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Abstract: Spontaneous leiomyomas of the oviduct are common tumors of the Japanese quail (Coturnix coturnix japonica), and fibroid tumors in the laying hen are similar to human fibroid tumors with respect to estrogen and progesterone receptors. This makes the quail a good animal model for screening potential agents for that aid in the prevention and treatment of human myoma uteri. We have previously reported a decreased incidence of leiomyomas in the oviduct of Japanese quail with antioxidant supplementation, for example, lycopene and soy isoflavones. Most of the health benefits associated with green tea consumption is attributed to EGCG, one of 4 major catechins found in green tea. This study investigated the effects of epigallocatechin-3-gallate supplementation on the development of leiomyomas in the oviduct of Japanese quail. We also measured serum and tissue levels of malondialdehyde and TNF-α. One hundred eighty quail (8 months old) were assigned to 3 treatment groups consisting of 6 replicates of 10 quail in each group. Animals were fed either a basal diet (control group) or the basal diet supplemented with 200 or 400 mg of EGCG/kg of diet. The animals were euthanized at the end of the 12-month study period, and the tumors were characterized. Epigallocatechin gallate supplementation significantly decreased the number of leiomyomas as compared with the controls (P = .001). The tumors in the EGCG fed birds were smaller than those found in the control birds (P = .001). Serum and liver malondialdehyde and TNF-α concentrations decreased (P = .001) with EGCG supplementation. The results indicate that dietary supplementation with EGCG reduces the incidence and size of spontaneously occurring leiomyoma of the oviduct in Japanese quail. Clinical trials should be conducted to investigate the efficacy of EGCG supplementation in the prevention and treatment of uterine leiomyoma in humans. [Copyright &y& Elsevier]

The objective of this study was to investigate the effects of different chromium histidinate (CrHis) complexes added to the diet of rats fed a high-fat diet (HFD) on body weight changes, glucose and lipid metabolism parameters, and changes in biomarkers such as PPAR-γ, IRS-1, GLUTs, and NF-κB proteins. Forty-two Sprague–Dawley rats were divided equally into six groups and fed either a control, an HFD, or an HFD supplemented with either CrHis1, CrHis2, CrHis3, or a combination of the CrHis complexes as CrHisM. Feeding an HFD to rats increased body weights, HOMA-IR values, fasting serum glucose, insulin, leptin, free fatty acid, total cholesterol, low-density lipoprotein cholesterol, and MDA concentrations as well as AST activities, and decreased serum and brain serotonin concentrations compared with rats fed a control diet (P < 0.0001). The levels of the PPAR-γ, IRS-1, and GLUTs in the liver and brain decreased, while NF-κB level increased, with feeding an HFD (P < 0.05). Although all the CrHis supplements reversed the negative effects of feeding an HFD (P < 0.05), the CrHis1 complex was most effective in changing the protein levels, while CrHisM was most effective in influencing certain parameters such as body weight and serum metabolites. The results of the present work suggest that the CrHis1 complex is most potent for alleviating the negative effects of feeding an HFD. The efficacy of CrHisM is likely due to the presence of the CrHis1 complex. [ABSTRACT FROM AUTHOR]

Chromium picolinate (CrPic) is commonly used to reduce muscle fatigue after exercise. We aimed to elucidate the effects of CrPic on glucose and lipid metabolism and the expression of glucose transporters in exercised rats. Forty-two male Wistar rats (8-week-old) were distributed into six groups (n = 7) as follows: Control, CrPic, Chronic Exercise (CEx), CEx + CrPic, Acute Exercise (AEx), and AEx + CrPic. CEx consists of 30 m/min, 30 min/day, and 5 days/week for 6 weeks. CrPic was supplemented at 400 μg elemental Cr/kg of diet for 6 weeks. In the AEx groups, animals were run on the treadmill at 30 m/min until exhaustion. CEx significantly lowered blood glucose (BG), total cholesterol (TC) and triglyceride (TG) levels, but elevated insulin concentration (IC), compared with control (P < 0.05). CEx significantly decreased the level of malondialdehyde (MDA) in the serum, liver, and muscle while AEx elevated it (P < 0.001 for all). CrPic significantly decreased BG, TC, TG levels, and increased IC with a remarkable effect in CEx rats (P < 0.01). CrPic also significantly reduced serum, liver, and muscle MDA levels (P < 0.001). Both AEx and CEx increased the expression of liver glucose transporter 2 (GLUT-2) and muscle GLUT-4 with the highest level in CEx rats (P < 0.05). Moreover, CrPic supplementation significantly elevated GLUT-2 and GLUT-4 expressions in the liver and muscle of sedentary and exercise-treated rats (P < 0.05). CrPic improves various metabolic parameters and reduces oxidative stress in CEx and AEx rats by decreasing BG, TC, TG, MDA levels in serum and elevating GLUT-2 and GLUT-4 expression in the liver and muscle samples. The efficacy of CrPic was more pronounced in CEx rats. [ABSTRACT FROM AUTHOR]

Background and Aims Despite it being a highly potent antineoplastic drug, cisplatin has important toxic adverse effects limiting its use such as nephrotoxicity, neurotoxicity and ototoxicity. It is thought that cisplatin-induced hepatotoxicity is caused by oxidative stress resulting from increased reactive oxygen species (ROS). Apocynin (APO) exerts its antioxidant effect by reducing ROS production via inhibition of NADPH oxidase. The present study intended to demonstrate effects of cisplatin on hepatic pro-oxidant/antioxidant systems and to investigate protective effects of APO against cisplatin-induced hepatotoxicity. Methods Rats were randomly assigned into four groups ( n = 8 each): a) control group; b) single dose of cisplatin (5 mg/kg); c) APO group (20 mg/kg on three consecutive days; i.p.); and d) APO plus cisplatin group. Liver tissue was assessed in all groups by biochemical and histopathological means. Also, serum alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase levels were studied in all groups. Results When cisplatin group was compared to controls, it was seen that lipid peroxidation product, total oxidant status and ALT levels were markedly increased, whereas superoxide dismutase and glutathione peroxidase levels were overtly decreased. APO therapy markedly prevented cisplatin-induced harmful changes in liver. Our histopathological findings such as central vein dilatation, perivenuler and periportal sinusoidal dilatation, parenchymal inflammation, vacuolar changes in hepatocytes, biliary duct proliferation and caspase-3 positive hepatocytes were in accordance with the biochemical changes. Conclusion In light of these results, it is our thought that APO has a protective role against cisplatin-induced hepatotoxicity at both biochemical and histopathological levels. [ABSTRACT FROM AUTHOR]

Abstract: Cisplatin is used against various types of solid tumors. However, its use is limited by its nephrotoxicity, with about 25–35% patients experiencing a significant decline in renal function after a single dose of cisplatin. This study reports that lycopene mitigates the nephrotoxic effect of cisplatin in rat through Nrf2-mediated induction of heme oxygenase-1 (HO-1). Eight weeks old male rats (200–215g) were supplemented with lycopene complex containing 6% lycopene, 1.5% tocopherols, 1% phytoene and phytofluene, and 0.2% β-carotene for 10days at a dose level of 6mg/kgbw, followed by a single i.p. injection of cisplatin (7mg/kgbw). Western blot analysis of renal Nrf2, HO-1 and NF-κB p65 showed that cisplatin-induced decrease in the levels of Nrf-2 and HO-1 was counteracted by lycopene. On the other hand, cisplatin mediated increase in NF-κB p65 was brought down by lycopene. Lycopene supplementation is reported to significantly improve the changes associated with cisplatin nephrotoxicity, as also evident by increased level of antioxidant enzymes. The study suggests that Nrf2/HO-1 signaling pathway may be the prime target for chemoprevention of cisplatin-induced nephrotoxicity by lycopene, and reduces inflammation by inhibiting NF-κB. Correlation between NF-κB and Nrf2 is discussed. [Copyright &y& Elsevier]

Abstract: Lycopene, a carotenoid present predominantly in tomatoes, is one of the most efficient antioxidants. This experiment was conducted to evaluate the effects of dietary lycopene supplementation on performance, carcass characteristics, biomarkers of oxidative stress (malondialdehyde (MDA) and homocysteine), and concentrations of vitamins C, E, A, cholesterol, triglyceride, and glucose in Japanese quails (Coturnix coturnix Japonica) exposed to high-ambient temperature of 34°C. Two hundred and forty Japanese quails (10day-old) were randomly assigned to eight treatment groups consisting of 10 replicates of three birds. The birds were kept at a temperature-controlled room at 22°C (Thermoneutral, TN groups) or 34°C (for 12h/day; 09.00am–05.00pm; Heat stress, HS groups). Birds were fed either a basal (control) diet (TN and HS) or the basal diet supplemented with 50, 100 or 200mg of lycopene/kg of diet. Lycopene supplementation linearly increased feed intake (), live weight gain (), feed efficiency () and cold carcass weight () and yield () under heat stress conditions but did not show the same effect at thermoneutral conditions (). The interaction Serum vitamin C, E, and A () concentrations increased linearly in birds reared at high temperature while non-significant changes occurred at TN groups. Homocysteine level in serum and malondialdehyde (MDA) levels in serum, liver, and heart () linearly decreased in all birds of both TN and HS groups as dietary lycopene supplementation increased. Heat stress-induced increase in serum cholesterol (), triglycerides () and glucose () concentrations were linearly reversed by lycopene supplementation. Supplementation of lycopene increased the HDL concentration whereas, the VLDL and LDL concentrations reduced with lycopene supplementation (, linear), particularly at a dietary concentration of 200mg/kg. Lycopene could not be detected in control birds while a linear increase was observed in the sera of lycopene supplemented birds The results of the study indicate that lycopene supplementation attenuated the increase in oxidative stress and depletion in antioxidants caused by heat stress in Japanese quails. [Copyright &y& Elsevier]

This study was conducted to examine the effects of dietary taurine supplementation on productive performance, nutrient digestibility, antioxidant status, and the gene expression of ileal nutrient transporters in laying quails reared under heat stress (HS). One hundred and eighty laying Japanese quails (Coturnix coturnix japonica) were fed a basal diet or basal diet supplemented with either 2.5 or 5 g of taurine per kg of diet, and reared at either 22 ± 2 °C for 24 h/d (thermoneutral, TN) or 34 ± 2 °C for 8 h/d (HS) for 12 weeks. The quails reared under HS consumed less feed, produced less egg, and had lower dry matter, organic matter and crude protein apparent digestibilities compared with the quails reared under the TN condition (P = 0.001). However, increasing taurine concentrations in the diet improved feed intake and egg production (P = 0.001), but also the apparent digestibilities (P ≤ 0.027) in quails reared under HS. The greater doses (5 g/kg) of taurine resulted in more responses. The quails reared under HS had greater serum and liver MDA concentrations (P = 0.0001) which decreased with dietary taurine supplementations, particularly greater doses. The gene expressions of ileal PEPT1, EAAT3, CAT1, CAT2, SGLT1, SGLT5, GLUT2, and GLUT5 decreased under HS conditions (P = 0.001). However, supplementing taurine, in a dose-dependent fashion, to the diet of quails reared under HS resulted in increases in the gene expressions of the transporters (P < 0.05) except for CAT1. The results of the present work showed that taurine supplementation, particularly with greater doses (5 g/kg), to the diet of laying quails kept under HS acts as alleviating negative effects of HS, resulting in improvements in productive performance and nutrient digestion, and also upregulation of ileal nutrient transporters. • Heat stress causes economic loses in poultry. • One of the ways to overcome heat stress is to add antioxidant feed additives to the diet. • Taurine supplementation improves live performance, digestion and gene expression of nutrient transporters. • Taurine with its antioxidant properties has alleviating effects on heat stress. [ABSTRACT FROM AUTHOR]

Abstract The purpose of this study was to test the effects of arginine-silicate-inositol complex (ASI), compared to a combination of the individual ingredients (A+S+I) of the ASI, on inflammatory markers and joint health in a collagen-induced arthritis (CIA) rat model. A total of 28 Wistar rats were divided into four groups: (i) Control; (ii) Arthritic group, rats subjected to CIA induction by injection of bovine collagen type II (A); (iii) Arthritic group treated with equivalent doses of the separate components of the ASI complex (arginine hydrochloride, silicon, and inositol) (A+S+I); (iv) Arthritic group treated with the ASI complex. The ASI complex treatment showed improved inflammation scores and markers over the arthritic control and the A+S+I group. ASI group had also greater levels of serum and joint-tissue arginine and silicon than the A+S+I group. Joint tissue IL-6, NF-κB, COX-2, TNF-α, p38 MAPK, WISP-1, and β-Catenin levels were lower in the ASI group compared to the other groups (P < 0.05 for all). In conclusion, these results demonstrate that the ASI complex may be effective in reducing markers of inflammation associated with joint health and that the ASI complex is more effective than a combination of the individual ingredients. Highlights • Rheumatoid arthritis (RA) is the leading cause of major disability. • Arginine silicate inositol (ASI) has beneficial effects on vascular and bone health. • ASI shows anti-inflammatory effects by modulation of NF-κB pathway. [ABSTRACT FROM AUTHOR]

The aim of this experiment was to determine the effects of β-cryptoxanthin (BCX) on the cardiometabolic health risk factors and NF-κB and Nrf2 pathway in insulin resistance induced by high-fat diet (HFD) in rodents. Twenty-eight Sprague-Dawley rats were allocated into four groups: (1) Control, rats fed a standard diet for 12 weeks; (2) BCX, rats fed a standard diet and supplemented with BCX (2.5 mg/kg BW) for 12 weeks; (3) HFD, rats fed a HFD for 12 weeks, (4) HFD + BCX, rats fed a HFD and supplemented with BCX for 12 weeks. BCX reduced cardio-metabolic health markers and decreased inflammatory markers ( P < 0.001). Rats fed a HFD had the lower total antioxidant capacity and antioxidant enzymes activities and higher MDA concentration than control rats ( P < 0.001 for all). Comparing with the HFD group, BCX in combination with HFD inhibited liver NF-κB and TNF-α expression by 22% and 14% and enhanced liver Nrf2, HO-1, PPAR-α, and p-IRS-1 by 1.43, 1.41, 3.53, and 1.33 fold, respectively ( P < 0.001). Furthermore, in adipose tissue, BCX up-regulated Nrf2, HO-1, PPAR-α, and p-IRS-1 expression, whereas, down-regulated NF-κB and TNF-α expression. In conclusion, BCX decreased visceral fat and cardiometabolic health risk factors through modulating expressions of nuclear transcription factors. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a musculoskeletal disorder mainly found in elderly individuals. Modern treatment of OA, like nonsteroidal anti-inflammatory drugs, corticosteroids, hyaluronic acid injections, etc., is linked to long-term side effects. We evaluated the anti-osteoarthritic properties of a novel joint health formula (JHF) containing Bisdemethoxycurcumin enriched curcumin, 3-O-Acetyl-11-keto-beta-Boswellic acid-enriched Boswellia , and Ashwagandha in monosodium iodoacetate (MIA)‐induced knee OA in rats. Twenty-eight female rats were distributed into four groups: Control, OA, OA + JHF (100 mg/kg), and OA + JHF (200 mg/kg). JHF decreased the right joint diameters but increased the paw area and stride length compared to the OA group with no treatment. JHF significantly reduced the arthritic conditions after four weeks of supplementation (p < 0.05). JHF significantly decreased TNF-α, IL-1β, IL-10, COMP, and CRP in the serum of osteoarthritic rats (p < 0.0001). We observed reduced lipid peroxidation but increased SOD, GSH-Px, and CAT activities in response to JHF treatment in OA animals. JHF down-regulated MMP-3, COX-2, and LOX-5 and improved the histological structure of the knee joint of osteoarthritic rats. JHF demonstrated a protective effect against osteoarthritis, possibly due to anti-inflammatory and antioxidant activity in experimentally induced osteoarthritis in rats, and could be an effective option in the management of OA. • Osteoarthritis (OA) is a type of arthritis commonly found in elderly patients. • Joint health formula (JHF) has antioxidant, and anti-inflammatory effect. • JHF reduced the arthritic conditions after four weeks of supplementation. • JHF significantly decreased expression of pro-inflammatory cytokines. [ABSTRACT FROM AUTHOR]

Abstract: Aims: This experiment investigated if chromium (Cr) as Cr-histidinate (CrHis) and Cr29 picolinate (CrPic) have a protective role in rats with hypoglycemia-induced brain injury, assessed by neuronal plasticity and regeneration potential. Main methods: Male Sprague–Dawley rats were prospectively divided into 2 groups: control and hypoglycemic (induced by insulin administration, 15U/kg, i.p., n=56). Hypoglycemic rats were then received randomly 1) none, 2) dextrose (on the day of sampling), 3) CrHis, or 4) CrPic. Cr-chelates were delivered via drinking water (providing 8μg elemental Cr per day) for one week prior to the hypoglycemia induction. The expressions of neuroplasticity markers [neural cell adhesion molecule (NCAM), growth-associated protein-43 (GAP-43), glial fibrillary acidic protein (GFAP)], glucose transporters (GLUT), and nuclear transcription proteins [nuclear factor-kappa (NF-κB), nuclear factor (erythroid-derived 2)-like 2 (Nrf2), and 4-hydroxyl nonenal (HNE)] were determined using Western blot. Key findings: Hypoglycemia caused increases in the expressions of GLUT-1, GLUT-3, GFAP, NF-κB and HNE and decreases in the expression of NCAM's, GAP-43 and Nrf2 in the hippocampus, cerebellum, and cortex. Cr-chelates suppressed expressions of GLUTs, GFAP, NF-κB and HNE expressions and enhanced expressions of NCAM, GAP-43 and Nrf2, which were more notable for CrHis than for CrPic. Significance: In conclusion, hypoglycemia leads to cerebral injury and Cr-chelates, particularly CrHis have protective and regeneration potential in cerebral tissues through modulating neuroplasticity markers and nuclear transcription proteins as well as facilitating glucose transporters. [Copyright &y& Elsevier]

Abstract: Aims: Cisplatin-induced nephrotoxicity is associated with increased oxidative stress and inflammatory cytokines in the kidney. Epigallocatechin-3-gallate (EGCG) has anti-oxidant, anti-inflammatory, and anti-tumorigenic properties. In this study, we investigated the effects of EGCG on cisplatin-induced nephrotoxicity and potential mechanisms by which it enhances antioxidant activities and resolves inflammation after EGCG treatment during cisplatin-induced nephrotoxicity. Main methods: Twenty-eight rats were divided into four groups as control (group 1; no treatment; n=7), EGCG (group 2; n=7), cisplatin (group 3; n=7) or cisplatin and EGCG (group 4; n=7). After 2days of EGCG treatment at a dose of l00mg/kg BW, rats were treated with a single i.p. injection of cisplatin (7mg/kg BW). On day 12 (10days after the cisplatin treatment), all rats were sacrificed by cervical dislocation. The level of protein was examined by Western blotting. Key findings: Cisplatin caused a significant decrease in the expression nuclear levels of NF-E2-related factor-2 (Nrf2), heme oxygenase-1(HO-1), and an increase in the levels of nuclear factor-kappa B (NF-κB p65) and 4-hydroxynonenal (HNE) an oxidative stress marker. EGCG supplementation significantly improved the changes associated with cisplatin nephrotoxicity by increasing levels of Nrf-2 and HO-1, and decreasing levels of NF-κB and HNE. Renal activities of antioxidant enzymes (catalase, superoxide dismutase, glutathione peroxidase) and glutathione were significantly lower in cisplatin-treated rats compared with control rats, and EGCG treatment significantly increased the activities of antioxidant enzymes and glutathione (P <0.001). Significance: The results suggest that Nrf2/HO-1 signaling pathway may be the primary target for prevention of cisplatin-induced nephrotoxicity by EGCG, and that reduces it inflammation by inhibiting NF-κB. [ABSTRACT FROM AUTHOR]