2-O-β-D-Glucopyranosyl-L-ascorbic acid,an ascorbic acid derivative isolated from the fruits of Lycium barbarum L.,ameliorates high fructose-induced neuroinflammation in mice:involvement of gut microbiota and leaky gut

Western diet(rich in highly refined sugar and fat)can induce a range of metabolic dysfunctions in animals and humans,including neuroinflammation and cognitive function decline.Neuroinflammation and cognitive impairment,two critical pathological characteristics of Alzheimer’s disease,have been closely associated with microbial alteration via the gut-brain axis.Thus,the present study aimed to investigate the influence of 2-O-β-D-glucopyranosyl-L-ascorbic acid(AA-2βG)isolated from the fruits of Lycium barbarum on preventing the high-fructose diet(HFrD)induced neuroinflammation in mice.It was found that AA-2βG prevented HFr D-induced cognitive deficits.AA-2βG also predominantly enhanced the gut barrier integrity,decreased lipopolysaccharide entry into the circulation,which subsequently countered the activation of glial cells and neuroinflammatory response.These beneficial effects were transmissible by horizontal fecal microbiome transplantation,transferring from AA-2βG fed mice to HFr D fed mice.Additionally,AA-2βG exerted neuroprotective effects involving the enrichment of Lactobacillus and Akkermansia,potentially beneficial intestinal bacteria.The present study provided the evidence that AA-2βG could improve indices of cognition and neuroinflammmation via modulating gut dybiosis and preventing leaky gut.As a potential functional food ingredient,AA-2βG may be applied to attenuate neuroinflammation associated with Western-style diets.

Measurement and Correlation on Viscosity and Apparent Molar Volume of Ternary System for L-ascorbic Acid in Aqueous D-Glucose and Sucrose Solutions

Viscosities and densities at several temperatures from 293.15 K to 313.15K are reported for L-ascorbic acid in aqueous glucose and sucrose solutions at different concentrations. The parameters of density, viscosity coefficient B and partial molar volume are calculated by regression. The experimental results show that densities and viscosities decrease as temperature increases at the same solute and solvent (glucose and sucrose aqueous solution) concentrations, and increase with concentration of glucose and sucrose at the same solute concentration and temperature. B increases with concentration of glucose and sucrose and temperature. L-ascorbic acid is structure-breaker or structure-making for the glucose and sucrose aqueous solutions. Furthermore, the solute-solvent interactions in ternary systems of water-glucose-electrolyte and water-sucrose-electrolyte are discussed.

Development of a miniature silicon wafer fuel cell using L-ascorbic acid as fuel

In the current studies a miniature silicon wafer fuel cell(FC) using L-ascorbic acid as fuel was developed. The cell employs L-ascorbic acid and air as reactants and a thin polymer electrolyte as a separator. Inductively coupled plasma(ICP) silicon etching was employed to fabricate high aspect-ratio columns on the silicon substrate to increase the surface area. A thin platinum layer deposited directly on the silicon surface by the sputtering was used as the catalyst layer for L-ascorbic acid electro-oxidation. Cyclic voltammetry shows that the oxidation of L-ascorbic acid on the sputtered platinum layer is irreversible and that the onset potentials for the oxidation of L-ascorbic acid are from 0.27 V to 0.35 V versus an Ag/AgCl reference electrode. It is found that at the room temperature,with 1 mol/L L-ascorbic acid/PBS(phosphate buffered solution) solution pumped to the anode at 1 ml/min flow rate and air spontaneously diffusing to the cathode as the oxidant,the maximum output power density of the cell was 1.95 mW/cm2 at a current density of 10 mA/cm2.

Alteration of chemical behavior of L-ascorbic acid in combination with nickel sulfate at different pH solutions in vitro

Objective:To evaluate the alteration of chemical behavior of L-ascorbic acid(vitamin C) with metal ion(nickel) at different pH solutions in vitro.Methods:Spectra of pure aqueous solution of L-ascorbic acid(E mark) compound and NiSO_4(H_2O)(sigma USA) were evaluated by UV visible spectrophotometer.Spectral analysis of L-ascorbic acid and nickel at various pH(2.0, 7.0,7.4 and 8.6) at room temperature of 29℃ was recorded.In this special analysis,combined solution of L-ascorbic acid and nickel sulfate at different pH was also recorded.Results:The result revealed that λ_(max)(peak wavelength of spectra) of L-ascorbic acid at pH 2.0 was 289.0 run whereas at neutral pH 7.0,λ_(max) was 29S.4 run.In alkaline pH 8.6,λ_(max) was 295.4 nm and at pH 7.4 the λ_(max) of L-ascorbic acid remained the same as 295.4 nm.Nickel solution at acidic pH 2.0 was 394.5 nm,whereas at neutral pH 7.0 and pH 7.4 were the same as 394.5 nm.But at alkaline pH 8.6,λ_(max) value of nickel sulfate became 392.0 nm.The combined solution of L-ascorbic acid and nickel sulfate(6 mg/mL each) at pH 2.0 showed 292.5 nm and 392.5 nm,respectively whereas at pH 7.0,L-ascorbic acid showed 296.5 nm and nickel sulfate showed 391.5 nm.At pH 7.4,L-ascorbic acid showed 297.0 nm and nickel sulfate showed 394.0 nm in the combined solution whereas at pH 8.6(alkaline) L-ascorbic acid and nickel sulfate were showing 297.0 and 393.5 nm,respectively. Conclusions:Results clearly indicate an altered chemical behavior of L-ascorbic acid either alone or in combination with nickel sulfate in vitro at different pH.Perhaps oxidation of L-ascorbic acid to L-dehydro ascorbic acid via the free radical(HSc*) generation from the reaction of H,ASc + Ni(Ⅱ) is the cause of such alteration of λ_(max),value of L-ascorbic acid in the presence of metal nickel.

Supplementation of L-ascorbic acid improves the in vitro development of buffalo(Bubalus bubalis)embryos and alters the expression of apoptosis-related genes

Objective:To study the effect of L-ascorbic acid supplementation on the in vitro development of buffalo embryos and evaluate the relative mRNA abundance of some pro-apoptotic,anti-apoptotic,and embryonic development-related genes.Methods:In experiment 1,we evaluated the effect of the addition of 0(control),50,and 100μM L-ascorbic acid to the in vitro maturation medium on the developmental competence in terms of blastocyst rate and relative mRNA abundance of some pro-apoptotic(BAX,BID),anti-apoptotic(BCL-XL,MCL1),and embryonic development(GDF9,BMP15)related genes.Based on the results,we chose 50μM as the suitable dose of L-ascorbic acid for the subsequent experiments.We further evaluated the blastocyst rates following the addition of 50μM L-ascorbic acid to the in vitro culture medium(experiment 2),and in vitro maturation and in vitro culture media(experiment 3).In all three experiments,the maturation and culture media devoid of L-ascorbic acid served as the control group.Results:The blastocyst rate after adding 50μM L-ascorbic acid to the in vitro maturation medium was significantly higher than the control group(P<0.05),whereas 100μM L-ascorbic acid exhibited a negative effect on the blastocyst rate.The blastocyst rates for embryos cultured in 50μM L-ascorbic acid in the in vitro culture medium alone and both in vitro maturation and in vitro culture media were significantly higher than their corresponding control groups(P<0.05).The relative mRNA abundance of BAX significantly decreased in blastocysts produced after the addition of 50μM L-ascorbic acid as compared with the control group(P<0.05),whereas,for MCL1,it significantly decreased in blastocysts produced after the addition of 100μM L-ascorbic acid(P<0.05).Conclusions:The supplementation of 50μM L-ascorbic acid to in vitro maturation and in vitro culture media supports in vitro embryonic development in buffaloes by improving developmental competence and altering the expression of apoptosis-related genes.

Synthesis, Crystal Structure and Antioxidant Activity of 5,6-O-(4-bromophenyl)-L-ascorbic Acid

The title compound 5,6-O-（4-bromophenyl）-L-ascorbic acid （C13H11BrO6, Mr = 343.13） has been synthesized and its structure was characterized by IR, 1H NMR and single-crystal X-ray diffraction. The product is a mixture of two diastereomer compounds （a （7S） and b （7R））. The crystal of a （7S） belongs to orthorhombic system, space group P212121 with a = 6.5362（10）, b = 7.8226（11）, c = 25.294（4） ？, V = 1293.3（3） ？3, Z = 4, Dc = 1.762 g/cm3, μ（MoKα） = 3.202 mm-1, F（000） = 688, R = 0.0235 and wR （I 〉 2σ（I）） = 0.0566. The hydrogen bonding interactions link the molecules to form a three-dimensional system. In addition, 5,6-O-（4-bromophenyl）-L-ascorbic acid （BPAA） exhibits strong free-radical scavenging activities in vitro against 2,2-diphenyl-1-picrylhy- drazyl and superoxide anion. BPAA should be investigated further as a worthy antioxidant.

Synthesis of L-Ascorbic Acid Lactone Derivatives

A small focused library which comprised of L-AA lactone derivatives was built with a facile method.This reported method was optimized by modifying the acidity of the solvent.As a result,12 L-AA lactones were synthesized.Among these lactones,lactones 8–12 were new compounds.The cytotoxicity of these synthetic compounds were investigated.

Conductive Polyacrylonitrile Fiber Prepared by Copper Plating with L-Ascorbic Acid as Reducing Agent

Conductive polyacrylonitrile fibers were prepared by electroless copper plating under weak alkaline conditions,with L-ascorbic acid as reducing agent.The influences of CuSO_(4)·5H_(2)O,L-ascorbic acid,2,2′-bipyridine and K_(4)Fe(CN)_(6) concentration on the conductivity and mass gain percentage of the fibers were studied.The morphological structure of the fibers was characterized by scanning electron microscopy(SEM),and the mechanical properties of the fibers were analyzed through the mechanical property test.The results showed that the optimal reaction conditions were as follows:26 g/L CuSO_(4)·5H_(2)O,26 g/L L-ascorbic acid,12 mg/L 2,2′-bipyridine,7 mg/L K 4Fe(CN)6,and 38℃.The volume resistivity of the conductive PAN fibers prepared by the process was only 3.84×10^(-3)Ω·cm.

Decoding the nexus:branched-chain amino acids and their connection with sleep,circadian rhythms,and cardiometabolic health

The sleep-wake cycle stands as an integrative process essential for sustaining optimal brain function and,either directly or indirectly,overall body health,encompassing metabolic and cardiovascular well-being.Given the heightened metabolic activity of the brain,there exists a considerable demand for nutrients in comparison to other organs.Among these,the branched-chain amino acids,comprising leucine,isoleucine,and valine,display distinctive significance,from their contribution to protein structure to their involvement in overall metabolism,especially in cerebral processes.Among the first amino acids that are released into circulation post-food intake,branched-chain amino acids assume a pivotal role in the regulation of protein synthesis,modulating insulin secretion and the amino acid sensing pathway of target of rapamycin.Branched-chain amino acids are key players in influencing the brain's uptake of monoamine precursors,competing for a shared transporter.Beyond their involvement in protein synthesis,these amino acids contribute to the metabolic cycles ofγ-aminobutyric acid and glutamate,as well as energy metabolism.Notably,they impact GABAergic neurons and the excitation/inhibition balance.The rhythmicity of branchedchain amino acids in plasma concentrations,observed over a 24-hour cycle and conserved in rodent models,is under circadian clock control.The mechanisms underlying those rhythms and the physiological consequences of their disruption are not fully understood.Disturbed sleep,obesity,diabetes,and cardiovascular diseases can elevate branched-chain amino acid concentrations or modify their oscillatory dynamics.The mechanisms driving these effects are currently the focal point of ongoing research efforts,since normalizing branched-chain amino acid levels has the ability to alleviate the severity of these pathologies.In this context,the Drosophila model,though underutilized,holds promise in shedding new light on these mechanisms.Initial findings indicate its potential to introduce novel concepts,particularly in elucidating the intricate connections between the circadian clock,sleep/wake,and metabolism.Consequently,the use and transport of branched-chain amino acids emerge as critical components and orchestrators in the web of interactions across multiple organs throughout the sleep/wake cycle.They could represent one of the so far elusive mechanisms connecting sleep patterns to metabolic and cardiovascular health,paving the way for potential therapeutic interventions.

Increased excitatory amino acid transporter 2 levels in basolateral amygdala astrocytes mediate chronic stress–induced anxiety-like behavior

The conventional perception of astrocytes as mere supportive cells within the brain has recently been called into question by empirical evidence, which has revealed their active involvement in regulating brain function and encoding behaviors associated with emotions.Specifically, astrocytes in the basolateral amygdala have been found to play a role in the modulation of anxiety-like behaviors triggered by chronic stress. Nevertheless, the precise molecular mechanisms by which basolateral amygdala astrocytes regulate chronic stress–induced anxiety-like behaviors remain to be fully elucidated. In this study, we found that in a mouse model of anxiety triggered by unpredictable chronic mild stress, the expression of excitatory amino acid transporter 2 was upregulated in the basolateral amygdala. Interestingly, our findings indicate that the targeted knockdown of excitatory amino acid transporter 2 specifically within the basolateral amygdala astrocytes was able to rescue the anxiety-like behavior in mice subjected to stress. Furthermore, we found that the overexpression of excitatory amino acid transporter 2 in the basolateral amygdala, whether achieved through intracranial administration of excitatory amino acid transporter 2agonists or through injection of excitatory amino acid transporter 2-overexpressing viruses with GfaABC1D promoters, evoked anxiety-like behavior in mice. Our single-nucleus RNA sequencing analysis further confirmed that chronic stress induced an upregulation of excitatory amino acid transporter 2 specifically in astrocytes in the basolateral amygdala. Moreover, through in vivo calcium signal recordings, we found that the frequency of calcium activity in the basolateral amygdala of mice subjected to chronic stress was higher compared with normal mice.After knocking down the expression of excitatory amino acid transporter 2 in the basolateral amygdala, the frequency of calcium activity was not significantly increased, and anxiety-like behavior was obviously mitigated. Additionally, administration of an excitatory amino acid transporter 2 inhibitor in the basolateral amygdala yielded a notable reduction in anxiety level among mice subjected to stress. These results suggest that basolateral amygdala astrocytic excitatory amino acid transporter 2 plays a role in in the regulation of unpredictable chronic mild stress-induced anxiety-like behavior by impacting the activity of local glutamatergic neurons, and targeting excitatory amino acid transporter 2 in the basolateral amygdala holds therapeutic promise for addressing anxiety disorders.

Microencapsulation of L-Ascorbic Acid by Spray Drying Using Sodium Alginate as Wall Material

L-ascorbic acid is a water soluble vitamin (vitamin C) widely used as an additive in foods and cosmetics. It has high instability against certain environmental factors;the main cause of its deterioration is oxidation. Microencapsulation is an effective protection technique of L-ascorbic acid from its degradation reactions. This work is focused on the encapsulation of L-ascorbic acid by spray drying technique using sodium alginate as wall material. The microcapsules morphology was observed by scanning electron microscopy (SEM) and the encapsulation efficiency was determined by spectrophotometric analysis. Results showed that encapsulation efficiency was of 93.48% and after 30 days was of 92.55%;differences were not significant, so that the stability of L-ascorbic acid was not affected. Encapsulation yields obtained were low, at around 30%, but the microcapsules morphology obtained is spherical.

Targeting harmful effects of non-excitatory amino acids as an alternative therapeutic strategy to reduce ischemic damage

The involvement of the excitatory amino acids glutamate and aspartate in ce rebral ischemia and excitotoxicity is well-documented.Nevertheless,the role of non-excitatory amino acids in brain damage following a stroke or brain trauma remains largely understudied.The release of amino acids by necrotic cells in the ischemic core may contribute to the expansion of the penumbra.Our findings indicated that the reversible loss of field excitato ry postsynaptic potentials caused by transient hypoxia became irreversible when exposed to a mixture of just four non-excitatory amino acids(L-alanine,glycine,L-glutamine,and L-serine)at their plasma concentrations.These amino acids induce swelling in the somas of neurons and astrocytes during hypoxia,along with permanent dendritic damage mediated by N-methyl-D-aspartate receptors.Blocking N-methyl-D-aspartate receptors prevented neuronal damage in the presence of these amino acids during hypoxia.It is likely that astroglial swelling caused by the accumulation of these amino acids via the alanine-serine-cysteine transporter 2 exchanger and system N transporters activates volume-regulated anion channels,leading to the release of excitotoxins and subsequent neuronal damage through N-methyl-D-aspartate receptor activation.Thus,previously unrecognized mechanisms involving non-excitatory amino acids may contribute to the progression and expansion of brain injury in neurological emergencies such as stroke and traumatic brain injury.Understanding these pathways co uld highlight new therapeutic targets to mitigate brain injury.

Simultaneous Determination of Dopamine and L-Ascorbic Acid by Modified Carbon Paste Electrode with Ni (II) Cyclam Complex

The electroanalysis of dopamine (DA) and ascorbic acid (AA) by square wave voltammetry has been performed at a modified carbon paste electrode with macrocyclic ligand 1, 4, 8, 11-tetraazacyclotetradecane (cyclam) and monolayer of Ni (II) cyclam. In pH 7.2 buffer solutions, the electrostatic reaction of AA with di-positive monolayer shifts the oxidation potential to less positive potential, while the electrostatic repulsion of DA with the monolayer shifts the oxidation potential of DA to more positive potential. The separation between the oxidation peaks of AA and DA at the present di-positive monolayer modified electrode (252 mV) was larger than that (187 mV) at the cyclam modified electrode. In addition, the catalytic oxidation of AA by oxidized DA has been advantageously eliminated at the modified carbon paste electrode with cyclam and Ni (II) cyclam complex. Thus, the determination of DA in the presence of an excess of AA is possible with the present modified electrodes.

Organic Media Enhanced Spectrofluorimetric Determination of L-Ascorbic Acid

A novel spectrofluorimetric method for the determination of L ascorbic acid is proposed. It is based on the inhibition of L ascorbic acid on the formation of 2,3 diaminophenazine, which is an oxidation product of o phenylenediamine catalyzed by laccase .The fluorescence (at λ ex /λ em =464 nm /530 nnm) was enhanced strongly in the presence of organic media . The mechanism of o phenylenediamine oxidation reaction catalyzed by laccase in the presence of L ascorbic acid is discussed .L ascorbic acid is determined in the ethanol, 1,4 dioxane and acetone over the linear range of 4.0×10 -7 ～1.2×10 -4 mol/L, 4.0×10 -7 ～ 8.0×10 -5 mol/L and 4.0×10 -7 ～1.0×10 -4 mol/L with a detection limit of 1.20×10 -8 mol/L,1.19×10 -8 mol/L and 1.24×10 -8 mol/L, respectively. The method has been successfully applied to the simple and rapid determination of L ascorbic acid in pharmaceuticals and milk powder.

Additive neurorestorative effects of exercise and docosahexaenoic acid intake in a mouse model of Parkinson’s disease

There is a need to develop interventions to slow or reverse the degeneration of dopamine neurons in Parkinson’s disease after diagnosis.Given that preclinical and clinical studies suggest benefits of dietary n-3 polyunsaturated fatty acids,such as docosahexaenoic acid,and exercise in Parkinson’s disease,we investigated whether both could synergistically interact to induce recovery of the dopaminergic pathway.First,mice received a unilateral stereotactic injection of 6-hydroxydopamine into the striatum to establish an animal model of nigrostriatal denervation.Four weeks after lesion,animals were fed a docosahexaenoic acid-enriched or a control diet for the next 8 weeks.During this period,the animals had access to a running wheel,which they could use or not.Docosahexaenoic acid treatment,voluntary exercise,or the combination of both had no effect on(i)distance traveled in the open field test,(ii)the percentage of contraversive rotations in the apomorphine-induction test or(iii)the number of tyrosine-hydroxylase-positive cells in the substantia nigra pars compacta.However,the docosahexaenoic acid diet increased the number of tyrosine-hydroxylase-positive terminals and induced a rise in dopamine concentrations in the lesioned striatum.Compared to docosahexaenoic acid treatment or exercise alone,the combination of docosahexaenoic acid and exercise(i)improved forelimb balance in the stepping test,(ii)decreased the striatal DOPAC/dopamine ratio and(iii)led to increased dopamine transporter levels in the lesioned striatum.The present results suggest that the combination of exercise and docosahexaenoic acid may act synergistically in the striatum of mice with a unilateral lesion of the dopaminergic system and provide support for clinical trials combining nutrition and physical exercise in the treatment of Parkinson’s disease.

Maintaining moderate levels of hypochlorous acid promotes neural stem cell proliferation and differentiation in the recovery phase of stroke

It has been shown clinically that continuous removal of ischemia/reperfusion-induced reactive oxygen species is not conducive to the recovery of late stroke.Indeed,previous studies have shown that excessive increases in hypochlorous acid after stroke can cause severe damage to brain tissue.Our previous studies have found that a small amount of hypochlorous acid still exists in the later stage of stroke,but its specific role and mechanism are currently unclear.To simulate stroke in vivo,a middle cerebral artery occlusion rat model was established,with an oxygen-glucose deprivation/reoxygenation model established in vitro to mimic stroke.We found that in the early stage(within 24 hours)of ischemic stroke,neutrophils produced a large amount of hypochlorous acid,while in the recovery phase(10 days after stroke),microglia were activated and produced a small amount of hypochlorous acid.Further,in acute stroke in rats,hypochlorous acid production was prevented using a hypochlorous acid scavenger,taurine,or myeloperoxidase inhibitor,4-aminobenzoic acid hydrazide.Our results showed that high levels of hypochlorous acid(200μM)induced neuronal apoptosis after oxygen/glucose deprivation/reoxygenation.However,in the recovery phase of the middle cerebral artery occlusion model,a moderate level of hypochlorous acid promoted the proliferation and differentiation of neural stem cells into neurons and astrocytes.This suggests that hypochlorous acid plays different roles at different phases of cerebral ischemia/reperfusion injury.Lower levels of hypochlorous acid(5 and 100μM)promoted nuclear translocation ofβ-catenin.By transfection of single-site mutation plasmids,we found that hypochlorous acid induced chlorination of theβ-catenin tyrosine 30 residue,which promoted nuclear translocation.Altogether,our study indicates that maintaining low levels of hypochlorous acid plays a key role in the recovery of neurological function.

Enhanced autophagic clearance of amyloid-βvia histone deacetylase 6-mediated V-ATPase assembly and lysosomal acidification protects against Alzheimer's disease in vitro and in vivo

Recent studies have suggested that abnormal acidification of lysosomes induces autophagic accumulation of amyloid-βin neurons,which is a key step in senile plaque formation.Therefore,resto ring normal lysosomal function and rebalancing lysosomal acidification in neurons in the brain may be a new treatment strategy for Alzheimer's disease.Microtubule acetylation/deacetylation plays a central role in lysosomal acidification.Here,we show that inhibiting the classic microtubule deacetylase histone deacetylase 6 with an histone deacetylase 6 shRNA or thehistone deacetylase 6 inhibitor valproic acid promoted lysosomal reacidification by modulating V-ATPase assembly in Alzheimer's disease.Fu rthermore,we found that treatment with valproic acid markedly enhanced autophagy.promoted clearance of amyloid-βaggregates,and ameliorated cognitive deficits in a mouse model of Alzheimer's disease.Our findings demonstrate a previously unknown neuroprotective mechanism in Alzheimer's disease,in which histone deacetylase 6 inhibition by valproic acid increases V-ATPase assembly and lysosomal acidification.

First Oxidation Product of Vitamin C, the Dehydro-L-Ascorbic Acid Dimer： A Study Based on FTIR-Raman and DFT Calculations

We studied the first oxidation product of vitamin C, the dehydro-L-ascorbic acid dimer and characterized it by infrared and Raman spectroscopies in the solid phase. The Density functional theory was used to study its structure and vibrational properties. These calculations gave us a precise knowledge of the normal modes of vibration taking into account that the molecule comprises a system of five fused rings; non planar γ-lactone and furonose rings are attached to a central dioxan ring in the twisted boat conformation. The calculated harmonic vibrational frequencies are consistent with the experimental vibrational spectra. An assignment of the observed spectral features is proposed. The shift of the band located in the infrared spectrum of the ascorbic acid from 3409 cm^-1 to 3299 cml and the remarkable increase in the band intensity at 1784 cm^-1 evidences the acid decomposition into its first product, the dehydro-L-ascorbic acid. The theoretical vibrational calculations allowed us to obtain a set of scaled force constants. The nature of the different -γ-lactone, furanose and dioxan rings and their topological properties were investigated by means of natural bond orbital and Bader＇s atoms in the molecule theory, respectively.

Activation of adult endogenous neurogenesis by a hyaluronic acid collagen gel containing basic fibroblast growth factor promotes remodeling and functional recovery of the injured cerebral cortex

The presence of endogenous neural stem/progenitor cells in the adult mammalian brain suggests that the central nervous system can be repaired and regenerated after injury.However,whether it is possible to stimulate neurogenesis and reconstruct cortical layers II to VI in non-neurogenic regions,such as the cortex,remains unknown.In this study,we implanted a hyaluronic acid collagen gel loaded with basic fibroblast growth factor into the motor cortex immediately following traumatic injury.Our findings reveal that this gel effectively stimulated the proliferation and migration of endogenous neural stem/progenitor cells,as well as their differentiation into mature and functionally integrated neurons.Importantly,these new neurons reconstructed the architecture of cortical layers II to VI,integrated into the existing neural circuitry,and ultimately led to improved brain function.These findings offer novel insight into potential clinical treatments for traumatic cerebral cortex injuries.

Study of Diffusion through the Skin of Coated L-Ascorbic Acid by Fluid Bed Technology

Coating protects substances such as L-ascorbic acid from natural processes like oxidation. In this study, L-ascorbic acid was coated by fluid bed technology. A pH-dependent polymer was used as a coating material in order to release L-ascorbic acid (dissolution above pH 5.5) under conditions closest to the skin’s natural condition. Different techniques were used to determine the coating (SEM and size distribution) and to evaluate the percentage of coated L-ascorbic acid and its diffusion through the skin.