- Reversing Effects of Ginsenosides on LPS-induced Hepatic CYP3A11/3A4 Dysfunction Through the Pregnane X Receptor. [Journal Article]
- JEJ Ethnopharmacol 2018 Oct 17
- CONCLUSIONS: Ginsenosides reverse the effects of LPS-induced hepatic CYP3A11/3A4 dysfunction, suggesting that the stabilization of the CYP3A11/3A4 expression in an injured liver appears a novel hepatoprotective mechanism of ginsenosides.
- Studies on effects of static electric field exposure on liver in mice. [Journal Article]
- SRSci Rep 2018 Oct 19; 8(1):15507
- With the development of ultra-high-voltage direct-current transmission, the intensity of static electric field (SEF) under transmission lines increased, which has aroused public attention on its pote...
With the development of ultra-high-voltage direct-current transmission, the intensity of static electric field (SEF) under transmission lines increased, which has aroused public attention on its potential health effects. In order to examine effects of SEF exposure on liver, institute of cancer research mice were exposed to SEF with intensities of 27.5 kV/m, 34.7 kV/m and 56.3 kV/m, respectively. In each intensity of SEF exposure, a corresponding sham exposure group was used. Several indices relating to liver function (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)) and oxidative stress (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA)) were tested after exposure of 7, 14, 21 and 35 days. Results showed that exposure to SEF with intensities of 27.5 kV/m and 34.7 kV/m for 35 days did not significantly influence any detected indices above. Under SEF exposure with intensity of 56.3 kV/m, the SOD activity in liver was significantly increased after exposure of 7 and 14 days. However, no significant increase was found in MDA content as well as the activities of AST and ALT between exposure group and sham exposure group during SEF exposure of 56.3 kV/m. It suggested that from three SEF intensities, only exposure to SEF with intensity of 56.3 kV/m (7 and 14 days) caused a temporary oxidative stress response in liver expressed by the increase in activity of SOD, but it did not produce oxidative damage. This biological effect may be related to the increase of mitochondrial membrane potential of hepatocytes caused by SEF exposure. When the membrane potential exceeds a threshold, Q cycle in mitochondria will be affected, which will result in an increase of superoxide anion concentration and ultimately an oxidative stress.
- Iron Overload in an HFE Heterozygous Carrier: A Case Report and Literature Review. [Journal Article]
- LMLab Med 2018 Oct 18
- Hereditary hemochromatosis (HH) is an autosomal recessive disorder of iron metabolism characterized by increased iron absorption and tissue deposition. Three loss-of-function mutations in the hemochr...
Hereditary hemochromatosis (HH) is an autosomal recessive disorder of iron metabolism characterized by increased iron absorption and tissue deposition. Three loss-of-function mutations in the hemochromatosis gene (HFE), namely, C282Y (c.845G>A), H63D (c.187C>G), and S65C (c.193A>T), account for the vast majority of HH cases. These mutations cause alterations in HFE membrane expression, structure, and/or activity, leading to dysregulation of iron absorption. It is well established that the phenotypic expression of HFE mutations varies markedly. Herein, we describe a 64-year-old Caucasian woman with a reported history of hemochromatosis. The father of the patient had died of complications due to iron overload. Testing of HFE codon C282Y, H63D, and S65C mutations showed heterozygous C282Y. The patient had significantly elevated transferrin saturation (TS) and serum ferritin (SF) levels. Her liver function test results showed elevated alanine transaminase (ALT) and aspartate aminotransferase (AST) levels. The patient has been treated with regular phlebotomy to prevent the clinical manifestations of hemochromatosis.
- Modulation of macrophage polarization by level-1 Yo-Yo intermittent recovery test in young football players. [Journal Article]
- MMedicine (Baltimore) 2018; 97(42):e12739
- The aim of this study was to examine the effect of the level-1 Yo-Yo intermittent recovery test (YYIRT1) on polarization of macrophages in young football players.Fourteen male football players (19.9 ...
The aim of this study was to examine the effect of the level-1 Yo-Yo intermittent recovery test (YYIRT1) on polarization of macrophages in young football players.Fourteen male football players (19.9 ± 1.4 years old) were enrolled in this study. YYIRT1 was performed with 20-meter shuttle runs at increasing speeds and 10-second active recovery in a 5-meter distance between runs till exhaustion. Fasting blood samples were collected before and immediately after YYIRT1. Analysis for macrophage polarization by flow cytometry, reactive oxygen species (ROS) by flow cytometry, biochemical parameters by chemical reactions, and serum cytokines by ELISA were performed. The rating of perceived exertion (RPE) and cardiovascular parameters were recorded.The time to exhaustion was 714.1 ± 114.4 seconds. The oxygen uptake ((Equation is included in full-text article.)) was 48.7 ± 5.6 mL/min/kg, RPE scale was 19 ± 1, resting heart rate and maximal heart rate were 64.9 ± 8.8 beat/min and 181.9 ± 9.3 beat/min, respectively, indicating a high level of cardiopulmonary fitness. The expression of macrophage-specific CD14 and M1 marker HLA-ABC, but not M2 marker CD206, was down-regulated after YYIRT1. The intracellular ROS levels in macrophages had no significant change. In biochemical profile, the serum levels of lactic dehydrogenase (LDH), a marker of muscle damage, increased after YYIRT1 whereas no significant alteration was noted in creatine phosphokinase (CPK), blood urine nitrogen, creatinine, aspartate transaminase (AST), alanine transaminase (ALT), and C-reactive protein. The serum levels of interleukin (IL)-6, IL-10 and tumor necrosis factor (TNF)-α had no significant change.The YYIRT1 may induce muscle damage accompanied by modulation of macrophage polarization toward suppression of M1 phenotype in young football players.
- Humulus japonicus Extracts Protect Against Lipopolysaccharide/d-Galactosamine-Induced Acute Liver Injury in Rats. [Journal Article]
- JMJ Med Food 2018; 21(10):1009-1015
- It has been described that Humulus japonicus has potential antituberculosis and anti-inflammatory effects. The antiaging activity of H. japonicus extract (HJE) was also examined not only in yeast but...
It has been described that Humulus japonicus has potential antituberculosis and anti-inflammatory effects. The antiaging activity of H. japonicus extract (HJE) was also examined not only in yeast but also in human fibroblast cells. We evaluated the protective effect of HJE on hepatotoxicity in this study. We demonstrated the expression of antioxidative enzyme and cytokines in plasma. The vehicle control group received orally administered normal saline. Acute hepatotoxicity rat model was induced by lipopolysaccharide (LPS) (30 μg/kg) and d-galactosamine (D-GalN) (500 mg/kg) by intraperitoneal injection. The positive control group received orally administered silymarin (10 mg/kg). Three HJE groups received 8, 16, and 32 mg/kg. The blood samples were prepared to evaluate malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) level to examine oxidative stress, and hepatic tissue was assayed for myeloperoxidase (MPO). Aspartate aminotransferase (AST), alanine aminotransferase (ALT), and tumor necrosis factor-α (TNF-α) activities were also assayed to examine liver cell viability. Pretreatment with HJE decreased levels of AST, ALT, MDA, MPO, and TNF-α and increased levels of SOD and CAT compared with the LPS/D-GalN-treated group. These results suggested that HJE has the potential to reduce oxidative damage and inflammatory reactions in LPS/D-GalN-induced liver injury in the rat model. It can also increase survival rate in LPS/D-GalN-induced hepatotoxicity rat models.
- Long-term treatment with pegvisomant: observations from 2090 acromegaly patients in ACROSTUDY [Journal Article]
- EJEur J Endocrinol 2018 Oct 01
- CONCLUSIONS: This second interim analysis confirms that long-term use of PEGV is an effective and safe treatment inpatients with acromegaly.
- Effect on Serum Parameters and Immune Responses of Carassius auratus gibelio Exposed to Dietary Lead and Bacillus subtilis. [Journal Article]
- BTBiol Trace Elem Res 2018 Oct 15
- Lead (Pb), a heavy metal and an environmental stressor, may affect many physiological processes, including the serum index and the immune response. The aim of this study was to explore the toxic effe...
Lead (Pb), a heavy metal and an environmental stressor, may affect many physiological processes, including the serum index and the immune response. The aim of this study was to explore the toxic effects of Pb on the serum index and the immune response of Carassius auratus gibelio (C. gibelio) fed 0, 120, or 240 mg/kg Pb, and 109 cfu/g Bacillus subtilis (B. subtilis). After 15 and 30 days of dietary exposure, the serum indices and the immune responses of the fish were assessed. Dietary Pb exposure significantly affected various components of the serum index, including calcium, magnesium, glucose, cholesterol, total protein, glutamic-pyruvic transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH). However, sIgA activity in the gut increased significantly following B. subtilis supplementation. Notable changes were also observed in the expression levels of immune-related genes, including HSP70, IgM, HSP90, IL-1β, IL-6, and TNF-α. B. subtilis supplementation effectively attenuated the effects of dietary Pb exposure.
- Small heterodimer partner negatively regulates C-X-C motif chemokine ligand 2 in hepatocytes during liver inflammation. [Journal Article]
- SRSci Rep 2018 Oct 15; 8(1):15222
- Recently, we reported that orphan nuclear receptor small heterodimer partner (SHP) is involved in neutrophil recruitment through the regulation of C-X-C motif chemokine ligand 2 (CXCL2) expression in...
Recently, we reported that orphan nuclear receptor small heterodimer partner (SHP) is involved in neutrophil recruitment through the regulation of C-X-C motif chemokine ligand 2 (CXCL2) expression in a concanavalin A (ConA)-induced hepatitis model. In the present study, we examined the mechanisms underlying CXCL2 regulation by SHP and the cell types involved in liver inflammation. To this end, either Shp knockout (KO) or wild-type (WT) bone marrow cells were transferred into sublethally-irradiated WT (KO → WT or WT → WT) or Shp KO (KO → KO or WT → KO) recipients, followed by intravenous injection of ConA (20-30 mg/kg) 8 weeks later. The KO recipient groups showed higher ConA-induced lethality than the WT recipient groups. Accordingly, plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, and inflammatory cytokine expressions were significantly higher in the KO recipients than in the WT recipients regardless of donor genotype. Massively increased hepatocyte death in KO recipients, as determined by H&E and TUNEL staining, was observed after ConA challenge. Bone marrow chimera experiments and in vitro chemotaxis assay also showed that SHP-deficient hepatocytes have an enhanced ability to recruit neutrophils to the injured liver. In vitro promoter assays showed that SHP is a negative regulator of Cxcl2 transcription by interfering with c-Jun binding to the AP-1 site within the Cxcl2 promoter. Collectively, SHP regulates Cxcl2 transcription in hepatocytes, playing a pivotal role in the recruitment of neutrophils. SHP-targeting strategies may represent alternative approaches to control fulminant hepatitis.
- The possible association between AQP9 in the intestinal epithelium and acute liver injury‑induced intestinal epithelium damage. [Journal Article]
- MMMol Med Rep 2018 Oct 10
- The present study aimed to investigate the expression and function of aquaporin (AQP)9 in the intestinal tract of acute liver injury rat models. A total of 20 Sprague Dawley rats were randomly divide...
The present study aimed to investigate the expression and function of aquaporin (AQP)9 in the intestinal tract of acute liver injury rat models. A total of 20 Sprague Dawley rats were randomly divided into four groups: Normal control (NC) group and acute liver injury groups (24, 48 and 72 h). Acute liver injury rat models were established using D‑amino galactose, and the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (Tbil) and albumin were determined using an automatic biochemical analyzer. Proteins levels of myosin light chain kinase (MLCK) in rat intestinal mucosa were investigated via immunohistochemistry. Pathological features were observed using hematoxylin and eosin (H&E) staining. MLCK, AQP9 and claudin‑1 protein expression levels were detected via western blotting. Levels of ALT and AST in acute liver injury rats were revealed to steadily increase between 24 and 48 h time intervals, reaching a peak level at 48 h. Furthermore, TBil levels increased significantly until 72 h. Levels of ALT were revealed to significantly increase until the 48 h time interval, and then steadily decreased until the 72 h time interval. The acute liver injury 72 h group exhibited the greatest levels of MLCK expression among the three acute liver injury groups; however, all three acute liver injury groups exhibited enhanced levels of MLCK expression compared with the NC group. Protein levels of AQP9 and claudin‑1 were enhanced in the NC group compared with the three acute liver injury groups. H&E staining demonstrated that terminal ileum mucosal layer tissues obtained from the acute liver injury rats exhibited visible neutrophil infiltration. Furthermore, the results revealed that levels of tumor necrosis factor‑α, interleukin (IL)‑6 and IL‑10 serum cytokines were significantly increased in the acute liver injury groups. In addition, AQP9 protein expression was suppressed in acute liver injury rats, which induced pathological alterations in terminal ileum tissues may be associated with changes of claudin‑1 and MLCK protein levels.
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- Tinospora cordifolia extract prevents cadmium-induced oxidative stress and hepatotoxicity in experimental rats. [Journal Article]
- JAJ Ayurveda Integr Med 2018 Oct 10
- CONCLUSIONS: The results of the present investigation reveal the hepatoprotective nature of T.cordifolia against Cd induced hepatotoxicity.