Carbon-supported T-Nb2O5 nanospheres and MoS2 composites with a mosaic structure for insertion-conversion anode materials.

Reasonably combining the strengths of insertion and conversion anode materials to create an advanced anode material remains a formidable challenge for rechargeable lithium-ion batteries (LIBs). In this work, bulk MoS2 embedded with T-Nb2O5 nanospheres was synthesized via a simple hydrothermal process and a polydopamine carbon source was introduced by heat treatment. The design strategy can effectively accelerate the charge transfer and reduce the volume expansion during electrochemical cycling, leading to an improvement in lithium storage performance. As a consequence, the coexistence of T-Nb2O5, MoS2 and C can achieve the best synergistic effect when the molar ratio of Nb and Mo sources was 1 : 1. Notably, the T-Nb2O5@MoS2@C-1-1 electrode not only delivered an excellent reversible capacity of 518 mA h g-1 at a current density of 0.1 A g-1 but also exhibited superb cycling stability. The specific capacity of this electrode maintained 187 mA h g-1 at 2 A g-1 after 1000 cycles with a negligible capacity fading rate of only 0.015% per cycle.

Intracranial infectious aneurysm caused by infective endocarditis resulting in intracerebral rebleeding following previous surgery for intracerebral hemorrhage: A case report and literature review.

Intracranial infectious aneurysm (IIA) is one of the most severe complications of infective endocarditis (IE). Approximately 2-9% of patients with IE have IIA, which possibly results in severe neurological deficits. Currently, the most common treatment for IIA is endovascular treatment, while excision surgery is less common. The present study describes the case of a 33-year-old male patient who underwent a primary evacuation of an intracerebral hemorrhage (ICH) in the right temporal lobe. The patient was diagnosed with IE and IIA by examinations with an enhanced computed tomography scan, echocardiography and blood culture. In the recovery period after surgery, the patient suffered intracerebral rebleeding and underwent a surgery of IIA excision. The patient finally achieved a good prognosis without severe neurological dysfunction. In summary, IIAs are extremely rare entities, and a rare cause of spontaneous ICH. Previous research has demonstrated that the majority of ruptured IIAs receive endovascular treatment rather than conventional surgery. In the case presented herein, IIA surgical excision was successfully performed and complete pathological results were obtained, which has rarely been reported in the literature. The present case report reinforces the validity of traditional craniotomy according to the characteristics of IIAs.

[Predictive value of magnetic resonance spectroscopy combined with diffusion weighted imaging in patients with secondary brain insult after spontaneous intra-cerebral hemorrhage].

OBJECTIVE: To investigate the correlations between the changes of N-acetylaspartate/creatine (NAA/Cr) detected by magnetic resonance spectroscopy (MRS), and of the relative apparent diffusion coefficient (rADC) detected by diffusion weighted imaging (DWI) and the occurrence and outcome of secondary brain injury (SBI) in patients with spontaneous intra-cerebral hemorrhage (SICH). METHODS: One hundred and eight SICH patients diagnosed by CT from January 2014 to December 2019 in the First People's Hospital of Huzhou were selected as the research objects. MRS and DWI examinations were performed on day 2 after admission. The body temperature, blood pressure, blood glucose, blood sodium, arterial oxygen partial pressure (PaO2) and other indexes were continuously monitored. The patients were divided into two groups: SBI group (46 cases) and control group (62 cases) according to whether there were secondary brain injury factors (SBIF). The differences in NAA/Cr and rADC of the edema area and Glasgow outcome score (GOS) after 6 months were compared between the two groups; multivariate Logistic regression analysis was used to analyze the risk factors of SBI. RESULTS: The NAA/Cr and rADC of perihematoma edema area and GOS after 6 months in SBI group were significantly lower than those in control group [NAA/Cr: 1.64±0.35 vs. 1.87±0.41, rADC: 2.57±0.39 vs. 2.75±0.45, GOS after 6 months (points): 3.47±0.59 vs. 3.76±0.65], with significant differences (all P < 0.05). Logistic regression analysis showed that NAA/Cr and rADC were the risk factors for the occurrence of SBI [odds ratio (OR) values were 0.172, 0.343, 95% confidence intervals (95%CI) were 0.048-0.609 and 0.118-0.996, respectively, both P < 0.05]. CONCLUSIONS: MRS combined with DWI has a certain value in predicting SBI after SICH. SBI can aggravate brain injury and affect the prognosis of patients. SBI should be actively prevented and intervention, carried out.

miR-494-3p Regulates Cellular Proliferation, Invasion, Migration, and Apoptosis by PTEN/AKT Signaling in Human Glioblastoma Cells.

Malignant gliomas are the most common primary brain tumors, and the molecular mechanisms involving their progression and recurrence are still largely unclear. Substantial data indicate that the oncogene miR-494-3p is significantly elevated in gliomas, but the molecular functions of miR-494-3p in gliomagenesis are largely unknown. The present study aimed to explore the role of miR-494-3p and its molecular mechanism in human brain gliomas, malignant glioma cell lines, and cancer stem-like cells. The expression level of miR-494-3p in 48 human glioma issues and 8 normal brain tissues was determined using stem-loop real-time polymerase chain reaction (PCR). To study the function of miR-494-3p inhibitor in glioma cells, the miR-494-3p inhibitor lentivirus was used to transfect glioma cells. Transwell invasion system was used to estimate the effects of miR-494-3p inhibitor on the invasiveness of glioma cells. A mouse model was used to test the effect of miR-494-3p inhibitor on glioma proliferation and invasion in vivo. Results showed that the expression of miR-494-3p in human brain glioma tissues was higher than in normal brain tissues. Downregulated expression of miR-494-3p can inhibit the invasion and proliferation and promote apoptosis in glioma cells. Quantitative reverse transcription PCR and Western blotting analysis revealed that the expression of PTEN was increased after downexpression of miR-494-3p in glioma cells (U87 and U251). miR-494-3p inhibitor could prevent migration, invasion, proliferation, and promote apotosis in gliomas through PTEN/AKT pathway. Therefore, the study results have shown that miR-494-3p may act as a therapeutic target in gliomas.

Anti-inflammatory effect of chlorogenic acid on the IL-8 production in Caco-2 cells and the dextran sulphate sodium-induced colitis symptoms in C57BL/6 mice.

Chlorogenic acid (CHA) is an antioxidant polyphenol prevalent in human diet, with coffee, fruits, and vegetables being its main source. Effects of CHA and CHA metabolites were evaluated on the IL-8 production in human intestinal Caco-2 cells induced by combined stimulation with tumour necrosis factor alpha (TNFα) and H2O2. CHA and caffeic acid (CA) inhibited TNFα- and H2O2-induced IL-8 production. We also examined the in vivo effects of CHA and CA using dextran sulphate sodium (DSS)-induced colitis in mice. CHA attenuated DSS-induced body weight loss, diarrhea, fecal blood, and shortening of colon and dramatically improved colitis histological scores. Furthermore, increases in the mRNA expression of colonic macrophage inflammatory protein 2 and IL-1ß, which were induced by DSS, were significantly suppressed by CHA supplementation. These results suggest that dietary CHA use may aid in the prevention of intestinal inflammatory conditions.

Identification of a NFKBIA polymorphism associated with lower NFKBIA protein levels and poor survival outcomes in patients with glioblastoma multiforme.

The aberrant constitutive activation of nuclear factor-κB (NF-κB) has been observed in glioblastomas, while NF-κB inhibitor alpha (NFKBIA) inhibits the NF-κB signaling pathway under several physiological processes. However, the contribution of NFKBIA to glioblastomas is poorly understood. In the present study, using gene sequencing, we identified rs1957106 as a novel single nucleotide polymorphism (SNP) in NFKBIA in glioblastoma and found that it was more frequently present in glioblastoma patients. In addition, we examined the association between different genotypes of the rs1957106 SNP of NFKBIA and the gene copy number, mRNA level and protein expression of NFKBIA. The SNP rs1957106 CT and TT genotypes were found to be associated with lower NFKBIA protein levels and a poor prognosis of pateints with glioblastoma. Hence, by identifying rs1957106 as a novel SNP in NFKBIA in glioblastoma patients, we provide a new platform for further investigating the function of NFKBIA in the pathobiology of glioblastoma.

MicroRNA-16 inhibits glioma cell growth and invasion through suppression of BCL2 and the nuclear factor-κB1/MMP9 signaling pathway.

Recent studies have identified a class of small non-coding RNA molecules, named microRNA (miRNA), that is dysregulated in malignant brain glioblastoma. Substantial data have indicated that miRNA-16 (miR-16) plays a significant role in tumors of various origins. This miRNA has been linked to various aspects of carcinogenesis, including cell apoptosis and migration. However, the molecular functions of miR-16 in gliomagenesis are largely unknown. We have shown that the expression of miR-16 in human brain glioma tissues was lower than in non-cancerous brain tissues, and that the expression of miR-16 decreased with increasing degrees of malignancy. Our data suggest that the expression of miR-16 and nuclear factor (NF)-κB1 was negatively correlated with glioma levels. MicroRNA-16 decreased glioma malignancy by downregulating NF-κB1 and MMP9, and led to suppressed invasiveness of human glioma cell lines SHG44, U87, and U373. Our results also indicated that upregulation of miR-16 promoted apoptosis by suppressing BCL2 expression. Finally, the upregulation of miR-16 in a nude mice model of human glioma resulted in significant suppression of glioma growth and invasiveness. Taken together, our experiments have validated the important role of miR-16 as a tumor suppressor gene in glioma growth and invasiveness, and revealed a novel mechanism of miR-16-mediated regulation in glioma growth and invasiveness through inhibition of BCL2 and the NF-κB1/MMP-9 signaling pathway. Therefore, our experiments suggest the possible future use of miR-16 as a therapeutic target in gliomas.

Wild rice (Zizania palustris L.) prevents atherogenesis in LDL receptor knockout mice.

OBJECTIVES: Dietary modifications including healthy eating constitute one of the first line strategies for prevention and treatment of cardiovascular disease (CVD) risk factors including high cholesterol and atherosclerosis. The purpose of the present study was to investigate the potential cardiovascular benefits of wild rice in male and female LDL-receptor-deficient (LDLr-KO) mice. METHODS: Wild rice was used to create a semi-synthetic diet containing approximately 60% of total energy from carbohydrate. Two other experimental diets were similar in macronutrient composition, but containing either white rice or commercial carbohydrate sources. All diets were supplemented with 0.06% (w/w) dietary cholesterol. The mice were divided into six experimental groups and fed with these diets over 24 weeks. RESULTS: Consumption of wild rice significantly reduced the size and severity of atherosclerotic lesions in the aortic roots of male and female mice by 71 and 61% respectively, compared to the control group of the same gender. This effect was associated with significant reductions of plasma cholesterol levels by 15 and 40%, low density lipoprotein (LDL) levels by 12 and 42%, and very low density lipoprotein (VLDL) levels by 35 and 75% respectively, in male and female mice compared to the control group of the same gender. Increased fecal cholesterol excretion of up to 34% was also noted, compared to the control group of the same gender. However, the antiatherogenic effect of wild rice was not associated with increased superoxide dismutase (SOD) and catalase (CAT) activities. CONCLUSION: Current data suggest that cholesterol-lowering effects of wild rice may be the main factor for the prevention of atherogenesis in LDLr-KO mice. Additional studies are needed to understand the mechanism of action.

Ultrasensitive electrochemical immunosensor for HE4 based on rolling circle amplification.

A novel electrochemical immunoassay system for the detection of human epididymis-specific protein 4 (HE4) was developed. A chitosan-titanium carbide (TiC) nanocomposition film was first electrodeposited onto a tin-doped indium oxide (ITO) electrode at a constant potential. Gold (Au) nanoparticles were then electrodeposited on the surface of the chitosan-TiC film by cyclic voltammetry (CV). The capture antibody (anti-HE4) was adsorbed onto the Au and TiC nanoparticles. After a specific sandwich immunoreaction among the capture antibody, HE4, and biotinylated secondary antibody, biotinylated primer DNA was immobilized on the secondary antibody by biotin-streptavidin system. Appropriate amounts of circular template DNA and biotinylated primer DNA were used for rolling circle amplification (RCA) under optimal conditions. The RCA products provided a large number of sites to link DNA detection probes. Doxorubicin hydrochloride intercalated the CG-GC steps between the RCA products and the DNA detection probes, which was monitored by differential pulse voltammetry (DPV) based on the current signal of doxorubicin hydrochloride. With the above-mentioned amplification factors, the current responded to HE4 linearly in the concentration range of 3-300 pM under optimal detection conditions, with a detection limit of 0.06 pM. Stepwise changes in the microscopic features of the surfaces and electrochemical properties upon the formation of each layer were confirmed by scanning electron microscopy (SEM), atomic force microscopy (AFM), and electrochemical impedance spectroscopy (EIS). This system was successfully employed for the detection of HE4 with good accuracy and renewable ability.

Synergistic effect of tumor necrosis factor-alpha and hydrogen peroxide on the induction of IL-8 production in human intestinal Caco-2 cells.

Oxidative stress and inflammatory cytokines such as TNF-α are thought to be involved in mucosal inflammation. The intestinal epithelium may be concurrently stimulated by both oxidative stress and inflammatory cytokines during the inflammation process in the intestines. However, experimental models for intestinal inflammation still employ single stimulation, either by an oxidative stress or inflammatory cytokine. We therefore examined an in vitro inflammation study using human intestinal epithelial Caco-2 cells, in which the cells were stimulated both by hydrogen peroxide and TNF-α, and measured the IL-8 production as an index of inflammation. The IL-8 production (secretion, mRNA expression, and transcriptional activity) induced by both TNF-α and H(2)O(2) was significantly higher than that by single stimulation. The synergistic effect of TNF-α and H(2)O(2) on the NF-κB signaling pathway (transcriptional activity and p65 nuclear translocation) was also observed. Oxidative stress and TNF-α may cooperatively enhance IL-8 production via NF-κB in Caco-2 cells.

[Clinic analysis of 16 patients of craniocerebral trauma with Labbé vein injury].

OBJECTIVES: To study the mechanism of Labbé vein injury, and its effect on traumatic cerebral infarction and prognosis in patients of craniocerebral trauma. METHODS: The clinic imageology and data of 16 patients of craniocerebral trauma with Labbé vein injury approved intraoperatively from June 2006 to February 2009 were analyzed. To compare the effect of the intraoperative finding of Labbé vein damage and blood vessel treatment on traumatic cerebral infarction, and to analyze the traumatic cerebral infarction size and prognosis. RESULTS: All the 16 patients had acute subdural hematoma and(or) intracerebral hematoma. And 15 of all the 16 patients with Labbé vein injury suffered from skull fractures. All patients accepted hematoma cleaning and intracranial decompression procedure by removing skull. The preoperative Glasgow coma scale (GCS) were as following: 5 patients being between 9 - 12, 7 patients being between 6 - 8 and 4 patients being between 3 - 5. Eight patients had cerebral hernia before operations on admission, and among them, 3 patients had corectasis of both sides and 5 patients had corectasis of only one side, the other 8 patients had no corectasis. Postoperatively, 14 patients suffered from traumatic cerebral infarction of different grades. After follow-ups of 24 months, 8 patients had relatively good prognosis, with 4 patients having good recoveries and 4 having middle disability; the other 8 had bad prognosis, including 3 patients being seriously disable and 5 kept vegetative state. CONCLUSIONS: Impact injury and counterblow are the main reasons to the injury of Labbé vein, which consequently leads to serious traumatic cerebral infarction and bad prognosis. Intraoperatively, it is quite important to protect Labbé vein during the surgery, which should not be easily cut or obstructed by electric coagulation, and this is an effective way to improve the prognosis of these patients.

A high-lipid diet potentiates left ventricular dysfunction in nitric oxide synthase 3-deficient mice after chronic pressure overload.

A high-lipid diet (HLD) may lead to adverse left ventricular (LV) remodeling and endothelial dysfunction in conditions of hemodynamic stress. Although congenital absence of nitric oxide synthase 3 (NOS3) leads to adverse LV remodeling after transverse aortic constriction (TAC), the effects of a HLD in this state remains unknown. Wild-type (WT) and NOS3 knockout mice (NOS3(-/-)) were randomized into the following 4 groups: 1) WT + low-lipid diet (LLD) (10% of energy); 2) WT + HLD (60% of energy); 3) NOS3(-/-) + LLD; and 4) NOS3(-/-) + HLD for a total of 12 wk. After 1 wk of randomization, TAC was performed on all groups. Serial echocardiography revealed a decrease in LV ejection fraction (LVEF) in WT and NOS3(-/-) mice fed the HLD compared with those fed the LLD diet at 12 wk post-TAC. Mice fed the NOS3(-/-) + HLD diet had a lower LVEF compared with mice in the other 3 groups (P < 0.05). There was greater myocyte hypertrophy, interstitial fibrosis, and percentage change in plasma cholesterol concentrations in the NOS3(-/-) + HLD group 12 wk post-TAC compared with the other 3 groups. Although high molecular weight fibroblast growth factor-2, a marker of cardiac hypertrophy, was more upregulated in the NOS3(-/-) + HLD group than in the other groups, markers of the renin-angiotensin system did not differ among them. A HLD potentiates LV dysfunction in NOS3(-/-) mice in a chronic pressure overload state.

Lack of evidence for antiatherogenic effects of wheat bran or corn bran in apolipoprotein E-knockout mice.

Epidemiological studies have suggested that intake of whole grains is inversely associated with coronary artery disease. The mechanisms, however, are not completely clear. We tested the hypothesis that intake of wheat bran or corn bran would (1) increase the plasma concentration of phenolic antioxidants and (2) reduce atherosclerosis in apo E-knockout mice. Apo E-knockout (E-KO) mice were fed for 18 weeks with a 0.1% cholesterol-supplemented diet in the absence of grain brans or the presence of 1.7% yellow dent corn bran or 3.3% hard red spring wheat bran. The concentration of antioxidant ferulic acid in plasma and urine was measured by HPLC to monitor the bioavailability of grain phenolics. Plasma lipoprotein profiles were determined by a combination of HPLC and online enzymatic methods. Urinary 15-isoprostane F(2t), an in vivo LDL oxidation biomarker, and atherosclerotic lesions were analyzed by ELISA and histological methods, respectively. Dietary supplementation with corn or wheat bran resulted in a 4- and 24-fold increase, respectively, in urinary excretion of ferulic acid. The urinary recovery rate of ferulic acid from the two brans in apo E-KO mice was approximately 1.9-2.9%. Dietary corn bran but not wheat bran also significantly increased the concentration of total ferulic acid in plasma. Nevertheless, the supplementation with either bran product for 18 weeks did not significantly alter the urinary excretion of 15-isoprostane F(2t), change the lipoprotein profiles, nor reduce the atherosclerotic lesion development in this animal model. The results suggest that phenolic antioxidants from the two types of bran may not be sufficient to reduce atherosclerosis in this animal model.

Pro-atherogenic effects of probucol in apo E-KO mice may be mediated through alterations in immune system: Parallel alterations in gene expression in the aorta and liver.

OBJECTIVE: To establish underlying molecular mechanisms of pro-atherogenic effects of probucol in apo E-KO mice. METHODS: Affymetrix Gene Chip System, GenMAPP/MAPPFinder software and real-time PCR techniques were used to identify alterations in gene expression and biological pathways in the liver and aorta of both male apo E-KO and male wild-type mice treated with or without probucol (1%, w/w) for 18 weeks. Plasma levels of lipids, cytokines, liver function test, and the extent of atherosclerosis and liver histology were examined. RESULTS AND CONCLUSIONS: Probucol treatment paradoxically reduced plasma cholesterol levels, increased plasma cytokine levels and atherogenesis in apo E-KO mice. Three hundred and sixty genes/transcripts and 110 biological processes were significantly differentially expressed in the liver of probucol-treated apo E-KO mice. The response to biotic stimulus, immune response and inflammatory response were the most prominent processes expressed in the liver. The expression of 60 of these genes involved in immune response including inflammatory responses, antigen presentation, humoral immune response, immune cell activation, innate immune response, and regulation of immune response was over-expressed. Many of these genes were also over-expressed in the aorta of probucol-treated apo E-KO mice. Such effects of probucol were not observed in the liver and aorta of wild-type mice. A significant interaction between apo E deficiency and probucol treatment was observed. Histological examinations showed a significant infiltration of inflammatory cells in the liver of probucol-treated apo E-KO mice, but not in C57BL/6 mice. These findings suggest that probucol-induced atherogenesis may be mediated through a pro-inflammatory state.

Effects of long-term consumption of a high-fructose diet on conventional cardiovascular risk factors in Sprague-Dawley rats.

We investigated the effects of a high-fructose (HF) diet on cardiovascular risks in Sprague-Dawley rats. Twelve rats were randomly assigned to standard chow or HF diet for 20 weeks. Systolic blood pressure and circulating insulin, total cholesterol, and triacylglycerol levels were significantly higher in the HF group. Aortic sections appeared normal, but liver sections from the HF group showed lipid accretion, mild inflammation, and bile pigmentation. Liver samples from the HF group showed significantly higher total lipid levels and changes in fatty acid profile. Levels of 16:0, cis-9-18:2, cis-11-20:1, cis-13-20:1, cis-11-20:2 and 24:0 were significantly raised in the phospholipid fraction. Lower levels of cis-11-18:1, cis-9-18:2, and cis-11-20:1 and increased levels of 16:1, cis-9-18:1, and cis-13-20:1 were found in the non-esterified fatty acid fraction. HF-feeding resulted in significant reductions in plasma levels of certain inflammatory biomarkers. HF intake over time may negatively impact cardiovascular health and liver function in rats.

Dietary taurine attenuates dextran sulfate sodium (DSS)-induced experimental colitis in mice.

Effects of dietary taurine on the experimental colitis induced by dextran sulfate sodium (DSS) were studied. C57BL/6 mice administrated taurine or placebo for 5 days were given 3% DSS to induce acute. The colitis was as-sessed using indices such as diarrhea/bleeding scores, colon length change, histological score and tissue myeloperoxidase (MPO) activity. Further, tissue mRNA levels of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and macrophage inflammatory protein (MIP)-2, were determined by real-time PCR. Taurine supplementation significantly attenuated the severity of diarrhea, colon shortening, histological score, MPO activity elevation and abnormal MIP-2 gene expression, indicating that taurine prevents DSS-induced colitis. Taurine also inhibited the TNF-alpha-induced secretion of IL-8 (a human homologue of MIP-2) from human intestinal epithelial Caco-2 cells. Inhibition of chemokine secretion from intestinal cells may be involved in the mechanisms underlying the cytoprotective function of taurine in the intestinal epithelium.

5-caffeoylquinic acid and caffeic acid down-regulate the oxidative stress- and TNF-alpha-induced secretion of interleukin-8 from Caco-2 cells.

Although chlorogenic acid (CHA) easily reaches a millimolar level in the gastrointestinal tract because of its high concentration in coffee and fruits, its effects on intestinal epithelial cells have been little reported. We investigated in this study the down-regulative effects of 5-caffeoylquinic acid (CQA), the predominant isomer of CHA, on the H(2)O(2-) or TNF-alpha-induced secretion of interleukin (IL)-8, a central pro-inflammatory chemokine involved in the pathogenesis of inflammatory bowel diseases, in human intestinal epithelial Caco-2 cells. After the cells had been pre- and simultaneously treated with CQA, the oversecretion of IL-8 and overexpression of its mRNA induced by H(2)O(2) were significantly suppressed in a dose-dependent manner in the range of 0.25-2.00 mmol/L. We further found that a metabolite of CQA, caffeic acid (CA), but not quinic acid, significantly inhibited the H(2)O(2)-induced IL-8 secretion and its mRNA expression in the same dose-dependent manner. Both CQA and CA suppressed the TNF-alpha-induced IL-8 secretion as well. Caffeic acid at 2.00 mmol/l was able to absolutely block the H(2)O(2)- or TNF-alpha-induced oversecretion of IL-8 in Caco-2 cells. However, CQA and CA did not suppress the TNF-alpha-induced increase in the IL-8 mRNA expression, indicating that the suppressive mechanisms are different between TNF-alpha-induced and H(2)O(2)-induced IL-8 production models. These results suggest that the habit of drinking coffee and/or eating fruits with a high CHA content may be beneficial to humans in preventing the genesis of inflammatory bowel diseases.

Chemistry, natural sources, dietary intake and pharmacokinetic properties of ferulic acid: A review.

Ferulic acid (FA) is an abundant dietary antioxidant which may offer beneficial effects against cancer, cardiovascular disease, diabetes and Alzheimer's disease. The impact of FA on health depends on its intake and pharmacokinetic properties. In this article, the literature pertaining to chemistry, natural sources, dietary intake and pharmacokinetic properties of FA is critically reviewed. High levels of FA are found in both free and bound forms in vegetables, fruits, cereals, and coffee. We have estimated that consumption of these foods may result in approximately 150-250mg/day of FA intake. FA can be absorbed along the entire gastrointestinal tract and metabolized mainly by the liver. The absorption and metabolism of FA seem to be dose dependent at least in experimental settings. Further pharmacokinetic and pharmacodynamic studies are required to characterize the impact of FA on human health.

Phenolic acids are absorbed from the rat stomach with different absorption rates.

The intestinal absorption characteristics of phenolic acids (PAs) have been elucidated in terms of their affinity for the monocarboxylic acid transporter (MCT). Recently, the involvement of the stomach has been implicated in the absorption of polyphenols. The present work demonstrates that the gastric absorption efficiency of each PA is apparently different between various PAs. Various PAs with different affinities for MCT were administered (2.25 mumol) to rat stomach, and then the plasma concentration of the PA was measured. The plasma concentration of ferulic acid (FA) peaked 5 min after administration in the stomach. At 5 min after administration, the plasma concentration of each PA increased in the order: gallic acid = chlorogenic acid < caffeic acid < p-coumaric acid = FA. This order matches their respective affinity for MCT in Caco-2 cells, which we have demonstrated in previous studies. These results indicated that MCT might be involved in the gastric absorption of PAs, similar to the intestinal absorption.

Oral exposure to cadmium chloride triggers an acute inflammatory response in the intestines of mice, initiated by the over-expression of tissue macrophage inflammatory protein-2 mRNA.

Intestinal inflammation is an indispensable protective response of the gut immune system to aggressive injury from pathogens and/or chemicals. Although the major route of exposure to cadmium for most people is via food, causing the gastrointestinal tract to become the first target organ, very little information is available on whether cadmium exposure triggers the intestinal inflammatory response. We investigated in the present study the acute inflammatory response in the intestines of mice orally challenged with a single dose of cadmium chloride (CdCl(2)) by determining the gene expression of pro-inflammatory mediators with real-time PCR, and by examining the infiltration of inflammatory cells with a myeloperoxidase (MPO) assay and histological analysis of hematoxylin and eosin (H&E)-stained intestinal sections. The results show that CdCl(2) significantly increased the expression of macrophage inflammatory protein-2 mRNA (30-40 times the normal level) 3h and the activity of MPO (about 2 times the normal level) 24h after the challenge in the duodenal and proximal jejunal tissue. Furthermore, these increases were dose-dependent over a dosage range of 25-100mg/kg of body weight. The histological analysis confirmed that CdCl(2) induced mild to moderate villus damage and infiltration of inflammatory cells into the lamina propria. All these results demonstrate that oral exposure to CdCl(2) triggered an acute inflammatory response in the proximal intestine of mice, suggesting that the gut immune system was involved in the toxic effects of Cd on the gastrointestinal tract.