scholarly journals Antioxidant Capacity and Hepatoprotective Role of Chitosan-Stabilized Selenium Nanoparticles in Concanavalin A-Induced Liver Injury in Mice

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 857 ◽  
Author(s):  
Kaikai Bai ◽  
Bihong Hong ◽  
Jianlin He ◽  
Wenwen Huang
Keyword(s):  
Liver Injury ◽  
Antioxidant Capacity ◽  
Concanavalin A ◽  
Radical Scavenging ◽  
Lactic Dehydrogenase ◽  
Selenium Nanoparticles ◽  
Con A ◽  
Ultra Filtration ◽  
Hepatocyte Necrosis

Selenium nanoparticles (SeNPs) have attracted wide attention for their use in nutritional supplements and nanomedicine applications. However, their potential to protect against autoimmune hepatitis has not been fully investigated, and the role of their antioxidant capacity in hepatoprotection is uncertain. In this study, chitosan-stabilized SeNPs (CS-SeNPs) were prepared by means of rapid ultra-filtration, and then their antioxidant ability and free-radical scavenging capacity were evaluated. The hepatoprotective potential of a spray-dried CS-SeNPs powder against autoimmune liver disease was also studied in the concanavalin A (Con A)-induced liver injury mouse model. CS-SeNPs with size of around 60 nm exhibited acceptable oxygen radical absorbance capacity and were able to scavenge DPPH, superoxide anion, and hydroxyl radicals. The CS-SeNPs powder alleviated Con A-caused hepatocyte necrosis and reduced the elevated levels of serum alanine transaminase, aspartate transaminase, and lactic dehydrogenase in Con A-treated mice. These results suggest that the CS-SeNPs powder protected the mice from Con-A-induced oxidative stress in the liver by retarding lipid oxidation and by boosting the activities of superoxide dismutase, glutathione peroxidase, and catalase, partly because of its ability to improve Se retention. In conclusion, SeNPs present potent hepatoprotective potential against Con A-induced liver damage by enhancing the redox state in the liver; therefore, they deserve further development.

scholarly journals The Role of Serotonin in Concanavalin A-Induced Liver Injury in Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-16 ◽  
Author(s):  
Qing Pang ◽  
Hao Jin ◽  
Xiquan Ke ◽  
Zhongran Man ◽  
Yong Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Inflammatory Response ◽  
Concanavalin A ◽  
Serum Levels ◽  
Hepatocyte Apoptosis ◽  
Con A ◽  
Serotonin 2A Receptor ◽  
Serotonin 2A

Serotonin is involved in the pathological processes of several liver diseases via the regulation of inflammatory response and oxidative stress. We aimed to investigate the role of serotonin in Concanavalin A- (Con A-) induced acute liver injury (ALI). ALI was induced in C57B/6 wild-type (WT) mice and tryptophan hydroxylase 1 (TPH1) knockout mice through tail vein injection of Con A (15 mg/kg body weight). Another group of TPH1 knockout ALI mice was supplied with 5-hydroxytryptophan (5-HTP) in advance to recover serotonin. The blood and liver tissues of mice were collected in all groups. Markedly increased serum levels of serotonin were identified after the injection of Con A. Increased serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and stronger hepatic tissue pathology were detected, suggesting that serotonin could mediate Con A-induced liver damage. Serotonin significantly facilitated the release of serum and intrahepatic inflammatory cytokines, including interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-17A (IL-17A), interferon-gamma (IFN-γ), and tumor necrosis-alpha (TNF-α), after the administration of Con A. In addition, serotonin significantly increased the intrahepatic levels of oxidative stress markers malonaldehyde (MDA), myeloperoxidase (MPO), and nitric oxide (NO) and decreased antioxidant stress indicator glutathione (GSH) in Con A-treated mice. Additionally, serotonin promoted hepatocyte apoptosis and autophagy based on B-cell lymphoma-2 (Bcl-2), Bcl-2-asociated X protein (Bax), and Beclin-1 levels and TUNEL staining. More importantly, serotonin activated nuclear factor kappa B (NF-κB) and upregulated the hepatic expressions of high mobility group protein B1 (HMGB1), toll-like receptor-4 (TLR4), and downstream molecules in Con A-mediated liver injury. Serotonin 2A receptor was upregulated in liver tissue after Con A injection, and serotonin 2A receptor antagonist Ketanserin protected against Con A-induced hepatitis. These results indicated that serotonin has the potential to aggravate Con A-induced ALI via the promotion of inflammatory response, oxidative stress injury, and hepatocyte apoptosis and the activation of hepatic HMGB1-TLR signaling pathway and serotonin 2A receptor.

The role of microbiota in concanavalin A-mediated liver injury

2018 ◽  
Vol 56 (01) ◽  
pp. E2-E89
Author(s):  
B Schiller ◽  
C Wegscheid ◽  
L Berkhout ◽  
A Zarzycka ◽  
U Steinhoff ◽  
...  
Keyword(s):  
Liver Injury ◽  
Concanavalin A

scholarly journals Concanavalin-A Induces Granulosa Cell Death and Inhibits FSH-Mediated Follicular Growth and Ovarian Maturation in Female Rats

Endocrinology ◽  
2013 ◽  
Vol 154 (5) ◽  
pp. 1885-1896 ◽  
Author(s):  
Ethel V. Velasquez ◽  
Mariana Ríos ◽  
María Elena Ortiz ◽  
Carlos Lizama ◽  
Elizabeth Nuñez ◽  
...  
Keyword(s):  
Cell Death ◽  
Granulosa Cell ◽  
Granulosa Cells ◽  
Concanavalin A ◽  
Ex Vivo ◽  
Female Rats ◽  
Carbohydrate Binding ◽  
Con A ◽  
Follicular Maturation

Abstract Reproductive success stems from a finely regulated balance between follicular maturation and atresia, in which the role of carbohydrate structure is poorly understood. Here, we describe for the first time a fraction of purified recombinant human FSH that is capable of bringing about the cell death of granulosa cells and preventing follicular maturation in a rat model. Further analysis by mass spectrometry revealed the presence of the lectin Concanavalin-A (Con-A) within this fraction of recombinant FSH. Using both the fractionated FSH and Con-A, the observed cell death was predominantly located to the granulosa cells. Ex vivo culture of rat follicles demonstrated that follicle degeneration occurred and resulted in the release of a denuded and deteriorated oocyte. Moreover, in vivo experiments confirmed an increase in atresia and a corresponding reduction confined to follicle in early antral stage. As a mechanism of action, Con-A reduces ovarian proliferation, Von Willebrand staining, and angiogenesis. Based on the observation that Con-A may induce granulosa cell death followed by follicle death, our results further demonstrate that follicular carbohydrate moiety is changing under the influence of FSH, which may allow a carbohydrate-binding lectin to increase granulosa cell death. The physiological consequences of circulating lectin-like molecules remain to be determined. However, our results suggest a potential exploitation of carbohydrate binding in fertility and ovarian cancer treatment. This work may shed light on a key role of carbohydrates in the still obscure physiological process of follicular selection and atresia.

scholarly journals The Protective Effect of Sheep Placental Extract on Concanavalin A-induced Liver Injury in Mice

Molecules ◽  
2018 ◽  
Vol 24 (1) ◽  
pp. 28 ◽  
Author(s):  
Jingwen Liu ◽  
Suting Luo ◽  
Jun Yang ◽  
Fazheng Ren ◽  
Yu Zhao ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Amino Acids ◽  
Liver Injury ◽  
Protective Effect ◽  
Concanavalin A ◽  
B Cell Lymphoma ◽  
Therapeutic Effects ◽  
Model Group ◽  
Con A ◽  
Placental Extract

Though the biological effects of human placental extract have been widely studied, it has limited availability and its use poses ethical problems. Thus, domestic animal placental extracts are suggested as alternatives. In this study, the protective effect of sheep placental extract (SPE) on concanavalin A (Con A)-induced liver injury was investigated. BALB/c mice were randomly divided into six groups, including one normal group and five experimental groups, which received different oral doses of SPE (0, 5, 10 and 50 mg/kg) or a mixture of amino acids for 3 days before Con A injection. Compared with Con A-induced model group, the SPE administration significantly decreased serum aminotransaminase activity, alleviated pathological changes, recovered liver antioxidant capacity and prevented the increase of nitric oxide. Secretion of pro-inflammatory cytokines in serum decreased and mRNA expression of hepatic intercellular adhesion molecule-1, interferon-inducible chemokine 10 and inducible nitric oxide synthase were downregulated, while B-cell lymphoma-2 expression increased. The administration of amino acids mixture had no significant effect in most measurements compared with the model group, which indicated proteins and peptides, rather than individual amino acid, were largely responsible for the bioactivity of SPE. The results indicate SPE has potential therapeutic effects against immune-mediated hepatitis.

scholarly journals Glycophorin A interferes in the agglutination of human erythrocytes by concanavalin A Explanation of the requirement for enzymic predigestion

1987 ◽  
Vol 241 (2) ◽  
pp. 505-511 ◽  
Author(s):  
S M Gokhale ◽  
N G Mehta
Keyword(s):  
Sialic Acid ◽  
Correlation Coefficient ◽  
Concanavalin A ◽  
Binding Sites ◽  
Band 3 ◽  
Human Erythrocytes ◽  
The Other ◽  
Glycophorin A ◽  
Con A

Human erythrocytes become agglutinable with concanavalin A (Con A) after treatment with various proteinases or neuraminidase. The extent of agglutinability achieved with different enzymes is, however, different: Pronase, papain, trypsin, neuraminidase and chymotrypsin enhance the agglutinability in decreasing order, the last being barely effective. The actions of the enzymes on band 3, the Con A receptor, do not correlate with their abilities to increase the agglutinability: Pronase, papain and chymotrypsin cleave the protein, but not trypsin or neuraminidase. No significant differences are found in the number of Con A-binding sites or the affinities for the lectin between the normal and trypsin- or Pronase-treated cells. Thus the receptor does not seem to play a role in determining the Con A-agglutinability of erythrocytes. On the other hand, the cleavage of glycophorins, especially glycophorin A, and the release of sialic acid (in the peptide-bound form) are well-correlated with the enhancement in agglutination after the action of proteinases. The release of sialic acid by graded neuraminidase digestion and the increase in Con A-agglutinability show a correlation coefficient of 0.88. The major inhibitory role of glycophorin A in the process is indicated by the agglutination of En(a) heterozygous erythrocytes; the cells, known to bear about 50% glycophorin A molecules in their membrane, are agglutinated approximately half as well without proteolysis as are the trypsin-treated cells. Possible mechanisms by which glycophorin A could affect Con A-mediated agglutination are discussed.

Critical role of NKT cell-derived IL-5 and eosinophils in liver injury induced by concanavalin a in mice

2001 ◽  
Vol 120 (5) ◽  
pp. A54-A54
Author(s):  
H LOUIS ◽  
A MOINE ◽  
E QUERTINMONT ◽  
F PAULART ◽  
N NAGY ◽  
...  
Keyword(s):  
Liver Injury ◽  
Concanavalin A ◽  
Critical Role ◽  
Nkt Cell

The role of the cell surface in the migration of primordial germ cells in early chick embryos: effects of concanavalin A

Development ◽  
1978 ◽  
Vol 46 (1) ◽  
pp. 5-20
Author(s):  
H. Lee ◽  
N. Karasanyi ◽  
R. G. Nagele
Keyword(s):  
Cell Surface ◽  
Germ Cells ◽  
Concanavalin A ◽  
Primordial Germ Cells ◽  
Sublethal Dose ◽  
Chick Embryos ◽  
Con A ◽  
And Migration ◽  
Coat Material

Effects of concanavalin A (Con A) on the morphology and migration of primordial germ cells (PGCs) in stage-6 to -12 chick embryos were investigated. Con A, at a sublethal dose (10µg/ml), inhibited migration of PGCs from the germinal crescent area to other parts of the embryo. Affected PGCs were more rounded without the usual cytoplasmic extensions, but the integrity of other structures was unaffected. Nearly identical results were obtained with another lectin, wheat germ agglutinin (10µg/ml). Histochemistry using Con A-horseradish peroxidase revealed that PGCs in control embryos had a thin, rather uniform layer of extracellular coat material (ECM). Con A appeared to alter the distribution of ECM on PGCs, i.e. some parts of the cell surface were devoid of any detectable ECM, while others had small, scattered patches of ECM. Con A effects were alleviated by α-methyl-d-mannoside. Overall results of the present study indicated that the observed inhibition of PGC migration in early chick embryos is a consequence of Con A-induced alterations of cell surface properties.

scholarly journals SHED ameliorated concanavalin A-induced autoimmune hepatitis by protecting hepatocytes from apoptosis

2020 ◽  
Author(s):  
Yikun Zhou ◽  
Ruili Yang ◽  
Lingsu Zhu ◽  
Huaming Huang ◽  
Shengjie Cui ◽  
...  
Keyword(s):  
Liver Injury ◽  
Autoimmune Hepatitis ◽  
Concanavalin A ◽  
Acute Liver Injury ◽  
Deciduous Teeth ◽  
Protective Effects ◽  
Hepatocyte Apoptosis ◽  
Con A ◽  
Tnf Α ◽  
Ifn Γ

Abstract Background：Autoimmune hepatitis (AIH) is serious autoimmune liver diseases that threaten people’s health worldwide, emphasizing the need to identify novel treatment. Stem cells from human exfoliated deciduous teeth (SHED), which is easy to obtain and non-invasive, showed pronounced proliferation and immunomodulation capacity. This study aims to investigate the effect of SHED on ConA-induced AIH and the potential underlying mechanisms.Methods: We used a concanavalin A (ConA) induced acute hepatitis mouse model and in vitro co-culture system to study the protective effects of SHED on ConA-induced autoimmune hepatitis and the underlying mechanisms.Results: SHED infusion could prevent aberrant histopathological architecture of liver with infiltration of abundant of CD3+, CD4+, TNF-α+ and IFN-γ+ inflammatory cells induced by ConA. The expression of ALT and AST which indicated the liver function significantly elevated in hepatitis mice. While SHED infusion could block the elevation of ALT and AST induced by ConA. Mechanistically, Con-A upregulated TNF-α and IFN-γ expression activated NF-κB pathways to induced hepatocyte apoptosis, resulting in acute liver injury. SHED administration protected hepatocytes from Con-A-induced apoptosis. Conclusions: These results demonstrated that SHED alleviated ConA-induced acute liver injury via inhibition of hepatocyte apoptosis mediated by the NF-κB pathways. Our findings could provide a potential prevention and therapeutic strategy for hepatitis and acute hepatic injury.

Critical role of NKT cell-derived IL-5 and eosinophils in liver injury induced by concanavalin a in mice

2001 ◽  
Vol 120 (5) ◽  
pp. A54
Author(s):  
Hubert Louis ◽  
Alain Le Moine ◽  
Eric Quertinmont ◽  
Frederic Paulart ◽  
Nathalie Nagy ◽  
...  
Keyword(s):  
Liver Injury ◽  
Concanavalin A ◽  
Critical Role ◽  
Nkt Cell
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