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The purpose of this study was to observe the effects of a novel combination of inositol-stabilized arginine silicate complex (ASI) and magnesium biotinate (MgB) on the prevention of skin damage after UVB exposure in rats. Forty-nine Sprague-Dawley rats were randomized into one of the following groups: (1) NC, normal control, (2) SC, shaved control, (3) UVB (exposed to UVB radiation), (4) ASI+MgB-L (Low Dose), (5) ASI+MgB-H (High Dose), (6) ASI+MgB-L+MgB cream, (7) ASI+MgB-H+MgB cream. The results showed that ASI+MgB treatment alleviated the macroscopic and histopathological damages in the skin of rats caused by UVB exposure. Skin elasticity evaluation showed a similar trend. ASI+MgB increased serum Mg, Fe, Zn, Cu, Si, biotin, and arginine concentrations and skin hydroxyproline and biotinidase levels while decreasing skin elastase activity (p < 0.05) and malondialdehyde (MDA) concentration (p < 0.001). Moreover, ASI+MgB treatment increased skin levels of biotin-dependent carboxylases (ACC1, ACC2, PC, PCC, MCC) and decreased mammalian target of rapamycin (mTOR) pathways and matrix metalloproteinase protein levels by the regulation of the activator protein 1 (AP-1), and mitogen activated protein kinases (MAPKs) signaling pathways. In addition, ASI+MgB caused lower levels of inflammatory factors, including TNF-α, NFκB, IL-6, IL-8, and COX-2 in the skin samples (p < 0.05). The levels of Bax and caspase-3 were increased, while anti-apoptotic protein Bcl-2 was decreased by UVB exposure, which was reversed by ASI+MgB treatment. These results show that treatment with ASI and MgB protects against skin damage by improving skin appearance, elasticity, inflammation, apoptosis, and overall health.

Retinal damage associated with loss of photoreceptors is a hallmark of eye diseases such as age-related macular degeneration (AMD) and diabetic retinopathy. Potent nutritional antioxidants were previously shown to abate the degenerative process in AMD. β-Cryptoxanthin (BCX) is an essential dietary carotenoid with antioxidant, anti-inflammatory, and provitamin A activity. It is a potential candidate for developing intervention strategies to delay the development/progression of AMD. In the current study, the effect of a novel, highly purified BCX oral formulation on the rat retinal damage model was evaluated. Rats were fed with BCX for four weeks at the doses of 2 and 4 mg/kg body weight in the form of highly bioavailable oil suspension, followed by retinal damage by exposing to the bright light-emitting diode (LED) light (750 lux) for 48 hrs. Animals were sacrificed after 48 hours, and eyes and blood samples were collected and analyzed. BCX supplementations (2 and 4 mg/kg) showed improvements in the visual condition as demonstrated by histopathology of the retina and measured parameters such as total retinal thickness and outer nuclear layer thickness. BCX supplementation helped reduce the burden of oxidative stress as seen by decreased serum and retinal tissue levels of malondialdehyde (MDA) and restored the antioxidant enzyme activities in BCX groups. Further, BCX supplementation modulated inflammatory markers (IL-1β, IL-6, and NF-κB), apoptotic proteins (Bax, Bcl-2, caspase 3), growth proteins and factors (GAP43, VEGF), glial and neuronal proteins (GFAP, NCAM), and heme oxygenase-1 (HO-1), along with the mitochondrial stress markers (ATF4, ATF6, Grp78, Grp94) in the rat retinal tissue. This study indicates that oral supplementation of BCX exerts a protective effect on light-induced retinal damage in the rats via reducing oxidative stress and inflammation, also protected against mitochondrial DNA damage and cellular death.

OBJECTIVES: The objective of this work was to investigate the effects of dietary supplementation of purified lycopene (LYC) or a source of LYC as in tomato powder (TP) on live hen performance, egg yolk cholesterol concentrations as well as the gene expressions related to mechanism and regulation of cholesterol, namely Niemann-Pick C1-like 1 protein (NPC1L1), acyl-CoA: cholesterol acyltransferase 2 (ACAT2), microsomal triacylglycerol transport protein (MTP), ATP binding cassette transporters sub-family G member 5 and 8 (ABCG5/8), ATP citrate lyase (ACLY), liver X receptor alpha (LXRα) and sterol regulatory element-binding proteins (SREBP1c). METHODS: A total of 150 20-week-old white laying hens were divided into one of 3 treatments, with 10 replicates of 5 hens per cage, totaling 50 hens per treatment. The birds were fed either a basal diet (Control) or basal diet supplemented with 20 mg purified lycopene/kg diet (LYC) or an equal amount of lycopene-containing tomato powder (TP) for 12 weeks. RESULTS: Feed intake, egg production and feed conversion ratio remained similar among treatments (P ≥ 0.27). However, egg weights from hens fed a diet supplemented with lycopene particularly the purified form were greater (P = 0.036). Supplementing lycopene either purified or as in TP increased the concentrations of serum and egg yolk lycopene but decreased serum and egg yolk cholesterol concentrations (P

Background A previous clinical study reported that the addition of an amylopectin/chromium complex (ACr; Velositol®) to 6 g of whey protein (WP) significantly enhanced muscle protein synthesis (MPS). Branched-chain amino acids (BCAAs) are also well-known to enhance MPS. The aim of this study was to determine if the addition of ACr to BCAAs can enhance MPS and activate expression of the mammalian target of the rapamycin (mTOR) pathway compared to BCAAs and exercise alone in exercise-trained rats. Methods Twenty-four male Wistar rats were randomly divided into three groups (n = 8 per group): (I) Exercise control, (II) Exercise plus BCAAs (0.465 g/kg BW, a 6 g human equivalent dose (HED)), and (III) Exercise plus BCAAs (0.465 g/kg BW) and ACr (0.155 g/kg BW, a 2 g HED). All animals were trained with treadmill exercise for 10 days. On the day of the single-dose experiment, rats were exercised at 26 m/min for 2 h and then fed, via oral gavage, study product. One hour after the consumption of study product, rats were injected with a bolus dose (250 mg/kg BW, 25 g/L) of phenylalanine labeled with deuterium to measure the fractional rate of protein synthesis (FSR). Ten minutes later, muscle tissue samples were taken to determine MPS measured by FSR and the phosphorylation of proteins involved in the mTOR pathway including mTOR, S6K1, and 4E-BP1. Results ACr combined with BCAAs increased MPS by 71% compared to the exercise control group, while BCAAs alone increased MPS by 57% over control (p

The objective of this work is to investigate the effects of Carnipure® Tartrate (CT) supplementation with or without exercise on endurance capacity, recovery, and fatigue by assessing time to exhaustion as well as body weight and composition in rats. In addition, antioxidant capacity has been evaluated by measuring malondialdehyde (MDA) levels and antioxidant enzyme (superoxide dismutase, SOD, catalase, CAT, glutathioneperoxidase, GSHPx) activities. Fifty-six male Wistar rats were divided into eight groups including seven rats each. A control group did not receive CT nor exercise. Another control group received 200 mg/kg CT without exercise. The other six groups of rats went through an exercise regimen consisting of a 5-day training period with incremental exercise capacity, which was followed by 6 weeks of the run at 25 m/min for 45 min every day. CT was supplemented at 0, 25, 50, 100, 200, and 400 mg/kg per day during the 6 weeks. Rats submitted to exercise and supplemented with CT had a significant and dose-dependent increase in time to exhaustion and this effect seems to be independent of exercise (p &lt, 0.05). Additionally, recovery and fatigue were improved, as shown by a significant and dose-dependent decrease in myoglobin and lactic acid plasma levels, which are two markers of muscle recovery. CT supplementation led to a dose-response decrease in body weight and visceral fat. These effects become significant at 200 and 400 mg/kg doses (p &lt, 0.05). Additionally, the antioxidant capacity was improved, as shown by a significant and dose-dependent increase in SOD, CAT, and GSHPx. Serum MDA concentrations decreased in exercising rats with CT supplementation. CT supplementation led to a decrease in serum glucose, triglycerides, and total cholesterol concentrations with the lowest levels observed at 400 mg/kg dose (p &lt, 0.05). These effects correlated with a significant dose-dependent increase in serum total L-carnitine, free L-carnitine, and acetyl-carnitine, which linked the observed efficacy to CT supplementation. These results demonstrate that CT supplementation during exercise provides benefits on exercise performance, recovery, and fatigue as well as improved the lipid profile and antioxidant capacity. The lowest dose leads to some of these effects seen in rats where 25 mg/kg corresponds to 250 mg/day as a human equivalent.

BACKGROUND: The purpose of the present study was to examine the chemopreventive effect of Stampidine, an aryl phosphate derivative of stavudine, in side by side comparison with the standard anti-breast cancer drug paclitaxel in the well-established 7,12-dimethylbenz(a)anthracene (DMBA)-induced murine breast cancer model. METHODS: Groups of 20 female mice were challenged with the chemical carcinogen DMBA. DMBA-challenged mice were assigned to various chemoprevention treatments, including stampidine alone, paclitaxel alone, and stampidine plus paclitaxel according to the same treatment schedules for 25 weeks. RESULTS: Stampidine treatments resulted in substantially reduced numbers of mammary tumors, tumor weight as well as tumor size in DMBA-treated mice. Stampidine was as effective as paclitaxel in the model and their combination exhibited greater chemopreventive activity, as measured by reduced tumor incidence and improved tumor-free survival as well as overall survival of DMBA-treated mice. The length of time for the initial tumor to appear in DMBA-challenged mice treated with stampidine was longer than that of mice treated DMBA-challenged control mice. Tumors from mice treated with stampidine or stampidine plus paclitaxel displayed unique changes of a signature protein cassette comprised of BRCA1, p21, Bax, and Bcl-2. CONCLUSION: Stampidine has potent chemopreventive activity and is as effective as the standard chemotherapy drug paclitaxel in the chemical carcinogenesis model of DMBA-induced murine breast cancer.

Scope To investigate the effects of chromium histidinate (CrHis) and chromium picolinate (CrPic) complex along with biotin to a high‐fat diet (HFD) fed to rats on the insulin sensitivity and the anti‐obesity properties. Methods Forty‐two Sprague–Dawley male rats were divided into six groups. The rats were fed either (a): a standard diet (Control) or (b): a HFD or (c): a HFD with biotin (HFD+B) or (d): a combination of HFD and biotin along with CrPic (HFD + B + CrPic) or (e): a combination of HFD and biotin along with CrHis (HFD + B + CrHis) or (f): a combination of HFD and biotin along with CrHis and CrPic (HFD + B + CrHis + CrPic). Results Adding biotin with chromium to HFD improved the glucose, insulin, HOMA‐IR, leptin, lipid profile, with HFD+B+CrHis treatment being the most effective (p = 0.0001). Serum, liver, and brain tissue Cr concentrations increased upon Cr supplementations (p = 0.0001). Supplementing CrHis along with biotin to a HFD (HFD + B + CrHis) provided the greatest levels of GLUT‐1, GLUT‐3, PPAR‐γ, and IRS‐1, but the lowest level of NF‐κB in the brain and liver tissues. Conclusion Biotin supplementation with chromium complexes, CrHis in particular, to a HFD pose to be a potential therapeutic feature for the treatment of insulin resistance.

Objective This study investigated the protective effects of magnesium biotinate (MgB) on propionic acid (PPA)-induced autistic features in rats. Background Biotin is involved in energy metabolism and various immune and nerve functions. MgB is a novel biotin complex that has enhanced absorption. Compared to D-Biotin, MgB has superior tissue uptake and anti-inflammatory effects. Neurological problems can occur in biotin-deficient individuals. Supplementation with MgB may prevent or reduce neurodevelopmental disorders such as those seen in autism spectrum disorder. Design/Methods Thirty-five male Wistar rats (3 weeks old) were randomized into the following five groups; 1: Control (received saline), 2: PPA alone, 3: PPA + 10 mg human equivalent dose (HED) MgB, 4: PPA + 100 mg HED MgB, 5: PPA + 500 mg HED MgB. Animals were fed a standard diet, with or without MgB, for 35 days and on day 30, rats were administered PPA (500 mg/kg BW/day) by subcutaneous injection for 5 days. Neurobehavioral tests were then performed for two days. Serum and tissue samples were then collected for analysis. Results Social interaction deficits and signs of brain toxicity, including higher brain levels of inflammatory and oxidative stress markers, were observed in PPA alone rats. Brain levels of inflammatory markers were lower in all MgB groups compared to PPA alone (p

The present study was undertaken to investigate the effect of the combination of soy protein, amylopectin, and chromium (SAC) on muscle protein synthesis and signal transduction pathways involved in protein synthesis (mTOR pathways, IGF-1, and Akt(Ser473)) and proteolysis (FOXO1(Ser256); MURF1, MAFbx) after exercise. Thirty-five Wistar rats were randomly divided into five groups: (1) control (C); (2) exercise (E); (3) exercise + soy protein (3.1 g/kg/day) (E + S); (4) exercise + soy protein + chromium (E + S + Cr); (5) exercise + soy protein + amylopectin + chromium (E + S + A + Cr). Post-exercise ingestion of SAC significantly increased the fractional rate of protein synthesis (FSR), insulin, glycogen, and amino acid levels with the highest effect observed in E + S + A + Cr group (P < 0.05). However, SAC supplementation decreased the lactic acid concentration (P < 0.05). A reduction in forkhead box protein O1 (FOXO1) and forkhead box protein O3 (FOXO3) (regulators of ubiquitin-related proteolysis) and muscle atrophy F-box (MAFbx) levels was noted after treatment with SAC (P < 0.05). Insulin-like growth factor 1(IGF-1) level was increased in the E + S, E + S + Cr, and E + S + A + Cr groups (P < 0.05). While the phosphorylation of 4E-BP1(Thr37/46), Akt(Ser473), mTOR(Ser2448), and S6K1(Thr389) levels increased after SAC supplementation, phosphorylated muscle ring finger 1 (MuRF-1, an E3-ubiquitin ligase gene) was found to be significantly lower compared with the E group (P < 0.05). These results indicate that SAC supplementation improves FSR, insulin, and glycogen levels after exercise. SAC improves protein synthesis by inhibiting the ubiquitin-proteasome pathway and inducing anabolic metabolism.

OBJECTIVES: Skin appearance and function begin to decline as humans age due to physiological changes as well as external factors such as prolonged sun exposure and inadequate nutrient intake. Replenishing the body with nutrients such as silicon and biotin has been shown to improve skin appearance. JDS-ASB is a novel combination of inositol-stabilized arginine silicate complex (ASI), a highly bioavailable form of arginine and silicon, and magnesium biotinate (MgB), a novel, well-absorbed biotin salt. This study was conducted to observe the effects of JDS-ASB on skin appearance and health in rats chronically exposed to ultraviolet (UV) radiation. METHODS: Thirty-five female Sprague-Dawley rats (8-weeks old) were randomized into one of the following groups; 1: Control (no treatment), 2: UV (exposed to UV radiation with no other treatment), 3: UV + ASI + Low Dose MgB (140 mg human equivalent dose (HED) of ASI and 1.5 mg HED of MgB), 4: UV + ASI + High Dose MgB (140 mg HED of ASI and 10 mg HED of MgB), 5: UV + ASI + High Dose MgB (140 mg HED of ASI and 10 mg HED of MgB) + MgB cream (10 mg HED). Rat diets included egg whites to standardize absorbable biotin levels. Rats had a dorsal area of hair shaved throughout the study and were exposed to UV lamps five times per week. Each day rats were dosed with study product by oral gavage and/or cream two hours before UV exposure for ten weeks. RESULTS: Rats exposed to UV radiation with no other treatment showed significant signs of skin damage. Skin appearance score improved with all treatments compared to UV exposure alone (p

OBJECTIVES: Curcumin, extracted from the rhizome Curcuma longa, has been shown to be beneficial for neuroprotection in previous studies. In a recent study, a novel formulation of curcumin resulted in an increased relative absorption by 46 times (CurcuWIN®) of the total curcuminoids over the unformulated standard curcumin form. However, the exact mechanisms by which curcumin demonstrates its neuroprotective effects are not fully understood. The present study aimed to investigate the effects of curcumin supplementation on the expression of brain-derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), a main component of the glial scar, and growth-associated protein-43 (GAP-43), a signaling molecule in traumatic brain injury (TBI). METHODS: Brain injury was induced using a cold trauma model in male mice that were treated with curcumin (50 mg/kg) or vehicle via intraperitoneal administration just after TBI. Mice were divided into two groups: TBI + vehicle group and TBI + curcumin (CurcuWIN) group. RESULTS: The results show that curcumin treatment reduced the infarct volume in the brain. TBI induction increased inflammatory cytokines (IL-1β and IL-6), nuclear factor-κB (NF-κB) and GFAP, and reduced BDNF, GAP-43, neural cell adhesion molecule (ICAM) and nuclear factor erythroid 2-related factor 2 (Nrf2) levels in the brain. Interestingly, curcumin decreased the levels of NF-κB, IL-1β, IL-6, and GFAP, and increased BDNF, GAP-43, ICAM and Nrf2 levels in the brain. CONCLUSIONS: In conclusion, these results showed that curcumin could increase the levels of BDNF, GAP-43, ICAM, and Nrf2 and attenuate brain injury in the model of TBI. FUNDING SOURCES: This study was supported by OmniActive Health Technologies Inc. (NJ, USA). This work was also supported in part by the Turkish Academy of Sciences. SUPPORTING TABLES, IMAGES AND/OR GRAPHS

OBJECTIVES: Aging, as well as inadequate intake of vitamins and minerals, can negatively affect the growth, strength, and appearance of hair and nails. For instance, biotin deficiency leads to brittle nails and hair loss. Moreover, certain nutrients, such as arginine and silicon, promote the biological conditions needed for optimal hair and nail growth. JDS-ASB is a novel combination of inositol-stabilized arginine silicate complex (ASI), a highly bioavailable form of arginine and silicon, and magnesium biotinate (MgB), a novel, well-absorbed biotin salt. The purpose of this study was to observe the effects of JDS-ASB on hair and nail growth in rats. METHODS: Twenty-one female Sprague-Dawley rats (8-weeks old) were randomized into one of the following groups; 1: Control (no treatment), 2: ASI + Low Dose MgB (140 mg human equivalent dose (HED) of ASI and 1.5 mg HED of MgB), 3: ASI + High Dose MgB (140 mg HED of ASI and 10 mg HED of MgB). Study product was dosed daily by oral gavage for six weeks. Rat diets included egg whites to standardize absorbable biotin levels. At baseline, hair was shaved from the dorsal area of the rats and hair growth was assessed on days 7, 14, 21, 28, 35, and 42. Hair growth measurements included hair density (per square cm), and percentage of hair follicles in the anagen (growing phase) and telogen (resting phase) phases of the hair cycle. Mean nail growth was measured on days 14, 28, and 42. Blood samples were collected on day 42. RESULTS: Visual observations revealed greater hair growth in both treatment groups compared to control, however the effect was more pronounced in group 3. Compared to control, the percentage of hair follicles in the anagen phase was significantly greater in group 3 from day 14 onward (Figure 1). Compared to control, hair density was significantly greater in group 3 from day 21 onward. These parameters improved in group 2 compared to control on day 42. Blood levels of vascular endothelial growth factor, a protein associated with hair growth, were higher in both treatment groups compared to control, with levels greatest in group 3 (p

OBJECTIVES: Biotin is a B vitamin that is critical for the metabolization of fats, carbohydrates, and amino acids. Deficiency in this vitamin can lead to a variety of adverse conditions. For these reasons, it is important to obtain adequate biotin levels from food sources or dietary supplements. Magnesium Biotinate (MgB) is a novel biotin salt that has been shown to be 40 times more soluble than D-Biotin. The following preclinical study was carried out to further explore the absorption and bioavailability of MgB compared to D-Biotin. METHODS: Forty two male Sprague-Dawley rats were divided into the following groups (n = 7 per group): 1) 0.01 mg D-Biotin/kg body weight (BW), 2) 1.0 mg D-Biotin/kg BW, 3) 100 mg D-Biotin/kg BW, 4) 0.01 mg MgB/kg BW, 5) 1.0 mg MgB/kg BW, 6) 100 mg MgB/kg BW. Rat diets included egg whites to standardize absorbable biotin levels. The duration of the study was 35 days. At the end of the study, blood samples were collected and rats were sacrificed to obtain tissue samples. RESULTS: Results showed that biotin serum levels were 47% higher when rats were given 100 mg of MgB compared to 100 mg of D-Biotin (p

This study reports the effects of Q10, coenzyme Q10 or ubiquinone, a component of the electron transport chain in mitochondria, on nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), inhibitors of kappa B (IκB), nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and hemeoxygenase 1 (HO-1) in rats after chronic exercise training for 6 weeks. 8-week old male Wistar rats were assigned randomly to one of four treatments planned in a 2 x 2 factorial arrangement of two condition (sedentary vs. exercise training), and two coenzyme Q10 levels (0 and 300 mg/kg per day for 6 weeks). The expression levels of the target proteins were determined in the heart, liver and muscle, and biochemical parameters including creatinine, urea, glucose and lipid profile were investigated in plasma. When compared with sedentary group, significant decreases in heart, liver and muscle NFκB levels by 45%, 26% and 44% were observed in Q10 supplemented rats after exercise training, respectively, while the inhibitory protein IκB increased by 179%, 111% and 127% in heart, liver and muscle tissues. Q10 supplementation caused an increase in Nrf2 (167%, 165% and 90%) and HO-1 (107%, 156% and 114%) after exercise training in heart, liver and muscle tissues (p < 0.05). No significant change was observed in any of the parameters associated with protein, carbohydrate and lipid metabolism, except that exercise caused a decrease in plasma triglyceride, which was further decreased by Q10. In conclusion, these results suggest that Q10 modulates the expression of NFκB, IκB, Nrf2 and HO-1 in exercise training, indicating an anti-inflammatory effect of Q10 and emphasizes its role in antioxidant defense.

Purpose. In the present study, we aimed to investigate the effects of tomato powder (TP) on glucose and lipid metabolism, as well as oxidative stress and the NF-κB, mTOR, and Nrf2 pathways during the aging process in healthy rats. Methods and Results. Male Wistar rats were randomly assigned to four groups as follows: (i) Control group 1 (n=15, 3-week old): rats were fed standard diet for 7 weeks; (ii) TP group 1 (n=15, 3-week old): rats were fed standard diet supplemented with TP for 7 weeks; (iii) Control group 2 (n=15, 8-week old): rats were fed standard diet for 69 weeks; and (iv) TP group 2 (8-week old): rats were fed standard diet supplemented with TP for 69 weeks. TP supplementation significantly reduced the hyperglycemia, hypertriglyceridemia, and hypercholesterolemia and improved liver function and kidney function in 77-week old rats compared with the control animals (P<0.05). In addition, TP significantly decreased the serum and liver MDA levels (P<0.003 and P<0.001, respectively) while increasing the activities of liver SOD (P<0.001), CAT (P<0.008), and GPx (P<0.01) compared with the control groups in both 10-week-old and 77-week-old rats (P<0.05). Age-related increases in phosphorylation of NF-κBp65, mTOR, 4E-BP1, and P70S6K were observed in livers of 77-week-old rats compared to those of 10-week-old rats (P<0.001). TP supplementation decreased the expression of NF-κBp65 and activation of mTOR, 4E-BP1, and P70S6K in livers of 77-week-old rats compared to the control animals. Moreover, TP supplementation significantly elevated Nrf2 expression in livers of both 10-week-old and 77-week-old rats (P<0.05). Conclusion. TP ameliorates age-associated inflammation and oxidative stress through the inhibition of NF-κBp65, mTOR pathways, and Nrf2 activation may explain the observed improvement in glucose and lipid metabolism as well as the improved liver and kidney functions.

WOS: 000462022300026 PubMed ID: 30406889 Traumatic brain injury (TBI) is the leading cause of mortality and morbidity in young adults and children in the industrialized countries; however, there are presently no FDA approved therapies. TBI results in oxidative stress due to the overproduction of reactive oxygen species and overwhelming of the endogenous antioxidant mechanisms. Recently, it has been reported that antioxidants including phytochemicals have a protective role against oxidative damage and inflammation after TBI. To analyze the effects of a naturally occurring antioxidant molecule, allyl isothiocyanate (AITC), on the nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor kappa B (NF-kappa B) signaling pathways in TBI, a cryogenic injury model was induced in mice. Here, we showed that AITC administered immediately after the injury significantly decreased infarct volume and blood-brain barrier (BBB) permeability. Protein levels of proinflammatory cytokines interleukin-1 beta (IL1 beta) and interleukin-6 (IL6), glial fibrillary acidic protein (GFAP) and NF-kappa B were decreased, while Nrf2, growth-associated protein 43 (GAP43) and neural cell adhesion molecule levels were increased with AITC when compared with vehicle control. Our results demonstrated that the antioxidant molecule AITC, when applied immediately after TBI, provided beneficial effects on inflammatory processes while improving infarct volume and BBB permeability. Increased levels of plasticity markers, as well as an antioxidant gene regulator, Nrf2, by AITC, suggest that future studies are warranted to assess the protective activities of dietary or medicinal AITC in clinical studies. OmniActive Health Technologies Inc.; Turkish Academy of Sciences This study was supported by OmniActive Health Technologies Inc. (NJ, USA). This work was also supported in part by the Turkish Academy of Sciences.

Mucuna pruriens, Ashwagandha, and Tribulus terrestris are known as the enhancers for sexual health, functional activities, vitality, and longevity. These herbs had been widely used in the Ayurveda medicine as aphrodisiacs through the ages, and their efficacy was also verified separately in our previous publication. Therefore, the aim of this study was to determine the effects of Mucuna, Ashwagandha, and Tribulus complexes on sexual function in rats. Twenty-eight male rats allocated to four groups as follows: (i) negative control (C); (ii) positive control or sildenafil citrate treated group (5 mg/kg) (S); (iii) MAT1 (combination of 10 mg Mucuna (M) + 10 mg Ashwagandha (A) + 10 mg Tribulus (T)/kg BW); (iv) MAT 2 (20 mg Mucuna + 20 mg Ashwagandha + 20 mg Tribulus/kg BW). There was no significant difference found between the MAT1 and MAT2 groups while they showed significantly increased testosterone, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) levels when compared to the negative control. Significant increases in Nrf2/HO1 levels and decreases in NF-κB were detected in MAT groups similar to the decrease in serum and testis malondialdehyde (MDA) levels as compared to both controls. The sperm motility, count, and rate also significantly improved in both MAT groups, while ALT, AST, creatinine, ALP, and urea levels did not change in any of the groups. Oral consumption of MATs combination in male rats resulted in inhibition of NF-κB and MDA and also increased sex hormones with Nrf2-mediated HO-1 induction. MAT combinations may improve sexual functions by increasing levels of sexual hormones and regulation of NF-κB and Nrf2/HO-1 signaling pathways.

Background: Cinnamon polyphenol extract is a traditional spice commonly used in different areas of the world for the treatment of different disease conditions which are associated with inflammation and oxidative stress. Despite many preclinical studies showing the anti-oxidative and antiinflammatory effects of cinnamon, the underlying mechanisms in signaling pathways via which cinnamon protects the brain after brain trauma remained largely unknown. However, there is still no preclinical study delineating the possible molecular mechanism of neuroprotective effects cinnamon polyphenol extract in Traumatic Brain Injury (TBI). The primary aim of the current study was to test the hypothesis that cinnamon polyphenol extract administration would improve the histopathological outcomes and exert neuroprotective activity through its antioxidative and anti-inflammatory properties following TBI. Methods: To investigate the effects of cinnamon, we induced brain injury using a cold trauma model in male mice that were treated with cinnamon polyphenol extract (10 mg/kg) or vehicle via intraperitoneal administration just after TBI. Mice were divided into two groups: TBI+vehicle group and TBI+ cinnamon polyphenol extract group. Brain samples were collected 24 h later for analysis. Results: We have shown that cinnamon polyphenol extract effectively reduced infarct and edema formation which were associated with significant alterations in inflammatory and oxidative parameters, including nuclear factor-κB, interleukin 1-beta, interleukin 6, nuclear factor erythroid 2-related factor 2, glial fibrillary acidic protein, neural cell adhesion molecule, malondialdehyde, superoxide dismutase, catalase and glutathione peroxidase. Conclusion: Our results identify an important neuroprotective role of cinnamon polyphenol extract in TBI which is mediated by its capability to suppress the inflammation and oxidative injury. Further, specially designed experimental studies to understand the molecular cross-talk between signaling pathways would provide valuable evidence for the therapeutic role of cinnamon in TBI and other TBI related conditions.

Objectives This study aims to examine the effects of sorafenib on a collagen-induced arthritis model. Materials and methods The study included 50 randomly selected female Wistar-albino rats (8-10-week-old, weighing between 200 g to 250 g). The rats were divided into five equal groups as control, arthritis, etanercept, sorafenib high-dose, and sorafenib low-dose groups, respectively. Arthritis was induced by injecting mixed intradermal chicken type II collagen and incomplete Freund's adjuvant. Twenty-four hours after the advent of arthritis; rats in group 3 were injected subcutaneous etanercept (6 mg/kg/week), while those in groups 4 and 5 were given sorafenib (10 or 30 mg/ kg/day) orally until they were sacrificed on the 34th day. The rat claws and trunk bloods were carefully examined to note perisynovial inflammation and cartilage/bone injury through histopathology. Tissue vascular endothelial growth factor (VEGF) and VEGF receptor levels were carefully checked using western blot analysis. Results Analysis of the experimental data showed that collagen-induced arthritis decreased in treatments groups after 12-13 days and 34th day in contrast with the arthritis group. Histopathological examination revealed broad perisynovial inflammation and cartilage/bone break down in the arthritis group. Compared to the control group, tissue VEGF and VEGF receptor levels increased in the arthritis group. Sorafenib and etanercept decreased tissue VEGF and VEGF receptor levels, perisynovial inflammation, damage of cartilage/bone. Conclusion Our findings indicate that sorafenib treatment ameliorates collagen-induced arthritis with anti-VEGF effectiveness.

WOS: 000372816600015, PubMed ID: 26965240, The objective of our study was to compare the serum concentrations of procalcitonin (PCT), neopterin, tumor necrosis factor alpha (TNF-), prostaglandin E-2, malondialdehyde, interleukin 8, and gamma interferon (IFN-) in neonatal calves with septicemic colibacillosis (n = 15) with healthy controls (n = 15). Septicemic colibacillosis was diagnosed based on clinical signs and the isolation of Escherichia coli from heparinized blood in clinically suspected cases. PCT, neopterin, TNF- (p < 0.05), and IFN- concentrations in calves with septicemic colibacillosis were significantly higher than in the healthy controls (p < 0.01). Serum PCT concentrations were similar to 4 times higher in the calves with septicemic colibacillosis than in the healthy calves, suggesting that PCT could be a useful marker of septicemic colibacillosis in neonatal calves., Scientific Research Projects Commission of Cumhuriyet University [V-013], The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported by the Scientific Research Projects Commission of Cumhuriyet University under project V-013.

WOS: 000387822300002, PubMed: 27895467, The purpose of this study was to induce experimental periodontitis in rats previously fed diets containing arginine silicate inositol (ASI) complex and examine the biochemical, immunological, and radiological effects. Fifty two 8-week-old female Sprague Dawley rats were equally divided into four groups. The control group included those fed a standard rat diet with no operation performed during the experiment. The periodontitis, ASI I, and ASI II groups were subjected to experimental periodontitis induction for 11 days after being fed a standard rat diet alone, a diet containing 1.81 g/kg ASI complex, or a diet containing 3.62 g/kg ASI complex, respectively, for 8 weeks. Throughout the 11-day duration of periodontitis induction, all rats were fed standard feed. The rats were euthanized on the eleventh day, and their tissue and blood samples were collected. In the periodontitis group, elevated tissue destruction parameters and reduced tissue formation parameters were found, as compared to the ASI groups. Levels of enzymes, cytokines, and mediators associated with periodontal tissue destruction were lower in rats fed a diet containing ASI complex after experimental periodontitis. These results indicate that ASI complex could be an alternative agent for host modulation., Scientific Research Project Fund of Inonu University [2013/88]; Turkish Academy of SciencesTurkish Academy of Sciences, We thank Nurhan Sahin and Cemal Orhan for their collaboration in our experiments. This work was supported by the Scientific Research Project Fund of Inonu University under project number 2013/88 and the Turkish Academy of Sciences (to KS).

Background Chromium (Cr) is commonly used as a complementary medicine for diabetes mellitus. Several studies suggest that Cr intakes may improve glucose metabolism and decrease oxidative stress. Therefore, we aimed to assess the effects of chromium histidinate (CrHis) supplementation using a range of reliable biomarkers of oxidative damage and histopathological changes in rats with diabetic retinopathy. Methods Diabetes was induced with streptozotocin [(STZ), 55 mg/kg] by intraperitoneal injection in male Long-Evans rats. Three weeks after STZ injection, rats were divided into four groups, namely, untreated normal controls, normal rats receiving CrHis (110 μg/kg/day); untreated diabetics and diabetics treated with CrHis (110 μg/kg/day) orally for 12 weeks. Results In the untreated diabetic group, levels of serum glucose, glycosylated haemoglobin (HbA1c), total cholesterol (TC) and retina malondialdehyde (MDA) were significantly increased, while expressions of retina insulin, and glucose transporter 1 (GLUT 1) and glucose transporter 3 (GLUT3) and level of serum insulin were decreased. CrHis supplementation was found to reduce the levels of glucose, HbA1c, total cholesterol and MDA and to improve the GLUT1, GLUT3 and insulin expressions in STZ-induced diabetic rats. CrHis prevents the changes in the expressions of GLUT1, GLUT3 and insulin and the level of MDA in the retina tissue, confirming the protective effect of CrHis supplementation against the retinopathy caused by STZ. Histopathologic findings suggest that the CrHis-treated diabetic group had normal retinal tissue appearance compared with the untreated diabetic group. Conclusions These results verify that CrHis has critical beneficial effects against retinal complications. Although detailed studies are required for the evaluation of the exact mechanism of the ameliorative effects of CrHis against diabetic complications, these preliminary experimental findings demonstrate that CrHis exhibits antidiabetic effects in a rat model of diabetic retinopathy by regulating the glucose metabolism and suppressing retinal tissue damage.