MiR-125a-3p inhibits cell proliferation and inflammation responses in fibroblast-like synovial cells in rheumatoid arthritis by mediating the Wnt/ß-catenin and NF-κB pathways via targeting MAST3.

OBJECTIVES: To explore the role and mechanism of miR-125a-3p in rheumatoid arthritis (RA) progression. METHODS: The RA-tissues and fibroblast-like synovial cells in rheumatoid arthritis (RA-FLS) were used in this study. qRT-PCR, western blot and ELISA assay were performed to detect the expression levels of IL-6, IL-ß and ΤΝF-α. Dual-luciferase reporter gene assay was used to observe the binding effect of miR-125a-3p and MAST3, and CCK-8 was used to observe the effect of miR-125a-3p on the proliferation of RA-FLS. RESULTS: miR-125a-3p was significantly downregulated in the RA-tissues and RA-FLS, and miR-125a-3p could inhibit the proliferation and reduce the inflammation response of RA-FLS. Besides, MAST3 was found as a target of miR-125a-3p, and increased MAST3 could reverse the effects of miR-125a-3p on RA-FLS including decreased proliferation, reduced inflammation level and the inactivation of Wnt/ß-catenin and NF-κB pathways. CONCLUSIONS: This study suggests that miR-125a-3p could inactivate the Wnt/ß-catenin and NF-κB pathways to reduce the proliferation and inflammation response of RA-FLS via targeting MAST3.

Lightweight pyramid network with spatial attention mechanism for accurate retinal vessel segmentation.

PURPOSE: The morphological characteristics of retinal vessels are vital for the early diagnosis of pathological diseases such as diabetes and hypertension. However, the low contrast and complex morphology pose a challenge to automatic retinal vessel segmentation. To extract precise semantic features, more convolution and pooling operations are adopted, but some structural information is potentially ignored. METHODS: In the paper, we propose a novel lightweight pyramid network (LPN) fusing multi-scale features with spatial attention mechanism to preserve the structure information of retinal vessels. The pyramid hierarchy model is constructed to generate multi-scale representations, and its semantic features are strengthened with the introduction of the attention mechanism. The combination of multi-scale features contributes to its accurate prediction. RESULTS: The LPN is evaluated on benchmark datasets DRIVE, STARE and CHASE, and the results indicate its state-of-the-art performance (e.g., ACC of 97.09[Formula: see text]/97.49[Formula: see text]/97.48[Formula: see text], AUC of 98.79[Formula: see text]/99.01[Formula: see text]/98.91[Formula: see text] on the DRIVE, STARE and CHASE datasets, respectively). The robustness and generalization ability of the LPN are further proved in cross-training experiment. CONCLUSION: The visualization experiment reveals the semantic gap between various scales of the pyramid and verifies the effectiveness of the attention mechanism, which provide a potential basis for the pyramid hierarchy model in multi-scale vessel segmentation task. Furthermore, the number of model parameters is greatly reduced.

IKWI-net: A cross-domain convolutional neural network for undersampled magnetic resonance image reconstruction.

Magnetic resonance imaging (MRI) is widely used to get the information of anatomical structure and physiological function with the advantages of high resolution and non-invasive scanning. But the long acquisition time limits its application. To reduce the time consumption of MRI, compressed sensing (CS) theory has been proposed to reconstruct MRI images from undersampled k-space data. But conventional CS methods mostly use iterative methods that take lots of time. Recently, deep learning methods are proposed to achieve faster reconstruction, but most of them only pay attention to a single domain, such as the image domain or k-space. To take advantage of the feature representation in different domains, we propose a cross-domain method based on deep learning, which first uses convolutional neural networks (CNNs) in the image domain, k-space and wavelet domain simultaneously. The combined order of the three domains is also first studied in this work, which has a significant effect on reconstruction. The proposed IKWI-net achieves the best performance in various combinations, which utilizes CNNs in the image domain, k-space, wavelet domain and image domain sequentially. Compared with several deep learning methods, experiments show it also achieves mean improvements of 0.91 dB in peak signal-to-noise ratio (PSNR) and 0.005 in structural similarity (SSIM).

SP600125 blocks the proteolysis of cytoskeletal proteins in apoptosis induced by gas signaling molecule (NO) via decreasing the activation of caspase-3 in rabbit chondrocytes.

NO plays a key role in the pathological mechanisms of articular diseases. As cytoskeletal proteins are responsible for the polymerization, stabilization, and dynamics of the cytoskeleton network, we investigated whether cytoskeletal proteins are the intracellular pathological targets of NO. We aimed at clarifying whether the cytoskeleton perturbations involved in apoptosis are induced in rabbit articular chondrocytes by NO, which can be liberated by sodium nitroprusside (SNP) treatment. The first passage rabbit articular chondrocytes were cultured as monolayer for the experiments, and the effects of NO were tested in the presence of JNK-specific inhibitor, SP600125. SNP treatment of cultured chondrocytes caused significant apoptosis in a concentration-dependent manner (time and dose), as evaluated by TUNEL assay and Annexin V flow cytometry, while the apoptosis was reduced by the SP600125 addition 30 min before SNP treatment. Besides, SP600125 decreased significantly the protein expression of total caspase-3 and the intracellular gene expression of caspase-3, measured by Western blot analysis and PCR. SP600125 also increased the cytoskeletal protein expressions. These results suggested that JNK pathway plays a critical role in the NO-induced chondrocyte apoptosis, and SP600125 treatment blocks the dissolution of the cytoskeletal proteins via activation of caspase-3 pathways.

Infusion of umbilical cord mesenchymal stem cells alleviates symptoms of ankylosing spondylitis.

The current study evaluated 5 patients with ankylosing spondylitis (AS). Patients received intravenous transfusions of umbilical cord mesenchymal stem cells (uMSCs). All therapeutic and adverse responses were assessed and recorded during uMSC therapy. No severe adverse reactions were observed in any of the patients, although a slight transient fever was observed in 3 patients within 2-6 h of intravenous administration of uMSCs. Following treatment, the Bath Ankylosing Spondylitis Disease Activity and Bath Ankylosing Spondylitis Metrology Indices decreased, however the Bath Ankylosing Spondylitis Functional Index increased. The erythrocyte sedimentation rate in 3 patients was reduced and C-reactive protein levels in 1 patient were markedly reduced. The symptoms of AS were alleviated in all patients. The present study indicates that intravenous transfusion of uMSCs is safe and well tolerated by patients and that it effectively alleviates disease activity and clinical symptoms. In the future, a larger cohort of patients with AS should be recruited to enable the systemic evaluation of uMSC therapy.

Loss of Reelin suppresses cell survival and mobility in non-Hodgkin lymphoma.

Reelin, a secreted glycoprotein, was recently demonstrated to be involved in the pathogenesis of cancer. However, its oncogenic activities in non-Hodgkin lymphoma (NHL) remain unclear. Therefore, we aimed to evaluate the functional role of reelin in NHL, and the underlying molecular mechanisms. In the present study, we analyzed reelin expression in lymphoma tissues and cell lines using immunohistochemistry, immunofluorescence staining, qRT-PCR and western blotting. Then, the expression of Reelin was silenced with short hairpin RNA (shRNA)-expressing plasmid in the NHL cell line A20. The effects of Reelin depletion on cell growth, migration and invasion in vitro were determined by CCK-8 and transwell assays. Flow cytometry was used to examine the cell cycle status and cellular apoptosis. Hoechst 33258 fluorescence staining was used to analyze morphologic changes caused by apoptosis. The second messenger, cAMP was analyzed by ELISA. In addition, we used nude mice to evaluate the tumorigenic ability of reelin. Aberrant upregulated levels of mRNA and protein of reelin were observed in lymphoma tissues and cell lines. Knockdown of reelin suppressed lymphoma growth, migration and invasion ability of A20. Furthermore, reelin depletion induced cell cycle arrest in G0/G1 phase and promoted apoptosis of A20 cells. Further analysis indicated that knockdown of reelin downregulated the expression of CDK5 and IL-10 and activated caspase-3 in shReelin group. ELISA assay showed cAMP at a lower level in shReelin group. SQ22536, a cAMP pathway inhibitor, treated A20 cells and revealed likely effects. The tumor size in a mouse model injected shReelin was significantly smaller than controls. There results suggest that reelin played essential roles in the development of lymphoma and might be a potential drug target in lymphoma.

Effect of lutein supplementation on visual function in nonproliferative diabetic retinopathy.

BACKGROUND AND OBJECTIVES: The purpose of this study was to determine whether supplementation with lutein improved visual function in patients with nonproliferative diabetic retinopathy (NPDR). METHODS AND STUDY DESIGN: In this randomized, double-blind, placebo-controlled trial, 31 patients with NPDR were assigned randomly to 10 mg/d of lutein or identical placebo for 36 weeks. Visual performance indices, including visual acuity (VA), contrast sensitivity (CS) and glare sensitivity (GS) at four different spatial frequencies, were measured at baseline, week 18 and 36. RESULTS: At 36 weeks, a slight improvement in VA was found in the lutein group. A significant association was observed between the changes in VA and the corresponding baseline values in treatment group (r=-0.53; p=0.04). At 36 weeks, the lutein treatment group increased CS at four spatial frequencies, and the improvement achieved statistical significance at 3 cycles/degree (p=0.02). The changes in CS at 3 cycles/degree for the lutein group was marginally significantly greater than those for the placebo group (p=0.09). There was also a slight increase in GS in the lutein group up to week 36, however, no significant changes were found over time in any cycles/degree. CONCLUSIONS: In patients with NPDR, supplementation with lutein resulted in potential improvements in CS at low spatial frequency. Further studies are required to determine the possibility that such intervention could be used as an adjunct therapy to prevent vision loss in diabetic patients.

T-2 Toxin Alters the Levels of Collagen II and Its Regulatory Enzymes MMPs/TIMP-1 in a Low-Selenium Rat Model of Kashin-Beck Disease.

The objectives of this study are to assess T-2 toxin's involvement in low selenium (Se)-induced Kashin-Beck disease (KBD) in rats and unveil the mechanisms underlying this disease. Two hundred thirty rats were randomly divided into two groups after weaning and fed normal or low-Se diets (n = 115), respectively, for a month. After low-Se model confirmation, rats in each group were subdivided into five: two subgroups (n = 20) were fed their current diets (normal or low-Se diets, respectively) for 30 and 90 days, respectively; two other subgroups (n = 25) received their current diets + low T-2 toxin (100 ng/g BW/day) for 30 and 90 days, respectively; and 25 rats were fed their current diets + high T-2 toxin (200 ng/g BW/day) for 30 days. Articular cartilage samples were extracted for hematoxylin and eosin (H&E) staining and immunohistochemistry. Western blot and reverse transcription-polymerase chain reaction (RT-PCR) were used to assess protein and mRNA levels, respectively, of collagen II, matrix metalloproteinase (MMP-1), MMP -3, MMP-13, and tissue inhibitor of metalloproteinase-1 (TIMP-1). Low Se and T-2 toxin synergistically affected animal fitness. Interestingly, low Se + T-2 toxin groups showed KBD characteristics. MMP-1, -3, and -13 mRNA and protein levels generally increased in low-Se groups, while collagen II and TIMP-1 levels showed a downward trend, compared with normal diet fed animals for the same treatment (P < 0.05). T-2 toxin's effect was dose but not time dependent. Low Se and T-2 toxin synergistically alter the expression levels of collagen II as well as its regulatory enzymes MMP-1, MMP-3, MMP-13, and TIMP-1, inducing cartilage damage. Therefore, T-2 toxin may cause KBD in low-Se conditions.

Determination of nitrofurans metabolites residues in aquatic products by ultra-performance liquid chromatography-tandem mass spectrometry.

A method was described for monitoring four nitrofuran metabolites including 5-methylmorpholino-3-amino-2-oxazolidinone (AMOZ), 3-amino-2-oxazolidone (AOZ), 1-amino-hydantoin (AHD) and semicarbazide (SEM) in aquatic products. The analytes were quantified by ultra-performance liquid chromatography-tandem mass spectrometry operating in positive ion multiple monitoring mode (MRM) after 2-nitrobenzaldehyde derivatization. The matrix calibration curve was established with correlation coefficient (R(2)>0.99) in the range of 1-100 ng ml(-1). Limit of detection and limit of quantification for all analytes were 0.5 and 1.5 µg kg(-1), respectively. Recovery rates and relative standard deviations ranged from 88% to 112% and 2% to 4%, respectively. The validated method was successfully applied to detect nitrofuran metabolites in 120 fish samples. The analytes were detected in 6/16 species of fish samples, with a total detection rate of 6.5%. AOZ was most frequently detected (8.3%), followed by AMOZ (7.5%), AHD (5.0%) and SEM (5.0%). The method is proposed for monitoring nitrofuran metabolites in aquatic products.

Cluster of differentiation 147 is a key molecule during hepatocellular carcinoma cell-hepatic stellate cell cross-talk in the rat liver.

The cross-talk between hepatocellular carcinoma (HCC) cells and activated hepatic stellate cells (HSCs) is considered to be important for modulating the biological behavior of tumor cells. However, the molecular links between inflammation and cancer in the activation of HSCs remain to be elucidated. The present study demonstrated that cluster of differentiation (CD)147 is a key molecule involved in the interaction between HCC cells and HSCs. The effects of conditioned medium from human HCC cells on the activation of the human HSC line, LX-2, were assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, western blotting and reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Western blotting, RT-qPCR and gelatin zymography were also used to investigate the effects of CD147 on the activation of LX-2. The expression levels of α-smooth muscle actin (α-SMA) and CD147 were assessed in a co-culture system of LX-2 and FHCC-98 cells by immunofluorescence staining and immunoblotting. In hepatic tissues from a rat model of fibrosis, immunohistochemistry and immunoblotting were performed to detect the expression levels of α-SMA and CD147. Tumor-conditioned medium and CD147 promoted cell proliferation, activated LX-2 cells, increased the expression levels of α-SMA, collagen I and tissue inhibitor of metalloproteinase-1 (TIMP-1), and increased the secretion of matrix metalloproteinase (MMP)-2. The HSCs, which were induced in the co-culture system of HCC cells and HSCs exhibited marked expression levels of CD147. In the hepatic tissue of rat models of fibrosis induced by CCl4, marked expression levels of CD147 were observed in the activated HSCs. Therefore, CD147 promoted the activation of HSCs and was a key molecule during HCC cell-HSC cross-talk in the rat liver.

Identification of therapeutic target genes with DNA microarray in multiple myeloma cell line treated by IKKß/NF-κB inhibitor.

PURPOSE: To explore the mechanism of resistance to IKKß inhibitor in multiple myeloma (MM) cells and uncover novel therapeutic targets for MM. METHODS: We downloaded the microarray data (GSE8476) from GEO (Gene Expression Omnibus) database. The data were derived from the human MM cells lines (L363 cells) treated with IKKß inhibitor MLN120b (MLN) for eight, 12 and 24 hours. Furthermore, we applied the Search Tool for the Retrieval of Interacting Genes (STRING) and Expression Analysis Systematic Explorer (EASE) database to construct protein-protein interaction networks and identified over-represented pathway among DEGs (differentially expressed genes). RESULTS: We obtained 108 DGEs in 8h vs. 12h group and 101 ones in 8h vs. 24h group. Most of DGEs were found to be involved in biological regulation. The significant pathways were Ig A pathway and the CAMs pathways. In addition, 24 common DGEs were found in the networks of the two groups such as ICAM 3 and SELL. CONCLUSION: Intercellular adhesion molecule 3 and SELL may be potential targets in multiple myeloma treatment in the future.

Identification of therapeutic target genes with DNA microarray in multiple myeloma cell line treated by IKKβ/NF-κB inhibitor

PURPOSE: To explore the mechanism of resistance to IKKβ inhibitor in multiple myeloma (MM) cells and uncover novel therapeutic targets for MM. METHODS: We downloaded the microarray data (GSE8476) from GEO (Gene Expression Omnibus) database. The data were derived from the human MM cells lines (L363 cells) treated with IKKβ inhibitor MLN120b (MLN) for eight, 12 and 24 hours. Furthermore, we applied the Search Tool for the Retrieval of Interacting Genes (STRING) and Expression Analysis Systematic Explorer (EASE) database to construct protein-protein interaction networks and identified over-represented pathway among DEGs (differentially expressed genes). RESULTS: We obtained 108 DGEs in 8h vs. 12h group and 101 ones in 8h vs. 24h group. Most of DGEs were found to be involved in biological regulation. The significant pathways were Ig A pathway and the CAMs pathways. In addition, 24 common DGEs were found in the networks of the two groups such as ICAM 3 and SELL. CONCLUSION: Intercellular adhesion molecule 3 and SELL may be potential targets in multiple myeloma treatment in the future. .

Saikosaponin­d suppresses the expression of cyclooxygenase­2 through the phospho­signal transducer and activator of transcription 3/hypoxia­inducible factor­1α pathway in hepatocellular carcinoma cells.

Hepatocellular carcinoma (HCC) is one of the most common malignancies and accounts for ~6% of all types of human cancer worldwide, particularly in Asia. The incidence and mortality rates in the USA have also rapidly increased. Saikosaponin­d (SSD), a saponin derivative extracted from several species of Bupleurum (Umbelliferae), possesses unique biological activities, including anti­inflammatory, antihepatitic and immunomodulatory effects. Our previous studies have demonstrated that SSD inhibits the proliferation and induces the apoptosis of HCC SMMC­7721 cells by downregulating the expression of cyclooxygenase (COX)­2 and decreasing the production of prostaglandin E2. However, the specific mechanism underlying how SSD controls the expression of COX­2 remains to be elucidated. In the present study, it was demonstrated that hypoxia inducible factor­1α (HIF­1α) was responsible for the expression of COX­2 under hypoxic conditions in HCC cells, and the activation of signal transducer and activator of transcription 3 (STAT3) was required for the expression of HIF­1α. SSD treatment inhibited STAT3 activation [phosphorylation of STAT3 (p­STAT3)], reduced the protein level of HIF­1α and decreased the expression of COX­2. These results suggested that SSD may target HCC cells by suppressing the expression of COX­2 through the p­STAT3/HIF­1α pathway.

Laminin 411 acts as a potent inducer of umbilical cord mesenchymal stem cell differentiation into insulin-producing cells.

BACKGROUND: Diabetes mellitus (DM) is an incurable metabolic disease constituting a major threat to human health. Insulin-producing cells (IPCs) differentiated from mesenchymal stem cells (MSCs) hold great promise in the treatment of DM. The development of an efficient IPC induction system is a crucial step for the clinical application of IPCs for DM. Laminin 411 is a key component of the basement membrane and is involved in the regulation of cell differentiation; however, little is known about a role of laminin 411 in the regulation of IPC differentiation from human MSCs. METHODS: MSCs were isolated from human umbilical cord (UC-MSCs) and expanded in an in vitro culture system. UC-MSCs were then cultured in the IPC induction and differentiation medium in the presence of laminin 411. Flow cytometry, Quantitative realtime PCR, immunofluorescence staining, ELISA, Western blotting and other techniques were applied to determine IPC generation, insulin expression and related mechanisms. To evaluate potential therapeutic efficacy of IPCs induced from UC-MSCs, a type-1 diabetes (T1DM) rat model was generated using streptozotocin. Blood glucose, insulin levels, and survival of rats were monitored periodically following intravenous injection of the tested cells. RESULTS: Laminin 411 markedly induced the expression of the genes Foxa2 and Sox17, markers for pancreatic precursor cells, efficiently induced IPC differentiation from MSCs, and up-regulated insulin expression at both mRNA and protein levels. Furthermore, the expression of the genes known to govern insulin expression including Pdx1 and Ngn3 was markedly induced by laminin 411, which suggests that Pdx1 and Ngn3 signaling pathways are involved in laminin 411 induced-insulin expression machinery. More importantly, administration of laminin 411-induced IPCs rapidly and significantly down-regulated fasting blood glucose levels, significantly reduced the HbA1c concentration and markedly improved the symptoms and survival of T1DM rats. CONCLUSIONS: Our results demonstrate that laminin 411 acts as a potent differentiation inducer of IPCs from UC-MSCs via the Pdx1 and Ngn3 signaling pathways. Moreover, transfusion of laminin 411 induced-IPCs more efficiently improves symptoms and survival of T1DM rats. These novel finding highlights a potential clinical application of laminin 411 induced-IPCs in the treatment of T1DM, which calls for further studies.

[Combined effects of T-2 toxin and selenium deficiency on lipid peroxidation in rat's brain].

OBJECTIVE: To explore the effects of T-2 toxin and it's synergy with low selenium on lipid peroxidation in rats' brain. METHODS: Early weaning male SD (Sprague-Dawley) rats were randomly divided into normal group and low-selenium model group by weight after 1 week for adaptive feeding, and respectively fed normal diet and low-selenium diet. After the low Se model was succeed, the normal group were randomly divided into control group, low T-2 group, high T-2 group, the model group were randomly divided into low Se group, low Se + low T-2 group, low Se + high T-2 group. Then give T-2 toxin to the low T-2 group, low Se + low T-2 group at the dose of 0.1 mg/(kg x d), and high T-2 group, low Se + high T-2 group at the dose of 0.2 (kg x d), intragastric administration for 4 weeks. We take the brain sample, observed the morphological changes of brain tissue after HE staining, measured the content of MDA and the activity of GSH-Px to observe the T-2 toxin' effect of antioxidant on rat brain. RESULTS: The activity of rats' brain GSH-Px in all low Se groups were lower than the control group (P < 0.05). The content of rats' brain MDA in all experimental group were higher than the control group (P < 0.05). In all experimental group, the structure, the neurons, the nuclei of rats' brain tissue have varying degrees of damage and destruction. CONCLUSION: The single factor of T-2 toxin can cause lipid peroxidation in brain, lower the activity of GSH-Px and higher the lever of MDA. The single factor of low Se can induce lipid peroxidation in rats' brain, lower the activity of GSH-Px, higher the level of MDA, With the condition of low Se, the effect of T-2 toxin on lipid peroxidation in rats' brain was more obviously than the single factor. There have synergistic effect T-2 toxin with low Se.

Increased levels of IL-6, IL-1ß, and TNF-α in Kashin-Beck disease and rats induced by T-2 toxin and selenium deficiency.

The objective of this study is to investigate the possible role of inflammatory mediators such as IL-6, IL-1ß, and TNF-α in Kashin-Beck disease (KBD) children and rats fed with T-2 toxin under a selenium-deficient nutrition status in order to determine possible mechanism underlying KBD. Sprague-Dawley rats were administered a selenium-deficient diet for 4 weeks prior to their exposure to T-2 toxin for 4 weeks. The morphology of joint cartilages of KBD children and rats was examined by light microscopy, and the expression of proteoglycans was determined by histochemical staining. The serum levels of IL-6, IL-1ß, and TNF-α were determined by enzyme-linked immunosorbent assay. IL-6, IL-1ß and TNF-α were localized by immunohistochemistry, and their mRNA levels were detected by real-time RT-PCR. The serum levels of IL-6 were significantly elevated in rats fed with selenium-deficient, T-2 toxin, and T-2 toxin plus selenium-deficient diets compared to those in the normal diet, while the serum levels of IL-1ß and TNF-α were significantly increased only in the T-2 toxin plus selenium-deficient diet group. IL-6, IL-1ß and TNF-α protein and mRNA levels in cartilage were significantly higher in rats with diets of T-2 toxin and T-2 toxin plus selenium deficiency than in rats fed normal or selenium-deficient diet. While staining for the cytokines in cartilages of KBD children was significantly higher than that in controls. T-2 toxin under a selenium-deficient nutritional status induces increased levels of IL-6, IL-1ß, and TNF-α in serum and cartilages, which may account for the pathological mechanism underlying the cartilage damage in KBD.

[Role of JNK signaling pathway in chondrocyte apoptosis induced by nitric oxide].

OBJECTIVE: To study the role of c-jun N-terminal kinase (JNK) signaling pathway in chondrocyte apoptosis induced by nitric oxide (NO) using NO donor sodium nitroprusside (SNP) and JNK inhibitor SP600125. METHODS: Articular chondrocytes were separated from New Zealand rabbits aged 3 weeks by mechanical digestion and enzyme digestion and identified by toluidine blue staining, and then the chondrocytes were treated with SNP and SP600125 for 24 h. The cell apoptosis was evaluated by Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL), and the expression levels of nuclear factor-kappa B (NF-κB) p65 and p53 were measured by western blot. RESULTS: Compared with those in control group, the early apoptotic rate of SNP-treated chondrocytes increased as the concentration of SNProse, exhibiting a concentration dependency (P < 0.05), and the expression levels of NF-κB p65 and p53 also increased (P < 0.05); JNK inhibitor SP600125 inhibited these increases (P < 0.05). CONCLUSION: JNK signaling pathway plays an important role in NO-induced chondrocyte apoptosis. JNK inhibitor SP600125 can reduce NO-induced apoptosis and expression of NF-κB p65 and p53 in articular chondrocytes of rabbits in a concentration-dependent manner.

Protective effects of selenium on oxidative damage and oxidative stress related gene expression in rat liver under chronic poisoning of arsenic.

Arsenic (As) is a toxic metalloid existing widely in the environment, and chronic exposure to it through contaminated drinking water has become a global problem of public health. The present study focused on the protective effects of selenium on oxidative damage of chronic arsenic poisoning in rat liver. Rats were divided into four groups at random and given designed treatments for 20 weeks. The oxidative damage of liver tissue was evaluated by lipid peroxidation and antioxidant enzymes. Oxidative stress related genes were detected to reflect the liver stress state at the molecular level. Compared to the control and Na2SeO3 groups, the MDA content in liver tissue was decreased and the activities of antioxidant enzymes were increased in the Na2SeO3 intervention group. The mRNA levels of SOD1, CAT, GPx and Txnrd1 were increased significantly (P<0.05) in the combined Na2SeO3+NaAsO2 treatment group. The expressions of HSP70 and HO-1 were significantly (P<0.05) increased in the NaAsO2 group and reduced in the combined treatment group. The results indicate that long-term intake of NaAsO2 causes oxidative damage in the rat liver, and Na2SeO3 protects liver cells by adjusting the expression of oxidative stress related genes to improve the activities of antioxidant enzymes.

Pesticide residues in market foods in Shaanxi Province of China in 2010.

The aim of this study was to investigate the pesticide residues in market vegetables in Shaanxi Province of China. The concentrations of 33 pesticides were determined by gas chromatography (GC) in 285 samples. Ten organophosphorus pesticides (OPs) were found in concentrations ranging from 0.004 to 0.257 mg/kg. The mean levels of omethoate, phorate, chlorpyrifos, methidathion, ethoprophos in vegetables exceeded the maximum residue limits (MRLs) allowed by the Ministry of Health, of China. Other detectable OP pesticide residues levels were below their MRLs. Dicofol were detectable in green pepper and chives samples. Five pyrethroid pesticides (PYRs) were detectable in vegetable samples respectively. The results provide useful information on the current contamination status of a key agricultural area in China, and point to the need for urgent action to control the excessive use of some chemicals.

Histopathology of chondronecrosis development in knee articular cartilage in a rat model of Kashin-Beck disease using T-2 toxin and selenium deficiency conditions.

The objective of this study is to observe pathogenic lesions of joint cartilages in rats fed with T-2 toxin under a selenium deficiency nutrition status in order to determine possible etiological factors causing Kashin-Beck disease (KBD). Sprague-Dawley rats were fed selenium-deficient or control diets for 4 weeks prior to their being exposed to T-2 toxin. Six dietary groups were formed and studied 4 weeks later, i.e., controls, selenium-deficient, low T-2 toxin, high T-2 toxin, selenium-deficient diet plus low T-2 toxin, and selenium-deficient diet plus high T-2 toxin. Selenium deficiencies were confirmed by the determination of glutathione peroxidase activity and selenium levels in serum. The morphology and pathology (chondronecrosis) of knee joint cartilage of experimental rats were observed using light microscopy and the expression of proteoglycans was determined by histochemical staining. Chondronecrosis in deep zone of articular cartilage of knee joints was seen in both the low and high T-2 toxin plus selenium-deficient diet groups, these chondronecrotic lesions being very similar to chondronecrosis observed in human KBD. However, the chondronecrosis observed in the rat epiphyseal growth plates of animals treated with T-2 toxin alone or T-2 toxin plus selenium-deficient diets were not similar to that found in human KBD. Our results indicate that the rat can be used as a suitable animal model for studying etiological factors contributing to the pathogenesis (chondronecrosis) observed in human KBD. However, those changes seen in epiphyseal growth plate differ from those seen in human KBD probably because of the absence of growth plate closure in the rat.