Ascorbic Acid Supplementation Research Articles

Effects of ascorbic acid supplementation on oxidative stress markers in healthy women following a single bout of exercise

BackgroundAscorbic acid is a water-soluble chain breaking antioxidant. It scavenges free radicals and reactive oxygen species (ROS), which are produced during metabolic pathways. Exercise can produce an imbalance between ROS and antioxidants, leading to oxidative stress-related tissue damages. This study was designed to determine the effects of ascorbic acid supplementation on circulating biomarkers of oxidative stress and muscle damage following a single bout of exercise.MethodsIn a crossover design with a 1 wk. wash-out period, 19 healthy women performed 30 min moderate-intensity cycling after ingesting 1000 mg of ascorbic acid (AA) or placebo. Blood samples were taken immediately before, immediately after and 30 min post-exercise to determine plasma albumin, total protein, glucose, oxidative stress and muscle damage markers.ResultsPlasma albumin and total protein levels increased immediately after exercise in placebo alongside slight reductions in glucose (p = 0.001). These effects were absent in AA cohort. Ferric reducing ability of plasma and vitamin C levels in AA cohort significantly increased after exercise (p < 0.05). Superoxide dismutase activity was significantly elevated after exercise (p = 0.002) in placebo but not AA. Plasma malondialdehyde did not change after exercise in placebo but was significantly decreased in AA (p < 0.05). The exercise protocol promoted slight muscle damage, reflected in significant increases in total creatine kinase in all subjects after exercise. On the other hand, plasma C-reactive protein and lactate dehydrogenase remained unchanged.ConclusionSupplementation with ascorbic acid prior exercise improves antioxidant power but does not prevent muscle damage.

Comparative Haemolymph Protein Content in Gen-3 Bivoltine Race of Bombyx Mori L. with Supplementation of Vitamin-C , E

Comparative Haemolymph Protein Content in Gen-3 Bivoltine Race of Bombyx Mori L. with Supplementation of Vitamin-C , E

Ascorbic acid insufficiency impairs spatial memory formation in juvenile AKR1A-knockout mice.

AKR1A, an aldo-keto reductase, is involved in the synthesis of ascorbic acid as well as the reduction of a variety of aldehyde compounds. AKR1A−/− mice produce considerably less ascorbic acid (about 10%) compared to AKR1A+/+ mice and require ascorbic acid supplementation in order to breed. To elucidate the roles played by AKR1A in spatial memory, AKR1A−/− male mice were weaned at 4 weeks of age and groups that received ascorbic acid supplementation and no supplementation were subjected to a Morris water maze test. Juvenile AKR1A−/− mice that received no supplementation showed impaired spatial memory formation, even though about 70% of the ascorbic acid remained in the brains of the AKR1A−/− mice at day 7 after weaning. To the contrary, the young adult AKR1A−/− mice at 13–15 weeks of age maintained only 15% of ascorbic acid but showed no significant difference in the spatial memory compared with the AKR1A+/+ mice or ascorbic acid-supplemented AKR1A−/− mice. It is conceivable that juvenile mice require more ascorbic acid for the appropriate level of formation of spatial memory and that maturation of the neural system renders the memory forming process less sensitive to an ascorbic acid insufficiency.

Combined supplementation of ascorbic acid and thyroid hormone T3 affects tenocyte proliferation. The effect of ascorbic acid in the production of nitric oxide

Combined supplementation of ascorbic acid and thyroid hormone T3 affects tenocyte proliferation. The effect of ascorbic acid in the production of nitric oxide

Effects of ascorbic acid treatment on developmental alterations in calcium-binding proteins and gamma-aminobutyric acid transporter 1 in the cerebellum of lead-exposed rats during pregnancy and lactation.

In the present study, we investigated the effects of lead (Pb) and ascorbic acid co-administration on rat cerebellar development. Female rats were randomly divided into the following groups: control, Pb, and Pb plus ascorbic acid (PA) groups. From one week prior to mating, female rats were administered Pb (0.3% Pb acetate in drinking water) and ascorbic acid (100 mg/kg, oral intubation). The chemical administration was stopped on postnatal day 21 when the morphology of the offspring's cerebellum is similar to that of the adult brain. The blood Pb level was significantly increased following long-term Pb exposure. Ascorbic acid reduced Pb levels in the dams and offspring. Nissl staining demonstrated that the number of Purkinje cells was significantly reduced following Pb exposure, while ascorbic acid ameliorated this effect in the cerebellum of the offspring. Calcium-binding proteins, such as calbindin, calretinin, and parvalbumin were commonly expressed in Purkinje cells, and Pb exposure and ascorbic acid treatment resulted in similar patterns of change, namely Pb-induced impairment and ascorbic acid-mediated amelioration. The gamma-aminobutyric acid transporter 1 (GABAT1) is expressed in the pinceau structure where the somata of Purkinje cells are entwined in inhibitory synapses. The number of GABAT1-immunoreactive synapses was reduced following Pb exposure, and ascorbic acid co-treatment prevented this effect in the cerebellar cortex. Therefore, it can be concluded that ascorbic acid supplementation to mothers during gestation and lactation may have potential preventive effects against Pb-induced impairments in the developing cerebellum via protection of inhibitory neurons and synapses.

Redox correlation in muscle lengthening and immune response in eccentric exercise.

This study was designed to examine the potential involvement of reactive oxygen species in skeletal muscle dysfunction linked with stretching in a mouse model and to explore the effects of combined antioxidant intake on peripheral leukocyte apoptosis following eccentrically-biased downhill runs in human subjects. In the mouse model, diaphragmatic muscle was stretched by 30% of its optimal length, followed by 5-min contraction. Muscle function and extracellular reactive oxygen species release was measured ex vivo. In human models, participants performed two trials of downhill running either with or without antioxidant supplementation, followed by apoptotic assay of inflammatory cells in the blood. The results showed that stretch led to decreased muscle function and prominent ROS increase during muscle contraction. In human models, we observed an elevation in circulating leukocyte apoptosis 24–48 hours following acute downhill runs. However, there is an attenuated leukocyte apoptosis following the second bout of downhill run. Interestingly, the combination of ascorbic acid (vitamin C) and α-tocopherol (vitamin E) supplementation attenuated the decrease in B-cell lymphoma 2 (Bcl-2) at 24 hours following acute downhill running. These data collectively suggest that significant ROS formation can be induced by muscle-lengthening associated with eccentric exercise, which is accompanied by compromised muscle function. The combination of antioxidants supplementation appears to have a protective role via the attenuation of decrease in anti-apoptotic protein.

Alleviation of heat-stress-related physiological perturbations in growing rabbits using natural antioxidants

The current study was performed to evaluate the effects of the dietary inclusion of extra virgin olive oil (EVOO), betaine (BET), lemongrass essential oil (LGEO), gallic acid (GA), vitamin C (VC) and vitamin E (VE) on different body temperature traits and stress hormone and glucose levels in heat-stressed growing rabbits. Rabbits were fed diets with no supplementation (control group) or supplemented with 15 g of EVOO, 400 mg of LGEO, 500 mg of GA, 1000 mg of BET, 500 mg of VC, or 200 mg of VE per kg of diet. All tested feed additives, especially EVOO, had a lowering effect on various rabbit temperature traits. Both triiodothyronine (T3) and tetraiodothyronine/thyroxine (T4) were increased (p&lt;0.05) by the addition of BET, VC, EVOO, and VE. With the exception of the VC group, all dietary groups showed no significant changes in the insulin level compared to the control group level. In contrast, the cortisol and glucose levels were diminished (p&lt;0.05) in all treated groups compared to the control levels. The results suggested that all tested supplementations had positive ameliorating effects on growing rabbits under a severe heat load in terms of lowered body temperatures and a favourable stress hormone balance, with the most favourable results found in the EVOO, VC, and BET supplementation groups.

A Meta-analysis of Randomized Control Trials: The Impact of Vitamin C Supplementation on Serum CRP and Serum hs-CRP Concentrations.

The present meta-analysis was designed to assess the effects of vitamin C supplementation on serum C-reactive Protein (CRP) levels. We conducted a comprehensive systematic search of the literature in Scopus, PubMed and Google Scholar until May 2018. The pooled Weighted Mean Difference (WMD) and its 95% Confidence Interval (CI) in baseline and at the end of the trial were calculated to assess the net change in serum CRP by using random-effects model. The heterogeneity was assessed by I2 test. Combined and stratified analyses were used in the metaanalysis. From 306 articles found and screened in our initial search, 12 studies were included with 446 participants in supplementation groups and 447 in control groups. The pooled effect size analysis showed a significant reducing effect of vitamin C supplementation on circulating CRP level (-0.23 mg/L, 95% CI, -0.44, -0.03, p=0.02), with a significant heterogeneity effect across the studies involved. Subgroup analyses showed that vitamin C supplementation significantly lowered CRP among trials. The most significant effect was found 1) on hs- CRP as the representative inflammatory marker (-0.43 mg/L, 95% CI -0.76, -0.1) 2) in subjects with a baseline CRP≥3 (-1.48 mg/L, 95% CI -2.84, -0.11) 3) in subjects under <60 years old of age (-0.23 mg/L, 95% CI -0.44,- 0.01) 4) or using intravenous administration of vitamin C (-0.89 mg/L, 95% CI -1.49,-0.3). The present meta-analysis shows that vitamin C supplementation reduces serum CRP level, particularly in younger subjects, with higher CRP baseline level, at a lower dosage and intravenous administration.

Ascorbic acid supplementation improves postprandial glycaemic control and blood pressure in individuals with type 2 diabetes: Findings of a randomized cross-over trial.

The primary aim of this study was to investigate whether ascorbic acid (AA) supplementation improves postprandial glucose responses under free-living conditions in individuals with type 2 diabetes. A secondary aim was to investigate the effect of AA supplementation on blood pressure. A total of 31 individuals with type 2 diabetes (26 males and 5 females; aged 61.8 ± 6.8 years; duration of diabetes, 5.6 ± 4.6 years; HbA1c, 7.6% ± 0.7% [mean ± SD]) were enrolled in a randomized cross-over study involving 4 months of supplementation with oral AA (2 × 500 mg/d) or placebo. Participants wore continuous glucose monitors for 48 hours and consumed standardized meals pre- and post-supplementation. Measurements included postprandial glucose incremental areas under the curve (iAUC), duration of day in hyper- and hypo-glycaemia status, average 24-hour and daily postprandial glucose concentrations, HbA1c, insulin, blood pressure (BP) and oxidative stress (F2 -isoprostanes). Following AA supplementation, significant decreases were observed in daily postprandial glucose iAUC (-36%), in duration of day with hyperglycaemia (-2.8 h/d) and postprandial hyperglycaemia (-1.7 h/d), in average 24-hour glucose (-0.8 mmol/L) and daily postprandial glucose (-1.1 mmol/L) concentrations, in systolic (-7 mm Hg) and diastolic (-5 mm Hg) blood pressures and in a specific fraction of free plasma F2 -isoprostanes (-47 pg/mL) as compared to placebo. Individuals with type 2 diabetes experienced improved postprandial and 24-hour glycaemia and decreased BP after 4 months of AA supplementation as compared to placebo. These findings offer evidence for the proposed use of AA as an adjunct therapy to improve glycaemic and BP control in individuals with type 2 diabetes.

Effect of tonophosphan, zinc oxide, and ascorbic acid on semen, sexual desire, and the fertility rate of Egyptian buffalo bulls

A twenty weeks experimental trial was conducted to evaluate the effects of using tonophosphan (8 ml injection), zinc oxide (ZnO) at 0.8 g oral dose and ascorbic acid (AA) at 0.5% oral dose of live body weight on reproductive performance of Egyptian buffalo bulls (n = 20, 550–600 kg). The overall mean of all treated groups yielded marked improvement in all semen physical characteristics. Reaction time (RT), scrotal circumference, testicular volume, the concentration of semen fructose, testosterone, total proteins, and albumin in blood plasma were significantly (P ≤ 0.05) improved in all treatment groups compared with the control, but were greater in tonophosphan group. The highest concentrations of phosphorus and zinc in blood or semen were observed in tonophosphan and zinc treatments, respectively as compared to other groups. Overall mean of all semen physical characteristics and sperm outputs were not affected by advancing collection weeks. Meanwhile, the testosterone concentration and testicular volume increased (P ≤ 0.05), whereas the reaction time did not vary. The conception rate of buffalo cows was the highest (P ≤ 0.05) in tonophosphan (82.8%), followed by ascorbic acid and zinc (77.1 and 74.2%) as compared to the control group (60%). These findings suggested that tonophosphan, zinc oxide, and ascorbic acid supplementation improved the reproductive performance of Egyptian buffalo bulls; however, tonophosphan showed better performance.

Ascorbic Acid Supplementation Prevents the Detrimental Effects of Prenatal and Postnatal Lead Exposure on the Purkinje Cell and Related Proteins in the Cerebellum of Developing Rats.

We investigated the effects of lead (Pb) and ascorbic acid co-administration on rat cerebellar development. Prior to mating, rats were randomly divided into control, Pb, and Pb plus ascorbic acid (PA) groups. Pregnant rats were administered Pb in drinking water (0.3% Pb acetate), and ascorbic acid (100mg/kg) via oral intubation until the end of the experiment. Offspring were sacrificed at postnatal day 21, the age at which the morphology of the cerebellar cortex in developing pups is similar to that of the adult brain. In the cerebellum, Pb exposure significantly reduced Purkinje cells and ascorbic acid prevented their reduction. Along with the change of the Purkinje cells, long-term Pb exposure significantly reduced the expression of the synaptic marker (synaptophysin), γ-aminobutyric acid (GABA)-synthesizing enzyme (glutamic acid decarboxylase 67), and axonal myelin basic protein while ascorbic acid co-treatment attenuated Pb-mediated reduction of these proteins in the cerebellum of pups. However, glutamatergic N-methyl-D-aspartate receptor subtype 1 (NMDAR1), anchoring postsynaptic density protein 95 (PSD95), and antioxidant superoxide dismutases (SODs) were adversely changed; Pb exposure increased the expression of NMDAR1, PSD95, and SODs while ascorbic acid co-administration attenuated Pb-mediated induction. Although further studies are required about the neurotoxicity of the Pb exposure, the results presented here suggest that developmental Pb exposure disrupted normal development of Purkinje cells by increasing glutamatergic and oxidative stress in the cerebellum. Additionally, ascorbic acid co-treatment is beneficial in attenuating prenatal and postnatal Pb exposure-induced maldevelopment of Purkinje cells in the developing cerebellum.

238 - Antioxidants ameliorate hyperoxia-induced lung injury by inhibition of HMGB1

Hyperoxia-induced acute lung injury (HALI) is mediated by the production of excessive reactive oxygen species (ROS), which overwhelms intracellular antioxidant systems and induces oxidative stress. This damages macromolecules critical for cell survival, inducing apoptosis in lung epithelial cells and compromising alveolar macrophage phagocytosis. In this study, we demonstrate that antioxidants protect against HALI and improve macrophage dysfunction by reducing ROS and inhibiting the release of the damage associated molecular pattern (DAMP), HMGB1. While hyperoxia exposure (≥98% O2, 72 h) alone induced alveolar thickening, leukocyte infiltration, and an increase in total protein in the broncheolar lavage fluid (BALF) of C57BL/6 mice, ascorbic acid (AA) supplementation reversed these hallmarks of HALI. Reduced lung injury was correlated to reduced oxidative redox potential and nitric oxide production in BALF and in RAW 264.7 macrophages, and decreased accumulation of airway HMGB1. Increased activation of the endogenous antioxidant regulator, Nrf-2, by sulforaphane (SUL) similarly showed protection against hyperoxia-compromised cell function in RAW 264.7 cells and in bone marrow derived macrophages (BMDM) by reducing both intracellular levels of ROS and the release of HMGB1. Our results suggest that supplementation of antioxidants during oxygen therapy can prevent lung damage and preserve macrophage function, providing a preventive measure for HALI.

Developmental lead (Pb)-induced deficits in hippocampal protein translation at the synapses are ameliorated by ascorbate supplementation.

BackgroundLead (Pb) is a persistent environmental neurotoxin and its exposure even in minute quantities has been known to induce neuronal defects. The immature brain is singularly sensitive to Pb neurotoxicity, and its exposure during development has permanent detrimental effects on the brain developmental trajectory and neuronal signaling and plasticity, culminating into compromises in the cognitive and behavioral attributes which persists even later in adulthood. Several molecular pathways have been implicated in the Pb-mediated disruption of neuronal signaling, including elevated oxidative stress, alterations in neurotransmitter biology, and mitochondrial dysfunction. Nevertheless, the neuronal targets and biochemical pathways underlying these Pb-mediated alterations in synaptic development and function have not been completely deduced. In this respect, recent studies have shown that synaptic signaling and its maintenance and plasticity are critically dependent on localized de novo protein translation at the synaptic terminals.Materials and methodsThe present study hence aimed to assess the alterations in the synapse-specific translation induced by developmental Pb exposure. To this end, in vitro protein translation rate was analyzed in the hippocampal synaptoneurosomal fractions of rat pups pre- and postnatally exposed to Pb using a puromycin incorporation assay. Moreover, we evaluated the therapeutic effects of ascorbic acid supplementation against Pb-induced deficits in synapse-localized protein translation.ResultsWe observed a significant loss in the rates of de novo protein translation in synaptoneurosomes of Pb-exposed pups compared to age-matched control pups. Interestingly, ascorbate supplementation lead to an appreciable recovery in Pb-induced translational deficits. Moreover, the deficit in activity-dependent synaptic protein translation was found to correlate significantly with the increase in the blood Pb levels.ConclusionDysregulation of synapse-localized de novo protein translation is a potentially critical determinant of Pb-induced synaptic dysfunction and the consequent deficits in behavioral, social, and psychological attributes of the organisms. In addition, our study establishes ascorbate supplementation as a key ameliorative agent against Pb-induced neurotoxicity.

Ascorbic acid inhibits visceral obesity and nonalcoholic fatty liver disease by activating peroxisome proliferator-activated receptor α in high-fat-diet-fed C57BL/6J mice.

Ascorbic acid is a known cofactor in the biosynthesis of carnitine, a molecule that has an obligatory role in fatty acid oxidation. Our previous studies have demonstrated that obesity is regulated effectively through peroxisome proliferator-activated receptor α (PPARα)-mediated fatty acid β-oxidation. Thus, this study aimed to determine whether ascorbic acid can inhibit obesity and nonalcoholic fatty liver disease (NAFLD) in part through the actions of PPARα. After C57BL/6J mice received a low-fat diet (LFD, 10% kcal fat), a high-fat diet (HFD, 45% kcal fat), or the same HFD supplemented with ascorbic acid (1% w/w) (HFD-AA) for 15 weeks, variables and determinants of visceral obesity and NAFLD were examined using metabolic measurements, histology, and gene expression. Compared to HFD-fed obese mice, administration of HFD-AA to obese mice reduced body weight gain, visceral adipose tissue mass, and visceral adipocyte size without affecting food consumption profiles. Concomitantly, circulating ascorbic acid concentrations were significantly higher in HFD-AA mice than in HFD mice. Ascorbic acid supplementation increased the mRNA levels of PPARα and its target enzymes involved in fatty acid β-oxidation in visceral adipose tissues. Consistent with the effects of ascorbic acid on visceral obesity, ascorbic acid not only inhibited hepatic steatosis but also increased the mRNA levels of PPARα-dependent fatty acid β-oxidation genes in livers. Similarly, hepatic inflammation, fibrosis, and apoptosis were also decreased during ascorbic acid-induced inhibition of visceral obesity. In addition, serum levels of alanine aminotransferase, aspartate aminotransferase, total cholesterol, and LDL cholesterol were lower in HFD-AA-fed mice than in those of HFD-fed mice. These results suggest that ascorbic acid seems to suppress HFD-induced visceral obesity and NAFLD in part through the activation of PPARα.

Ascorbic acid synthesis and transportation capacity in old laying hens and the effects of dietary supplementation with ascorbic acid

BackgroundLaying hens over 75 weeks of age commonly show great declines in immunity and production performance. It is unclear whether these declines can be relieved by supplementing with ascorbic acid (AA) in feed. Two trials were conducted to investigate the synthesis and metabolism of AA in layers of different ages and the effects of dietary supplemental AA on the performance and the immune and antioxidant statuses of 78 weeks old hens.MethodsIn Exp. 1, equal numbers (24 hens) of 35 weeks old (Young) and 75 weeks old (Old) layers were fed the same diet without AA supplementation for 4 weeks. In Exp. 2, 360 healthy 78 weeks old laying hens were randomly assigned to 4 treatments (basal diet supplemented with 0, 0.25, 0.5, or 1 g AA/kg diet) in an 8-week feeding trial.ResultsThe old hens tended to have decreased L-gulonolactone oxidase (GLO) synthase activity in the kidney and liver than that of the young hens (P = 0.07 and P = 0.05, respectively). Compared with the young hens, the old hens had lower hepatic antioxidant capacity allowing for the lower thioredoxin (TXN), thioredoxin reductase (TXNR) and cytochrome b5 reductase (CYB5R) gene expression (P < 0.05), whereas increased sodium-dependent vitamin C transporter (SVCT) 1 expression levels in the ileum and kidney and enhanced splenic and hepatic AA concentrations (P < 0.05). Dietary supplementation with AA significantly decreased GLO enzyme activity but increased splenic AA concentration and anti-bovine serum albumin IgG levels (P < 0.05) and tended to increase CD4+ T lymphocyte numbers (P = 0.06) in serum. Supplementation of 0.25 g AA/kg diet significantly increased hepatic total antioxidant capacity (T-AOC, P < 0.05) relative to the control group.ConclusionsLaying hens could synthesize AA in both the kidney and the liver, though the GLO enzyme activities were 100 times greater in kidneys than in livers. The old laying hens had greater absorption and reabsorption capacity and higher AA retention in some tissues that did the young hens. Dietary supplementation of AA can improve the health of old layers by enhancing immunity and antioxidant capacity.

Ascorbic acid supplementation ameliorates testicular hormonal signaling, sperm production and oxidative stress in male rats exposed to rosuvastatin during pre-puberty.

Dyslipidemias are occurring earlier in the population due to the augmentation of obesity. Rosuvastatin reduces cholesterol and triglycerides; however, previous studies have shown that it may affect male reproduction. Ascorbic acid (AA), an antioxidant compound, plays a protective role in the male reproductive system. This study aimed to evaluate whether pre-pubertal exposure to rosuvastatin may impair testicular structure and antioxidant status in male rats and if supplementation with AA may alleviate these damages. Male rats were randomly divided into six experimental groups (n=10) on postnatal day (PND) 23 and received the different treatments by gavage from PND 23 to 53. The experimental groups received vehicle (saline solution 0.9%), 3 or 10mg/kg/day of rosuvastatin diluted in saline solution 0.9%, supplementation with 150mg/day of AA, 3mg/kg/day of rosuvastatin in association with 150mg/day of AA or 10mg/kg/day of rosuvastatin associated with 150mg/day of AA. Testicular parameters were assessed on PND 53 and 110. There were diminished androgen receptors staining in the Sertoli cells and increased germ cell death in rosuvastatin-exposed groups, in both periods. Spermatids showed lower estrogen alpha-receptors staining in the group exposed to 10mg of statin at adulthood. There were androgen depletion and increased lipid peroxidation and catalase activity in statin-exposed groups. Rosuvastatin exposure during pre-puberty impaired testicular structure, steroid receptor distribution and increased oxidative stress; however, AA was able to ameliorate the impairment provoked by statin exposure.

Effects of vitamin C supplementation on blood pressure and hypertension control in response to ambient temperature changes in patients with essential hypertension

ABSTRACTEvidence for blood pressure-lowering effects of vitamin C (VC) supplementation in clinical trials is inconsistent and limited studies have examined the effect of VC supplementation on hypertension (HTN) control. In this study, eligible patients were cluster assigned to receive 300 mg VC per day or nothing for 6 months. During the 6-month follow-up period, a questionnaire survey was obtained and standardized blood pressure measurements were performed on all subjects. Oral administration of VC significantly decreased the diastolic blood pressure and pulse pressure with a significant increase in HTN control. After adjusting for confounding variables, treatment with VC was associated with ~ 0.5 risk reduction of uncontrolled HTN in subjects received anti-hypertensive medications, whereas lower indoor and outdoor and ground temperature were significantly associated with an increased risk of uncontrolled HTN in all patients. Our results warrant further studies investigating the mechanisms underlying the association between VC and HTN control.

Cajanine promotes osteogenic differentiation and proliferation of human bone marrow mesenchymal stem cells

Seed cells - mesenchymal stem cells (MSCs) - appear to be an attractive tool in the context of tissue engineering. Bone marrow represents the main source of MSCs for both experimental and clinical studies. However, the number limitation of bone marrow MSCs (BMSCs) and decreased function caused by proliferation make the search for adequate alternative sources of these cells for autologous and allogenic transplant necessary. This study was aimed to investigate the roles of cajanine isolated from the extracts of Cajanus cajan L. Millsp. in the proliferation and differentiation of BMSCs, and to discover the mechanism of proliferation of BMSCs promoted by cajanine. Bone marrow mesenchymal stem cells were cultured in high-glucose Dulbecco's Modified Eagle's Medium (DMEM) and osteogenic differentiation was induced by adding dexamethasone, ascorbic acid and β-glycerophosphate supplements. Bone marrow MSCs were cultured in medium without cajanine or supplemented with cajanine. The information about the proliferation and osteogenic differentiation of BMSCs was collated. The osteogenic differentiation potential of BMSCs was also assessed at the 3rd passage by Von Kossa staining. To observe cell signal transduction changes of BMSCs after culturing them with cajanine for 24 h, the western blot analysis was performed to detect phosphorylated cell cycle proteins and activated cyclins. After osteogenic induction, the differentiation of BMSCs was accelerated by cajanine treatment. Osteogenesis markers were upregulated by cajanine treatment at both protein and mRNA levels. Cajanine obviously promoted the proliferation of BMSCs. After BMSCs were cultured with cajanine for 24 h, the cell cycle regulator proteins were phosphorylated or upregulated. Cajanine can promote the expansion efficiency of BMSCs, at the same time keeping their multi-differentiation potential. Cajanine can activate the cell cycle signal transduction pathway, thus inducing cells to enter the G1/S phase and accelerating cells entering the G2/M phase. This study can contribute to the development of cajanine-based drugs in tissue engineering.

Vitamin C and Helicobacter pylori Infection: Current Knowledge and Future Prospects.

The gram-negative bacterium, Helicobacter pylori (H. pylori), infection is predominantly known for its strong association with development of gastric diseases, including gastritis, peptic ulcers, and stomach cancer. Numerous clinical reports show that ascorbic acid deficiency has been connect with gastritis. Vitamin C levels both in gastric acid and serum have constantly been affirmed to be low in subjects with H. pylori infected gastritis and peptic ulcers. Ascorbic acid supplementation likely relates to reduced incidences of bleeding from peptic ulcers and gastric cancer. H. pylori eradication is shown to increase vitamin C levels, while the benefits of ascorbic acid oral intake to increase the effectiveness of H. pylori-eradication therapy are controversial. Recent studies suggest that ascorbate intake intravenously, but not orally; pharmacologic ascorbate concentrations up to 30 mmol/L in blood, several millimolar in tissues as well as in interstitial fluid, are easily and safely achieved. Pharmacologic ascorbate can exert pro-oxidant effects locally as a drug by mediating hydrogen peroxide (H2O2) formation, which was applied to animal and clinical trials of cancer, sepsis, and severe burns etc. In this review, we summarize current understanding of the associations of vitamin C and H. pylori infection, and outline some potential strategies for H. pylori intervention from emerging advances on ascorbic acid physiology and pharmacology.

Effect of antioxidant ascorbic acid on in vitro maturation of Caprine oocytes under normal and elevated temperatures

The aim of the present study was to assess the effect of ascorbic acid on in vitro maturation of caprine oocytes under normal and elevated temperatures. Goat ovaries were collected at slaughter and both A and B grade cumulus-oocyte-complexes (COCs) were aspirated out and were matured in vitro under normal (38.5°C) and elevated temperatures (41°C). On the basis of cumulus expansion and nuclear maturation, the maturation competencewere compared with and without ascorbic acid supplementation (100 µM). Heat stress significantly (P£ 0.01) reduced cumulus expansion, maturation rate and lowered metaphase stage II of nuclear maturation. Ascorbic acid improved developmental competence of oocytes during heat stress (41 °C) and ascorbic acid supplemented COCs demonstrated significantly (P£ 0.05) higher maturation rates when compared to non-supplemented groups.