC-MS/MS. The Se species in both the low Se PSPL and high Se PSPL were determined to be selenomethionine (SeMet), methylselenocysteine (MeSeCys) and selenocystine (SeCys 2 ) with SeMet (15.6 mg/g) dominated the high Se PSPL. Their antioxidant activities were also evaluated using free radical scavenging assay, reducing power assay and ferric thiocyanate (FTC) test. As results, the PSPL exhibited potent DPPH radical (96.2%) and superoxide anion radical (98.4%) scavenging activities and showed strong reducing power in a Se-concentration-dependent manner, indicating that PSPL can be used as antioxidants and Se sources to improve health., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Epigallocatechin-3-gallate (EGCG), a major constituent of green tea catechin, has been used for antioxidant. This study aimed to evaluate the antihyperuricemic activity of EGCG on hyperuricemic mice. We demonstrated that serum uric acid (UA) level was decreased significantly with dose-dependence by EGCG treated with 10, 20, and 50mg/kg. Compared with the model, data on blood urea nitrogen (BUN) supported that there was significance with high dose of EGCG (50mg/kg). Levels of serum creatinine (Cr) in each EGCG-treated group were decreased but not significant; the activities of hepatic xanthine oxidase (XOD) and adenosine deaminase (ADA) in high dose groups' EGCG were notably lower than those of model group. EGCG could downregulate the renal mRNA expression levels of glucose transporter 9 (GLUT9) and urate transporter 1 (URAT1) on hyperuricemic mice. These results presented that EGCG had obvious hypouricemic and renal protective effects on hyperuricemic mice. Our data may have a potential value in clinical practice in the treatment of hyperuricemia., (Copyright © 2017. Published by Elsevier Masson SAS.)

Mercury (Hg) is a global pollutant that causes negative health effects. In order to assess Hg-induced hepatotoxicity in fish and examine whether gender differences existed in response to Hg exposure, adult zebrafish were exposed to 0, 15 and 30 μg L -1 Hg 2+ for 30 days, and histology, antioxidant status and the transcription levels of several immune-related genes were examined in the liver. Hg 2+ exposure caused a dose-dependent increase in histopathological lesions of the liver, including vacuolization, parenchyma disorganization and pyknotic nucleus, and these lesions were more severe in males than in females. In females, Hg 2+ exposure decreased CAT activity and its mRNA levels, while increased GSH content and the expressions of sod1, gpx1a, gstr and keap1. In males, the decrease in cat1 expression and the increase in GST activity, GSH and MDA contents as well as gpx1a, gstr, nrf2 and keap1 mRNA levels were observed in Hg 2+ -exposed groups, but the activities of CAT, SOD and GPX were only stimulated in the 15 μg L -1 Hg 2+ group. Moreover, both in females and males, Hg 2+ exposure down-regulated il-8 expression while up-regulated il-10 and lyz mRNAs. However, the down-regulation of il-1β and tnfα was detected only in males under Hg 2+ treatments. Thus, our results indicated that HgCl 2 exposure induced histopathological damage, oxidative stress and immunotoxicity in the liver of zebrafish. Different response patterns of histology, antioxidant status and immune defenses to Hg 2+ between females and males suggested sex-dependent effects of Hg, and males showed more vulnerable to Hg 2+ exposure than females., (Copyright © 2017 Elsevier Ltd. All rights reserved.)

Recently, accumulating evidence has indicated that glucocorticoid-induced osteoporosis (GIOP) is closely related to oxidative stress and apoptosis. Alpha-lipoic acid (LA), a naturally endogenous anti-oxidant, possesses anti-oxidative and anti-apoptosis activities, implicating LA as a therapeutic agent for the treatment of GIOP. In this study, the osteogenesis-promoting effects of LA against GIOP were investigated and the mechanisms were further probed. Here, the results showed that LA inhibited oxidative stress, suppressed apoptosis and improved osteopenia by promoting the expression of osteogenesis markers, including ALP, COL-I, OCN, BMP-2, RUNX2 and OSX. Further study revealed that the osteogenesis-promoting effects of LA likely occur via the regulation of the NOX4, NF-kappaB, JNK and PI3K/AKT pathways. The present study indicated that LA may prevent GIOP and promote osteogenesis and might be a candidate for the treatment of GIOP.

Background: Potentilla fruticosa, also called "Jinlaomei" and "Gesanghua", is widely used as folk herbs in traditional Tibetan medicine in China to treat inflammations, wounds, certain forms of cancer, diarrhoea, diabetes and other ailments. Previous research found P. fruticosa leaf extract (C-3) combined with Ginkgo biloba extracts (EGb) showed obvious synergistic effects in a variety of oxidation systems. The aim of the present study was to further confirm the synergy of P. fruticosa combined with EGb viewed from physiological bioavailability and explore the related bioactive mechanism behind the synergism., Methods: The microbial test system (MTS) was adopted to evaluate the related bioactive mechanism. The synergistic effects were evaluated by isobolographic analysis. The H 2 O 2 production rate and antioxidant enzyme (Catalase (CAT), Peroxidase (POD), Superoxide dismutase (SOD), Glutathione peroxidase (GSH-PX)) activities were determined by the colorimetric method. Enzyme gene (CAT, SOD) expression was measured by real time-PCR., Results: The MTS antioxidant activity results showed the combination of C-3 + EGb exhibited synergistic effects especially at the ratio 5:1. Components of isorhamnetin and caffeic acid in C-3 and EGb displayed strong antioxidant activities on MTS and their combination also showed significant synergy in promoting H 2 O 2 production. The combinations of C-3 + EGb and isorhamnetin + caffeic acid promoted CAT and SOD enzyme activities and the ratio 1:1 exhibited the strongest synergy while no obvious promotion on POD and GSH-PX enzyme activities was found. Both combinations above promoted gene expression of CAT and SOD enzymes and the ratio 1:1 exhibited the strongest synergy., Conclusions: Antioxidant activity results in MTS further confirmed the significant synergy of C-3 combined with EGb and isorhamnetin combined with caffeic acid. The synergy of C-3 combined with EGb may be attributed to the combination of isorhamnetin + caffeic acid, which promoted CAT and SOD enzyme gene expression and further promoted the enzyme activities in E. coli. This study could further provide rational basis for optimizing the physiological bioavailability of P. fruticosa by using natural and safe antioxidants in low doses to produce new medicines and functional products.

The objective of the present study was to investigate the effects of dietary supplemental Zinc (Zn) source and level on antioxidant ability and fat metabolism-related enzymes of broilers. Dietary treatments included the Zn-unsupplemented corn-soybean meal basal diet (control) and basal diets supplemented with 60, 120, or 180 mg Zn/kg as Zn sulfate, Zn amino acid chelate with a weak chelation strength of 6.5 quotient of formation (Qf) (11.93% Zn) (Zn-AA W), Zn proteinate with a moderate chelation strength of 30.7 Qf (13.27% Zn) (Zn-Pro M), or Zn proteinate with an extremely strong chelation strength of 944.0 Qf (18.61% Zn) (Zn-Pro S). The results showed that dietary supplemental Zn increased (P < 0.01) Zn contents in the liver, breast, and thigh muscles of broilers, and up-regulated mRNA expressions of copper and Zn containing superoxide dismutase (CuZnSOD) and metallothioneins (MT) in the liver (P < 0.01) and thigh muscle (P < 0.05), and also enhanced (P < 0.05) CuZnSOD activities in the breast and thigh muscles, which exerted antioxidant ability and a decreased malondialdehyde (MDA) level in the liver (P < 0.01) and breast and thigh muscles (P < 0.05) of broilers. Furthermore, supplemental Zn increased activities of malate dehydrogenase (MDH) and lipoprotein lipase (LPL) in the abdominal fat (P < 0.05), and fatty acid synthetase (FAS) and LPL in the liver (P < 0.01), which were accompanied with up-regulation (P < 0.01) of the mRNA expressions levels of these enzymes in the abdominal fat and liver of broilers. Dietary Zn source, and an interaction between Zn source and level, had no effects on any measurements. It is concluded that dietary Zn supplementation improved Zn status and resulted in promoting antioxidant ability and activities and gene expressions of fat metabolism-related enzymes of broilers regardless of Zn source and level, and the addition of 60 mg Zn/kg to the corn-soybean meal basal diet (a total dietary Zn of approximately 90 mg/kg) was appropriate for improving the above aspects of broilers., (© The Author 2015. Published by Oxford University Press on behalf of Poultry Science Association.)

The present study demonstrates the effect of DHPEA on suppression of irradiation-induced pulmonary fibrosis. A (60)Co irradiator was used to induce pulmonary fibrosis in a rat model at a dose of 22 Gy. The rats of the treatment and positive control group were intraperitoneally injected DHPEA (10 mg/kg) or dexamethasone (DEX; 5 mg/kg) daily for 30 days. Hydroxyproline assay was used to evaluate the fibrosis of pulmonary and lung tissue sections after irradiation. Hematoxylin and eosin (H&E) and Masson's trichrome stained lung section were used for alveolitis and fibrosis score analyses, respectively. Immunohistochemistry was used for surfactant protein-B (SPB) and α-SMA expression analysis. Western blot analysis was employed for analysis of nuclear transcription factor NF-E2-related factor 2 (Nrf-2) and its associated antioxidant enzymes like heme oxygenase-1 (HO-1) and NAD (P) H: quinone oxidoreductase-1 (NQO-1). Results revealed a significant decrease in mortality rates and lung index scores, decreased collagen deposition, reduced MDA content and enhanced superoxide dismutase (SOD) activity in DHPEA treated rats compared to DEX-treated rats. DHPEA treatment also inhibited (myo) fibroblast proliferation, and regulated serum levels of TGF-β1, IL-6, IL-10, and TNF-α. In addition, DHPEA-treatment activated Nrf-2 and its downstream antioxidant enzymes HO-1 and NQO-1. Thus DHPEA can be a promising agent for the suppression of irradiation-induced pulmonary fibrosis.

The effects of NaCl stress on the activity of antioxidant enzymes, lipid peroxidation, cell membrane stability, net photosynthetic rate, gas-exchange, and chlorophyll content were investigated in two Jerusalem artichoke cultivars, Dafeng (salt-tolerant) and Wuxi (salt-sensitive), grown under control (nutrient solution) or salt stress (nutrient solution containing 75, 150, and 225 mM NaCl) conditions for 7 days. In leaves of salt-tolerant cv. Dafeng, superoxide dismutase (EC 1.15.1.1), peroxidase (EC 1.11.1.7), and catalase (EC 1.11.1.6) activities significantly increased as compared to the controls, whereas no significant change was observed in cv. Wuxi. Lipid peroxidation and cell membrane injury were enhanced in both cultivars. Net photosynthesis and stomatal conductance decreased in response to salt stress, but cv. Dafeng showed a smaller reduction in photosynthesis than cv. Wuxi. The results indicated that stomatal aperture limited leaf photosynthetic capacity in the NaCl-treated plants of both cultivars. However, significant reduction in the leaf chlorophyll content due to NaCl stress was observed only in cv. Wuxi. These results suggested that salt-tolerant Jerusalem artichoke varieties may have a better protection against reactive oxygen species, at least in part, by increasing the activity of antioxidant enzymes under salt stress. [ABSTRACT FROM AUTHOR]