BACKGROUNDAs one of the intercellular adhesion molecules, CD58 plays important roles in promotion of the adhesion between T cells and target cells, hyperplasia, activation of T cells and natural killer cells, and balance between Th1 and Th2. We studied the relationship between the levels of CD58 expression in peripheral blood mononuclear cells (PBMCs) and severity of HBV infection.

METHODSThe levels of CD58 mRNA in PBMCs were detected using quantitative reverse transcription PCR. The percentage of CD58 positive cells was detected by flow cytometry in patients and healthy controls.

RESULTSThe levels of CD58 mRNA and the percentage of CD58 positive cells in patients infected with HBV were significantly higher than that in the control. Based on severity of HBV infection, the patients were classified into four groups. The expression of CD58 increased significantly in an order from mild chronic, moderate chronic, severe chronic to severe hepatitis groups. The levels of CD58 mRNA and the percentage of CD58 positive cells in PBMCs from patients with HBV infection were both positively correlated with serum levels of ALT and AST.

CONCLUSIONThe level of CD58 expression is related with the severity of HBV infection and the degree of liver damage.

Alanine Transaminase ; blood ; Aspartate Aminotransferases ; blood ; CD58 Antigens ; genetics ; Hepatitis B ; blood ; physiopathology ; Humans ; Leukocytes, Mononuclear ; metabolism ; RNA, Messenger ; analysis

BACKGROUND/AIMS: To assess the usefulness of magnetization-tagged magnetic resonance imaging (MRI) in quantifying cardiac-induced liver motion and deformation in order to predict liver fibrosis. METHODS: This retrospective study included 85 patients who underwent liver MRI including magnetization-tagged sequences from April 2010 to August 2010. Tagged images were acquired in three coronal and three sagittal planes encompassing both the liver and heart. A Gabor filter bank was used to measure the maximum value of displacement (MaxDisp) and the maximum and minimum values of principal strains (MaxP1 and MinP2, respectively). Patients were divided into three groups (no fibrosis, mild-to-moderate fibrosis, and significant fibrosis) based on their aspartate-aminotransferase-to-platelet ratio index (APRI) score. Group comparisons were made using ANOVA tests. RESULTS: The patients were divided into three groups according to APRI scores: no fibrosis (≤0.5; n=41), moderate fibrosis (0.5-1.5; n=23), and significant fibrosis (>1.5; n=21). The values of MaxDisp were 2.9±0.9 (mean±SD), 2.3±0.7, and 2.1±0.6 in the no fibrosis, moderate fibrosis, and significant fibrosis groups, respectively (P<0.001); the corresponding values of MaxP1 were 0.05±0.2, 0.04±0.02, and 0.03±0.01, respectively (P=0.002), while those of MinP2 were -0.07±0.02, -0.05±0.02, and -0.04±0.01, respectively (P<0.001). CONCLUSIONS: Tagged MRI to quantify cardiac-induced liver motion can be easily incorporated in routine liver MRI and may represent a helpful complementary tool in the diagnosis of early liver fibrosis.
Aged ; Aspartate Aminotransferases/analysis ; Blood Platelets/cytology ; Humans ; Liver Cirrhosis/*diagnostic imaging/metabolism/pathology ; *Magnetic Resonance Imaging ; Male ; Middle Aged ; Retrospective Studies ; Severity of Illness Index

A 61-year-old male patient was admitted because of unexplained abdominal pain and anemia. His past medical history was unremarkable except for having taken herbal medicine to treat facial palsy two months ago. The result of health examination performed about a month ago showed increased serum aspartate and alanine aminotransferase level, and he was diagnosed with toxic hepatitis by herbal medicine. When the patient presented to the outpatient department three weeks ago, follow-up liver function test results showed improvement but he complained of abdominal pain. Despite extensive blood chemistry tests and computed tomography, the cause of pain could not be found. After much deliberation, serum lead level and herbal medicines analysis was performed based on the fact that he took herbal medicine two months ago, and he could finally be diagnosed with lead poisoning. Since the serum lead level was high enough to be indicated for lead chelating therapy, conservative management was given. When a patient with toxic hepatitis due to herbal medication presents with abdominal pain, the possibility of lead poisoning should always be taken into consideration.
Acute Disease ; Alanine Transaminase/analysis ; Aspartate Aminotransferases/analysis ; Chemical and Drug Induced Liver Injury/*diagnosis ; Hemoglobins/analysis ; Humans ; Lead/analysis ; *Lead Poisoning ; Liver/enzymology/metabolism ; Liver Function Tests ; Male ; Middle Aged ; Plants, Medicinal/chemistry

OBJECTIVETo study the intervention effects of Jianpi Liqi Huoxue Decoction ( JLHD) on lipid peroxidative liver injury induced by alcohol.

METHODSThe rat alcoholic model of liver disease (ALD) induced by Lieber-DeCarli liquid diet was established. Thirty-two male SD rats were randomly divided into 4 groups: the normal group (n =5), the control group (n =9), the model group (n =9) and the JLHD group (n =9). From the 4th week after modeling, the rats were given JLHD or distilled water by gastrogavage respectively, and the samples of blood and liver tissues were taken out from the rats for determination by the end of the 8th week. The hepatic pathological changes were observed with HE staining; the liver injury related indices, including activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum, Y-glutamyl transpeptidase (Y-GT) activity and triglyceride (TG) content in liver tissues, as well as the lipid peroxidation related indices, including malonaldehyde (MDA) content and nitric oxide synthase (NOS) activity in liver tissue, serum Fe2+ level, and the anti-peroxidation capacity related indices, including superoxide dismutase (SOD) activity, glutathion (GSH) content and reactive oxygen species (anti-ROS) activity in liver tissues were determined.

RESULTS(1) There were obvious figures of fatty degeneration and inflammatory infiltration in liver tissues of the model group. As compared with the control group, in the model group, the activity of ALT and AST, and Fe2+ content in serum, Y-GT and NOS activity, TG and MDA content in liver tissues were significantly higher (P<0. 01), while the activity of SOD, GSH and anti-ROS in liver tissues were significantly lower (P<0.01). (2) The fatty degeneration and inflammatory infiltration of liver tissues in the JLHD group were significantly lessen as compared with those in the model group; and the abnormalities of all the indexes revealed in the model rats were restored to certain extent in the JLHD group, and especially significant were the levels of ALT activity, MDA content and Fe2+ , which were nearly normal.

CONCLUSIONJLHD has significant effects against alcoholic liver injury, the acting mechanism of which is likely to be related with its anti-lipid peroxidative effect.

Alanine Transaminase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Glutathione ; analysis ; Lipid Peroxidation ; drug effects ; Liver ; pathology ; Liver Diseases, Alcoholic ; drug therapy ; metabolism ; pathology ; Male ; Medicine, Chinese Traditional ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Triglycerides ; analysis

The aim of this study was to observe the protective effect of water extract from Sabia parviflora on mice with acute liver injury induced by acetaminophen, and investigate its possible mechanism. Fifty-eight Kunming mice were divided into 6 groups, 8 in the normal group, 10 in the model group, 10 in the biphenyl diester group, and 10 each in the low, medium and high dose groups. After adaptive feeding for one week, the mice in normal group were intragastrically administered with an equal volume of 0.5% sodium carboxymethylcellulose sodium(CMC-Na), and the mice in other groups were intragastrically administered with corresponding drugs at 20 mL·kg~(-1) once a day. Then acetaminophen(200 mg·kg~(-1)) was administered after the above drug administration except the normal group. The behavior and signs of the experimental animals were observed every day and the samples were taken for experiments on the next day of the final administration. The liver mass and mass index were calculated. The blood was collected from the abdominal aorta and centrifuged to obtain the serum for detecting aspartate aminotransferase(AST) activity and alanine aminotransferase(ALT) activity. The liver tissue homogenate was used to detect superoxide dismutase(SOD) activity, glutathione(glutathione, r-glutamyl cysteingl+glycine, GSH) activity and malondialdehyde(MDA) content. Liver tissue was analyzed for histological analysis. The results showed that S. parviflora could alleviate the lipid peroxidation damage in the liver caused by acetaminophen, reduce the ALT and AST activities in serum, increase the levels of SOD and GSH in liver tissue, decrease the content of MDA in liver tissue, and inhibit the apoptosis. S. parviflora could also improve the live histopathological profile, protect liver cells and restore liver function. Among them, the high dose had the most significant effect and showed dose-effect relationship. This study indicated that S. parviflora had a significant protective effect on acetaminophen-induced liver injury in mice, and its mechanism may be related to its anti-oxidation effect and inhi-bitory effect on apoptosis.
Acetaminophen/toxicity* ; Alanine Transaminase/metabolism* ; Animals ; Aspartate Aminotransferases/metabolism* ; Chemical and Drug Induced Liver Injury/drug therapy* ; Liver/enzymology* ; Malondialdehyde/analysis* ; Mice ; Oxidative Stress ; Plant Extracts/pharmacology* ; Superoxide Dismutase/metabolism*

OBJECTIVETo investigate the expression and pathobiological implications of angiotensin II type 1 receptor (AT1R) in development of myocardial fibrosis of rats.

METHODSRat myocardial necrosis model was established using isoproterenol injection (15 mg/kg). Rat serum aspartate transaminase (AST), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase isoenzymes (CK-MB) were detected by MD-100 automatic biochemical analyzer. Masson staining was used to evaluate the morphological changes. The expression of AT1R protein was determined by immunohistochemistry and its mRNA expression was analyzed by RT-PCR. The expression of collage type I and III was determined by immunohistochemistry.

RESULTSSerum LDH, CK and CK-MB reached their peaks at 4 h (chi2 = 16.90, P < 0.05), and AST achieved its peak in 6 h (chi2 = 16.90, P < 0.05). AT1R mRNA expression was increased 2 - 12 h after isoproterenol injection, but no statistical significance (P > 0.05) was observed comparing with the control. However, a significant AT1R mRNA increase was present at 24 h and decreased gradually after 48 h, and back to the control level after 3 weeks. Protein expression of AT1R increased proportionally with the severity of the fibrosis.

CONCLUSIONSAT1R mRNA and protein expressions increase significantly during myocardial ischemia, and is closely correlated with the fibrosis. These findings indicate that AT1R may play an important role in the pathogenesis of myocardial fibrosis.

Animals ; Aspartate Aminotransferases ; analysis ; genetics ; Cardiomyopathies ; metabolism ; Cell Differentiation ; physiology ; Creatine Kinase ; analysis ; genetics ; Fibrosis ; metabolism ; Immunohistochemistry ; Isoproterenol ; analysis ; L-Lactate Dehydrogenase ; genetics ; metabolism ; Male ; Myocardial Infarction ; pathology ; Myocardial Ischemia ; pathology ; Myocardium ; metabolism ; RNA, Messenger ; metabolism ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 1 ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVEThe prevalence of non-alcoholic fatty liver disease (NAFLD) has markedly increased. Insulin resistance has been implicated in the pathogenesis of NAFLD. This study was aimed at observing the relationship between insulin resistance and NAFLD, and evaluating the role of pioglitazone (PGZ) acting as insulin-sensitizing agents in the prevention and treatment of rat fatty liver induced by high fat feeding.

METHODSThe rats were separated randomly into 6 groups: model group I were fed high fat diet for 8 weeks, PGZ prevention group were given PGZ 4 mg/(kg.d) simultaneously, while control group I were fed normal food for 8 weeks; model group II were fed high fat diet for 16 weeks, PGZ treatment group were given PGZ 4 mg/(kg.d) orally simultaneous with high fat diet for 8 weeks after high fat feeding for 8 weeks, control group II were fed normal food for 16 weeks. The rats were sacrificed after 8 weeks and 16 weeks respectively. Liver weight, body weight, serum activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), tumor necrosis factor alpha (TNF-alpha), fasting blood glucose (FBG), fasting plasma insulin (FINS), HOMA (homeostasis model assessment) insulin resistance index (HOMA-IR), and the liver histology of rats of all groups were assayed.

RESULTSAfter 8 weeks, the liver in model group I showed typical steatosis, accompanied with mild to moderate lobular inflammatory cell infiltration, liver indexes and serum levels of ALT, AST, ALP, TNF-alpha were significantly increased (P<0.05) compared with control group I. Whereas, the degree of hepatic injury was attenuated in PGZ prevention group, liver indexes and serum levels of ALT, ALP were significantly decreased (P<0.05) compared with model group I. After 16 weeks, notable steatosis, and lobular inflammation were observed in model group II rat liver, while the degree of hepatic injury was attenuated in the PGZ treatment group. Liver index, serum levels of ALT, AST, ALP, FINS and HOMA-IR were significantly increased (P<0.05) in model group II compared with control group II. Whereas, in PGZ treatment group, serum levels of AST and FINS showed decreasing tendency, liver indexes, serum levels of ALT, ALP, TNF-alpha and HOMA-IR were significantly decreased compared with model group II.

CONCLUSIONInsulin resistance plays a role in the pathogenesis of NAFLD in rats. Pioglitazone can attenuate insulin resistance and biochemical and histological injury in high fat-induced fatty liver in rats.

Alanine Transaminase ; blood ; Alkaline Phosphatase ; blood ; Animals ; Aspartate Aminotransferases ; blood ; Fatty Liver ; drug therapy ; etiology ; metabolism ; pathology ; Insulin Resistance ; Liver ; pathology ; Male ; Rats ; Rats, Sprague-Dawley ; Thiazolidinediones ; therapeutic use ; Tumor Necrosis Factor-alpha ; analysis

OBJECTIVETo investigate the risk factors of Budd-Chiari syndrome (B-CS) complicated with hepatocellular carcinoma (HCC).

METHODSThe clinical data of 30 patients with B-CS complicated with HCC treated in the First Affiliated Hospital of Zhengzhou University from December 2012 to November 2014 were analyzed retrospectively, 106 another patients were selected randomly as control group in the same term. Gender, age, medical history, type of B-CS, hemoglobin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin, Child-Pugh classification, portal vein diameter, HBV infection and drinking history were recorded and analyzed between the two groups. Univariate analysis and unconditional Logistic regression model were performed to screen corresponding risk factors. Area under curve (AUC) was calculated according to receiver operator characteristic (ROC) curve to evaluate the diagnostic value of each indicator.

RESULTSUnivariate analysis showed that there were no statistical differences in gender (χ² =0.001), age (t=0.317), medical history (t=-0.906), type of B-CS (χ² =2.894), ALT (t=-1.581), Child-Pugh classification (Z=-0.777), HBV infection (χ² =0.016) and drinking history (χ² =0.285) between the two groups (all P > 0.05), but the hemoglobin (t=3.370) and albumin (t=2.152) in HCC group were lower and AST (t=-2.425) and portal vein diameter (t=-2.554) were higher than that in the other group, and the differences were statistically significant (all P <0.05). The results of unconditional Logistic regression model analysis indicated that hemoglobin, AST and portal vein diameter were independent risk factors of B-CS complicated with HCC (OR=0.972, 1.015, 1.206; P=0.004, 0.022, 0.012). ROC curve analysis indicated that the AUC of AST, hemoglobin and portal vein diameter was 0.704, 0.324 and 0.624, the predicate value was, in order, AST, portal vein diameter, hemoglobin.

CONCLUSIONHemoglobin, AST and portal vein diameter are independent risk factors of B-CS complicated with HCC.

Area Under Curve ; Aspartate Aminotransferases ; metabolism ; Budd-Chiari Syndrome ; complications ; Carcinoma, Hepatocellular ; complications ; Case-Control Studies ; Child ; Hemoglobins ; analysis ; Humans ; Liver Neoplasms ; complications ; Logistic Models ; Portal Vein ; pathology ; ROC Curve ; Retrospective Studies ; Risk Factors

UNLABELLEDWe investigated the relationship between ethanol exposure and heme oxygenase (HO-1) in human hepatocytes in order to ascertain if induction of HO-1 can prevent ethanol induced cellular damage.

METHODSDose-dependent (25-100 mmol/L) and time-dependent (0-24 h) ethanol exposure were used in the present study. HO-1 mRNA and protein expression were detected by PT-PCR and Western blot respectively. HO-1 activity was indicated by bilirubin and Fe2+ formation. Cytotoxicity was investigated by means of lactate dehydrogenate (LDH) and aspartate transaminase (AST) level in culture supernatants, as well as the intracellular formation of malondialdehyde (MDA), cellular glutathione (GSH) status and CYP 2E1 activity.

RESULTSWe first demonstrated a dose-dependent response between ethanol exposure and HO-1 mRNA and protein expression in human hepatocytes. We further observed a time-dependent increase of HO-1 mRNA expression using 100 mmol/L ethanol starting 30 minutes after ethanol exposure, reaching its maximum between 3 h and 9 h. Being similar increased protein expression started to what had been demonstrated with the mRNA level, at 6 h after ethanol exposure, and kept continuous elevated over 18 h. In addition, we found that ethanol exposure to hepatocytes markedly increased HO-1 enzyme activity in a time-dependent manner measured as bilirubin and Fe2+ formation in human hepatocytes. Our results clearly showed that ethanol exposure caused a significant increase of LDH, AST, and MDA levels, while the antioxidant GSH was time-dependently reduced. Furthermore, we demonstrated that pre-administration of cobalt protoporphyrin (CoPP) induced HO-1 in human hepatocytes, and prevented an increase of MDA and a decrease of GSH. These effects could be partially reversed by zinc protoporphyrin (ZnPP), an antagonist of HO-1 induction.

CONCLUSIONHO-1 expression in cells or organs could lead to new strategies for better prevention and treatment of ethanol-induced oxidative damage in human liver.

Aspartate Aminotransferases ; metabolism ; Bilirubin ; analysis ; Cell Survival ; Cells, Cultured ; Enzyme Induction ; drug effects ; Ethanol ; Gene Expression Regulation, Enzymologic ; drug effects ; Glutathione ; metabolism ; Heme Oxygenase (Decyclizing) ; metabolism ; Heme Oxygenase-1 ; Hepatocytes ; drug effects ; enzymology ; pathology ; Humans ; Iron ; analysis ; L-Lactate Dehydrogenase ; metabolism ; Malondialdehyde ; metabolism ; Membrane Proteins ; Protoporphyrins ; RNA, Messenger ; biosynthesis ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo investigate the expression of sonic hedgehog (Shh) signaling pathway in liver fluorosis and to explore related mechanism.

METHODSTo establish animal model, 48 normal SD rats (aged 4-5 weeks) were randomly divided into 4 groups (12 each): control group, fluoriosis group, blocking group and blocking control group. After 6 months, the blocking group and blocking control group were injected intraperitoneally once every 2 days for 3 times with 10 mg/kg cyclopamine or dimethysulfoxide, respectively. Rats were sacrificed at the end of the experiment and the fluoride content in urine and liver function was determined. The expression of Shh and Gli1 protein and mRNA in hepatocytes was detected by immunohistochemistry and real-time fluorescence quantitative PCR, respectively.

RESULTSThe fluoride contents in the urine and the incidence of dental fluorosis increased in the fluoride and blocking control groups as compared with those in the control group, but decreased in the blocking group compared with those of the fluoride and blocking control group. Compared with the control group, the titers of aspartate transaminase (AST) and alanine transaminase (ALT) significantly increased, while the activity of total protein and albumin decreased in the fluoride and blocking control groups. Compared with the fluoride and blocking control groups, the activity of the ALT slightly declined and the AST, total protein and albumin slightly increased in the blocking group. Histologically, the cells were disorganized and swollen with cytoplasmic clearing (balloon cells), compared with the control group. The expression of Shh and Gli1 significantly increased in all but the control group. Compared with the fluoride and blocking control groups, the expression of Shh and Gli1 declined in the blocking group.

CONCLUSIONSThe overexpression and cyclopamine inhibition of the Shh signaling pathway are closely related to the content of fluoride in the liver. The Shh signaling pathway plays an important role in the pathogenesis of liver injury caused by fluorosis, suggesting a preventive and therapeutic target of the disease.

Alanine Transaminase ; analysis ; Animals ; Aspartate Aminotransferases ; analysis ; Dimethyl Sulfoxide ; pharmacology ; Disease Models, Animal ; Fluoride Poisoning ; drug therapy ; metabolism ; Fluorosis, Dental ; diagnosis ; Hedgehog Proteins ; antagonists & inhibitors ; metabolism ; Hepatocytes ; metabolism ; Kruppel-Like Transcription Factors ; metabolism ; Liver ; metabolism ; Liver Diseases ; drug therapy ; metabolism ; RNA, Messenger ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; drug effects ; Veratrum Alkaloids ; pharmacology ; Zinc Finger Protein GLI1