Elevated Serum Aspartate Aminotransferase Research Articles

Effect of cannabinoid receptor-2 agonist AM1241 on platelet-derived growth factor expression in the liver tissue of mice with hepatic fibrosis

Objective: To investigate the effect of cannabinoid receptor-2 (CB2) agonist AM1241 on the mRNA and protein expression of platelet-derived growth factor (PDGF) and collagen-III (Col-III) in the liver tissue of mice with experimental liver fibrosis induced by carbon tetrachloride (CCl(4)). Methods: Totally 38 8-week-old male C57BL/6J mice were randomly divided into control group, model group, 3 mg/kg CB2 receptor agonist (AM1241) group, and 9 mg/kg AM1241 group. All mice, except for the control group, were treated with 30% CCl(4) (three times a week, 5 ml/kg body weight, 16 weeks) to establish a liver fibrosis model. Meanwhile, 3 and 9 mg/kg AM1421 was intraperitoneally injected for daily intervention, respectively. The dosage was adjusted according to actual body weight. The same solvent was given in the control group. The serum level of aspartate aminotransferase (AST) was measured by serum enzyme digestion. The liver inflammation and fibrosis were observed by HE staining of tissue slices. The mRNA and protein expression of PDGF and Col-III in hepatic tissue was determined by real-time PCR and immunohistochemistry. Results: Compared with the control group, the mice in model group showed severe liver fibrosis, significantly elevated serum AST level (742 ± 300.8 U/L vs 118.1 ± 31.1 U/L, P < 0.05), and significantly increased mRNA and protein expression of PDGF and Col-III in liver tissue (P < 0.05). Compared with the model group, the mice in 3 mg/kg AM1241 group and 9 mg/kg AM1241 group had less severe liver fibrosis, and significantly reduced serum AST levels (116.6 ± 13.68 U/L vs 742 ± 300.8 U/L, P < 0.05; 113.8 ± 16.01 U/L vs 742 ± 300.8 U/L, P < 0.05) and mRNA and protein expression of PDGF and Col-III in liver tissue (P < 0.05). Conclusion: CB2 receptor agonist AM1241 can inhibit the mRNA and protein expression of PDGF in the liver tissue of mice with hepatic fibrosis, and reduce extracellular matrix synthesis.

Unexplained High Activity of Aspartate Aminotransferase in an Asymptomatic Pediatric Patient

Elevated enzyme activities in plasma may at times be attributed to the presence of macro-enzymes. The macro-enzymes are often serum enzymes in complex with immunoglobulins, resulting in a greater molecular mass that cannot be filtered by renal glomeruli and are, hence, retained in the plasma. The aspartate aminotransferase (AST) can exist as a macro-enzyme, although it has been rarely reported. We describe a pediatric patient with persistently elevated serum AST activity, due to macro-enzyme formation between AST and an immunoglobulin. This is to highlight the importance of early diagnosis of macro-AST in an otherwise asymptomatic pediatric patient with isolated AST-elevation and to avoid unnecessary costly testing.

Influence of resveratrol on liver fibrosis induced by dimethylnitrosamine in male rats.

Liver fibrosis is a significant health problem which represents the liver’s scarring process and response to injury through deposition of collagen and extracellular matrix, and ultimately leads to cirrhosis. Resveratrol is a naturally occurring phytoalexin found predominantly in grapes. This study aimed to investigate the antifibrotic role of resveratrol on dimethylnitrosamine (DMN)-induced liver fibrosis in rats. Rats were divided into four groups and treated for three weeks; control, resveratrol administered orally (20 mg/kg daily), DMN intraperitoneally injected (10 mg/kg 3 days/week), and the last group was pre-treated daily with resveratrol then injected with DMN, 3 days/week. DMN administration induced severe liver pathological alterations. However, oral administration of resveratrol before DMN significantly prevented the induced loss in body weight, as well as the increase in liver weight which arise from DMN administration. Resveratrol has also inhibited the elevation of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and bilirubin levels. Furthermore, resveratrol significantly increased hepatic reduced glutathione (GSH) levels and reduced the levels of malondialdehyde (MDA) due to its antioxidants effect as well as increased serum protein levels. In addition, DMN induced elevation in hydroxyproline content. On the other hand, hydroxyproline level was significantly reduced in the resveratrol pretreated rats. Resveratrol has also remarkably maintained the normal liver lobular architecture. Moreover, resveratrol had displayed potent potentials to prevent collagen deposition, lymphocytic infiltration, necrosis, steatosis, vascular damage, blood hypertention, cholangiocyte proliferation. It can be concluded that resveratrol has a marked protective role on DMN-induced liver fibrosis in rats, and can be considered as antiproliferative, antihypertensive, as well as antifibrotic agent and may be used to block the development of liver fibrosis.

Targeting Sirt1 in a rat model of high-fat diet-induced non-alcoholic fatty liver disease: Comparison of Gegen Qinlian decoction and resveratrol.

The present study aimed to explore the mechanism of action of Gegen Qinlian decoction (GGQLD) in experimental non-alcoholic fatty liver disease (NAFLD). A total of 30 rats were randomly divided into five groups: The chow, model, high- and low-dose GGQLD (GGQLD-H and GGQLD-L, respectively) and resveratrol (Resl) groups, and were treated with saline, GGQLD and Resl when a model of high-fat diet (HFD)-induced NAFLD was established. Blood lipid and liver enzymes were detected following treatment for 8 weeks and liver tissue pathology was observed using Oil Red O and haematoxylin and eosin staining. Furthermore, the liver protein and mRNA expression of sirtuin (Sirt)1, peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α and nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) were measured using western blotting and reverse transcription-quantitative polymerase chain reaction. Compared with the chow group, the model group demonstrated significantly increased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels (P<0.01). GGQLD doses and Resl attenuated the elevated serum ALT and AST levels. GGQLD-H and Resl significantly increased the serum high-density lipoprotein cholesterol level compared with that in the model group (P<0.01), while GGQLD-L and Resl significantly decreased serum low-density lipoprotein cholesterol levels (P<0.01). The GGQLDs and Resl groups revealed an evident improvement in Sirt1 protein and mRNA expression. Although GGQLD and Resl significantly decreased NF-κB gene expression compared with the model group (P<0.01), the effect on NF-κB protein expression was not significant. Furthermore, the PGC-1α gene and protein expression in the HFD rat group slightly decreased compared to the levels in the chow group, but the decrease was insignificant. However, an evident increase in PGC-1α mRNA expression was observed in the GGQLD-H group compared with the model group (P<0.01). Histological staining revealed that GGQLD and Resl decreased the lipid droplets in hepatocytes and normalized steatosis in rats fed with a HFD. The results indicated that GGQLD treatment may be a potent strategy for managing NAFLD by managing lipid metabolism and inflammatory and histological abnormalities by triggering the Sirt1 pathway.

Protective effects of tropisetron on cerulein-induced acute pancreatitis in mice

Acute pancreatitis (AP) causes morbidity and mortality. The aim of the present study was to investigate the protective effect of tropisetron against AP induced by cerulein.Cerulein (50μg/kg, 5 doses) was used to induce AP in mice. Six hours after final cerulein injection, animals were decapitated. Hepatic/pancreatic enzymes in the serum, pancreatic content of malondialdehyde (MDA), pro-inflammatory cytokines and myeloperoxidase (MPO) activity were measured.Tropisetron significantly attenuated pancreatic injury markers and decreased the amount of elevated serum amylase, lipase, alanine aminotransferase (ALT), aspartate aminotransferase (AST), MPO activities and pro-inflammatory cytokines levels caused by AP in mice. Tropisetron didn’t affect the pancreatic levels of MDA.Our results suggest that tropisetron could attenuate cerulein-induced AP by combating inflammatory signaling. Further clinical studies are needed to confirm its efficacy in patients with AP.

Exogenous phosphatidylcholine supplementation retrieve aluminum-induced toxicity in male albino rats.

This study investigated the ameliorative potential of exogenous phosphatidylcholine (PC) against aluminum-induced toxicity in male albino rats. Four groups of rats were used for this study (N=8): group I served as the control, group II (PC treated) received L-α-phosphatidylcholine (egg yolk-derived) 100mg/kg bwt/day orally, group III (aluminum treated) received aluminum chloride 100mg/kg bwt/day orally, and group VI (aluminum+PC treated) received similar oral dose of aluminum and PC (100mg/kg bwt/day). Treatment was continued for 8weeks. Results revealed that aluminum chloride treatment leading to a significant elevation in serum aspartate aminotransferase, serum alanine aminotransferase, urea, creatinine, malondialdehyde, serum cytokines (tumor necrosis factor-α, interleukin-6), and brain content of acetylcholine, as well as a significant reduction in serum-reduced glutathione, serum testosterone, and brain content of acetylcholinesterase. Moreover, aluminum administration caused significant histopathological alteration in liver, kidney, brain, testes, and epididymis. Co-treatment with exogenous PC resulted in significant improvement in intensity of histopathologic lesions, serum parameters, testosterone level, proinflammatory cytokines, and oxidative/antioxidative status. However, it does not affect the brain content of acetylcholine and acetylcholinesterase. Conclusively, treatment with exogenous PC can retrieve the adverse effect of aluminum toxicities through its antioxidative and anti-inflammatory properties.

Protective Effects of Tormentic Acid, a Major Component of Suspension Cultures of Eriobotrya japonica Cells, on Acetaminophen-Induced Hepatotoxicity in Mice.

An acetaminophen (APAP) overdose can cause hepatotoxicity and lead to fatal liver damage. The hepatoprotective effects of tormentic acid (TA) on acetaminophen (APAP)-induced liver damage were investigated in mice. TA was intraperitoneally (i.p.) administered for six days prior to APAP administration. Pretreatment with TA prevented the elevation of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), total bilirubin (T-Bil), total cholesterol (TC), triacylglycerol (TG), and liver lipid peroxide levels in APAP-treated mice and markedly reduced APAP-induced histological alterations in liver tissues. Additionally, TA attenuated the APAP-induced production of nitric oxide (NO), reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and IL-6. Furthermore, the Western blot analysis showed that TA blocked the protein expression of inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2), as well as the inhibition of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) activation in APAP-injured liver tissues. TA also retained the superoxidase dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) in the liver. These results suggest that the hepatoprotective effects of TA may be related to its anti-inflammatory effect by decreasing thiobarbituric acid reactive substances (TBARS), iNOS, COX-2, TNF-α, IL-1β, and IL-6, and inhibiting NF-κB and MAPK activation. Antioxidative properties were also observed, as shown by heme oxygenase-1 (HO-1) induction in the liver, and decreases in lipid peroxides and ROS. Therefore, TA may be a potential therapeutic candidate for the prevention of APAP-induced liver injury by inhibiting oxidative stress and inflammation.

Shiftwork Is Not Associated with Increased Risk of NAFLD: Findings from the National Health and Nutrition Examination Survey.

There is increased focus on the metabolic impact of shiftwork, especially given the significant number of employees who work nighttime or rotating shifts. Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. We conducted a cross-sectional study to examine the association between shiftwork and the risk of NAFLD. We used aggregated data from the 2005-2006, 2007-2008, and 2009-2010 cycles of the National Health and Nutrition Examination Survey (NHANES). We defined NAFLD by elevated serum alanine aminotransferase (ALT) or aspartate aminotransferase (AST) levels (males: AST>40 or ALT>37; females: AST>31 or ALT>31) in the absence of excessive alcohol use and viral hepatitis. We defined shiftworkers as participants who self-reported currently working regular night shifts or rotating shifts. We calculated adjusted odds ratios (OR) and 95% confidence intervals (CI) using multivariable logistic regression. Overall, 8159 participants aged 20-79years reported working at a job or business using the NHANES Occupation Questionnaire and were included in the analysis. Of these, 11.1% were classified as shiftworkers. Compared to non-shiftworkers, shiftworkers were younger, were less likely to be non-Hispanic White, and have health insurance or health care. The overall prevalence of NAFLD was 15.7%. NAFLD occurred more frequently in shiftworkers (17.0%) than non-shiftworkers (15.5%). However, in the overall multivariable analysis, shiftwork was not associated with the risk of NAFLD (OR 1.11, 95% CI 0.87-1.43). The findings from this NHANES-based cross-sectional study do not support an association between shiftwork and increased risk of NAFLD.

Thymoquinone mitigate ischemia-reperfusion-induced liver injury in rats: a pivotal role of nitric oxide signaling pathway.

Oxidative and nitrosative stress-induced endothelial cell damage play an essential role in the pathogenesis of hepatic ischemia-reperfusion (IR) injury. IR is associated with reduced eNOS expression and exacerbated by superimposed stress. NOSTRIN induces intracellular endothelial nitric oxide synthase (eNOS) translocation and inducible nitric oxide synthase (iNOS) increases nitric oxide (NO) production. Our aim was to assess hepatic expression of iNOS, eNOS, and NOSTRIN in IR with or without N-acetylcysteine (NAC) or thymoquinone (TQ) pretreatment and to compare their hepatoprotective effects. Surgical induction of IR was performed by occlusion of hepatic pedicle for 30min with mini-clamp and reperfused for 30min. The effects of TQ (20mg/kg/day) or NAC (300mg/kg/day) administered orally for 10days were evaluated by serum ALT and AST, oxidative stress parameters, NO production, and histopathological analysis. Also, localization and expression of iNOS, eNOS, and NOSTRIN were assessed by immunofluorescence. TQ or NAC pretreatment significantly decreased elevated serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and myeloperoxidase (MPO) activities, malondialdehyde (MDA) level, and NO production. In addition, they restored the depleted GSH content and alleviated histopathological changes. Furthermore, they up-regulated eNOS and down-regulated iNOS and NOSTRIN expressions. TQ exerts its hepatoprotective effect, at least in part, by nitric oxide signaling pathway through modulation of iNOS, eNOS, and NOSTRIN expressions as well as suppression of oxidative stress.

Longitudinal Changes in Liver Aminotransferases Predict Metabolic Syndrome in Chinese Patients with Nonviral Hepatitis

ObjectiveThis study explored the correlation of longitudinal changes in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels with the incidence of metabolic syndrome (Mets) based on a dynamic health examination cohort. MethodsA Mets-free dynamic cohort involving 4541 participants who underwent at least three health examinations from 2006 to 2011 was included in the study. Mets was defined according to the Chinese Medical Association Diabetes Branch definition that included hypertension, obesity, hyperlipidemia, and hyperglycemia. Generalized estimating equation (GEE) model was used to analyze multivariate relative risk (RR) of repeated observations of ALT and AST in quartiles for Mets or its components according to gender. ResultsIn all, 826 Mets cases were reported. Adjustment of relevant parameters indicated that time-varying changes in ALT and AST levels were positively associated with the incidence of Mets in a dose-response manner. Positive association between high ALT levels and fatty liver was much stronger than that between high AST levels and fatty liver, particularly in male participants. These associations were consistently observed in the following subgroups: participants with ALT and AST levels of <40 U/L, participants with of <25 kg/m2, and participants with non-fatty liver. Furthermore, participants with 2 Mets components at baseline showed lower multivariate adjusted RRs of ALT and AST for Mets than participants with 0-1 Mets component. ConclusionThese results suggested that elevated serum ALT and AST levels were early biomarkers of Mets or its components.

Lipodystrophy Due to Adipose Tissue-Specific Insulin Receptor Knockout Results in Progressive NAFLD.

Ectopic lipid accumulation in the liver is an almost universal feature of human and rodent models of generalized lipodystrophy and is also a common feature of type 2 diabetes, obesity, and metabolic syndrome. Here we explore the progression of fatty liver disease using a mouse model of lipodystrophy created by a fat-specific knockout of the insulin receptor (F-IRKO) or both IR and insulin-like growth factor 1 receptor (F-IR/IGFRKO). These mice develop severe lipodystrophy, diabetes, hyperlipidemia, and fatty liver disease within the first weeks of life. By 12 weeks of age, liver demonstrated increased reactive oxygen species, lipid peroxidation, histological evidence of balloon degeneration, and elevated serum alanine aminotransferase and aspartate aminotransferase levels. In these lipodystrophic mice, stored liver lipids can be used for energy production, as indicated by a marked decrease in liver weight with fasting and increased liver fibroblast growth factor 21 expression and intact ketogenesis. By 52 weeks of age, liver accounted for 25% of body weight and showed continued balloon degeneration in addition to inflammation, fibrosis, and highly dysplastic liver nodules. Progression of liver disease was associated with improvement in blood glucose levels, with evidence of altered expression of gluconeogenic and glycolytic enzymes. However, these mice were able to mobilize stored glycogen in response to glucagon. Feeding F-IRKO and F-IR/IGFRKO mice a high-fat diet for 12 weeks accelerated the liver injury and normalization of blood glucose levels. Thus, severe fatty liver disease develops early in lipodystrophic mice and progresses to advanced nonalcoholic steatohepatitis with highly dysplastic liver nodules. The liver injury is propagated by lipotoxicity and is associated with improved blood glucose levels.

CRT-200.49 Hypoxic Liver Injury Diagnosed in the Emergency Room Predicts In-Hospital Death in Patients With Acute ST-segment Elevation Myocardial Infarction

Elevated serum aspartate and alanine aminotransferase (AST & ALT) are often observed in patients with ST-segment elevation myocardial infarction (STEMI). From 2007 to 2014, a total of 1540 consecutive patients (mean age 61±13 years old) with STEMI underwent primary PCI were analyzed

Metabolic Syndrome and Serum Liver Enzymes in the General Chinese Population.

Background: The aim of this study was to evaluate the associations between alanine aminotransferase (ALT) and aspartate aminotransferase (AST) with metabolic syndrome (MetS) in the general Chinese population. Methods: This study was a multicenter, cross-sectional study which was conducted in rural areas of China from the 2012 to 2013 Northeast China Rural Cardiovascular Health Study (NCRCHS), and 11,573 adults with complete data were included in our final analysis. Elevated ALT and AST levels were defined as >40 U/L. Serum ALT and AST levels within the reference range were divided into quartiles, and their associations with MetS were evaluated by logistic regressions. Results: A total of 7.4% and 3.5% participants had elevated serum ALT and AST levels, respectively. The prevalence of MetS was 37.3% in males and 45.8% in females. After adjusting for potential confounders, we found ALT level elevation, even within the reference range, was independently associated with MetS. The odds ratio (OR) values of MetS in the ALT quartiles 2–4 groups within the reference range were 1.113 (95% CI: 1.019–1.280), 1.375 (95% CI: 1.212–1.560), 1.878 (95% CI: 1.650–2.138) compared with the ALT quartile 1 group, and OR in the elevated ALT group was 3.020 (95% CI: 2.496–3.653). Positive relationship for MetS was also observed in elevated AST group (OR: 1.689, 95% CI: 1.314–2.171), but within the reference range, the AST level was not associated with MetS. Conclusions: Serum ALT level, even within the reference range, was significantly associated with MetS. However, only elevated AST levels above 40 U/L was positively associated with MetS. Within the reference range, we did not find a relationship between AST levels and MetS.

Protective effect of diallyl trisulfide against naphthalene-induced oxidative stress and inflammatory damage in mice.

The aim of this study was to investigate the possible protective effects of diallyl trisulfide (DATS) against naphthalene-induced oxidative and inflammatory damage in the livers and lungs of mice. Elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels showed significant hepatic damage after the challenge with 100 mg/kg naphthalene. Hepatic malondialdehyde (MDA) contents and the activity of myeloperoxidase (MPO) increased significantly, accompanying a decrease in the hepatic activity of total superoxide dismutase (SOD) and glutathione (GSH) levels after the naphthalene damage. In addition, the serum levels of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 8 (IL-8) increased significantly in the groups damaged with naphthalene. The main parameters related to oxidative stress and inflammatory responses in the lungs, including the NO, MPO, and GSH contents, were determined, and the histopathological and immunohistochemical changes in the lung and liver tissues were also observed. In the DATS-treated groups, all of the oxidative and inflammatory damage in the serum, liver, and lung tissues were significantly prevented.

Protective effect of Rabdosia amethystoides (Benth) Hara extract on acute liver injury induced by Concanavalin A in mice through inhibition of TLR4-NF-κB signaling pathway

Extract of Rabdosia amethystoides (Benth) Hara (ERA), a traditional Chinese medicine has antibacterial, antiviral, anti-tumor, anti-hepatitis and anti-inflammatory properties. However, the hepatoprotective effects and molecular mechanisms of ERA on acute liver injury have not been fully elucidated. This study aims to investigate the anti-inflammatory effect and liver protection of ERA against the acute liver injury induced by Concanavalin A (Con A) and its underlying molecular mechanisms in mice. Mice received ERA (50, 100, 150 mg/kg body weight) by gavage before Con A intravenous administration. We found that ERA pretreatment was able to significantly reduce the elevated serum alanine and aspartate aminotransferase levels and liver necrosis in Con A-induced hepatitis. In addition, ERA treatment significantly decreased the myeloperoxidase, malondialdehyde levels and augmented superoxide dismutase level in the liver tissue, and also suppressed the secretion of proinflammatory cytokines in the serum, compared with Con A group by enzyme linked immunosorbent assay. Furthermore, we observed that ERA pretreatment can significantly decrease the expression level of Toll-like receptor (TLR) 4 mRNA or protein in liver tissues. Further results showed that ERA pretreatment was capable of attenuating the activation of the NF-κB pathway by inhibiting IκBα kinase and p65 phosphorylation in Con A-induced liver injury. Our results demonstrate that ERA pretreatment has hepatoprotective property against Con A-induced liver injury through inhibition of inflammatory mediators in mice. The beneficial effect of ERA may be mediated by the downregulation of TLR4 expression and the inhibition of NF-κB activation.

A Herbal Formula, CGXII, Exerts Antihepatofibrotic Effect in Dimethylnitrosamine-Induced SD Rat Model.

We aimed to evaluate the antihepatofibrotic effects of CGXII, an aqueous extract which is composed of A. iwayomogi, A. xanthioides, and S. miltiorrhiza, against dimethylnitrosamine- (DMN-) induced hepatofibrosis. Male Sprague Dawley rats were intraperitoneally injected with 10 mg/kg of DMN for 4 weeks (three consecutive days weekly). Rats were orally given distilled water, CGXII (50 or 100 mg/kg), or dimethyl dimethoxy biphenyl dicarboxylate (50 mg/kg) daily. DMN injection caused substantial alteration of total body weight and liver and spleen mass, whereas they were notably normalized by CGXII. CGXII treatment also markedly attenuated the elevation of serum aspartate aminotransferase and alanine aminotransferase levels, hepatic lipid peroxidation, and protein carbonyl contents. Collagen accumulation in hepatic tissue evidenced by histopathological analysis and quantitative assessment of hepatic hydroxyproline was ameliorated by CGXII. Immunohistochemistry analysis revealed decreased α-smooth muscle actin supporting the antihepatofibrotic effect of CGXII. The profibrogenic cytokines transforming growth factor-β, platelet-derived growth factor-β, and connective tissue growth factor were increased by DMN injection. Administration of CGXII normalized the protein and gene expression levels of these cytokines. Our findings suggest that CGXII lowers the levels of profibrogenic cytokines and thereby exerts antifibrotic effects.

Ameliorative Effect of Ginger Extract on Serum Biochemical Alterations in Diethylnitrosamine Treated Rats

Present work was designed to study ameliorative effect of ginger extract (GE) on serum biochemical alterations in diethylnitrosamine (DEN) treated rats. Fifty one male Wistar albino rats were randomly allotted to four groups. DEN (0.01%) was given in drinking water ad libitum and ginger extract (50 mg/kg BW) was administered in olive oil per os either alone or in combination for 90 days. Hypoproteinaemia, hypoalbuminaemia, hypoglycaemia, elevated serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gammaglutamyl transferase (GGT) and total cholesterol levels were observed in the DEN treated rats. Concurrent administration of ginger extract with DEN significantly (P<0.05) alleviated the effects of DEN on serum enzyme level and other parameters. To conclude, present study demonstrated the ameliorative effect of ginger extract in partial to complete reversal in serum biochemical alterations.

Folate Deficiency Was Associated with Increased Alanine Aminotransferase and Glutamyl Transpeptidase Concentrations in a Chinese Hypertensive Population: A Cross-Sectional Study.

Alanine aminotransferase (ALT), aspartate transaminase (AST), and glutamyl transpeptidase (GGT) were three key enzymes in the hepatic metabolism. This study aimed to investigate the effect of homocysteine (Hcy) metabolism gene polymorphisms and serum Hcy and folate level on the hepatic functions in a Chinese hypertensive population. A representative sample with 480 subjects aged 28-75 was enrolled in 2005.9-2005.12 from six hospitals in different Chinese regions. Serum ALT, AST and GGT were measured by using an automatic biochemistry analyzer. Serum Hcy was measured by high-performance liquid chromatography, and serum folate was measured by chemiluminescent immunoassay. Known genotypes were detected by PCR-RFLP methods. The results showed that the MTHFR C677T mutation was related a decreased serum AST level (r=-0.11, p=0.026), whereas the MTHFR A1298C mutation elevated serum AST level (r=0.11, p=0.032). Furthermore, multiple regression analysis showed that folate deficiency was associated with higher serum ALT (β (SE): 0.13 (0.06), p=0.031) and GGT level (β (SE): 0.18 (0.07), p=0.011). However, serum Hcy level may not affect the hepatic functions. Our data suggested that hepatic functions were affected by MTHFR gene polymorphisms and serum folate level. Further studies are needed to confirm these correlations in a larger population.

감마선 조사로 유도된 간세포와 조혈계 손상 마우스에서 퀘르세틴 투여 후의 방사선방호 효과

This study was designed to evaluate the therapeutic effect of quercetin against radiation-induced hepatocellular and hematopoiectic damage in BALB/c mice. Mice were exposed to 6 Gy of γ-radiation and orally administered quercetin (25, 50 mg/kg b.w.) for 7 consecutive days. γ-Irradiation caused marked elevation of serum aspartate aminotransferase and alanine aminotransferase, levels as well as reduction of spleen index, thymus index, and the number of white blood cells. In addition, γ-irradiation induced significant elevation of lipid peroxidation as well as reduction of antioxidant enzyme activities, including superoxide dismutase, catalase, and glutathione peroxidase. However, post-treatment with quercetin resulted in a significant recovery of all of these parameters. These results suggest that quercetin acts as a potent radioprotector against irradiation-induced cellular damage in mice.

Hepatitis B virus reactivation and hepatitis in diffuse large B-cell lymphoma patients with resolved hepatitis B receiving rituximab-containing chemotherapy: risk factors and survival

IntroductionHepatitis B virus (HBV) reactivation has been reported in B-cell lymphoma patients with resolved hepatitis B (hepatitis B surface antigen [HBsAg]-negative and hepatitis B core antibody [HBcAb]-positive). This study aimed to assess HBV reactivation and hepatitis occurrence in diffuse large B-cell lymphoma (DLBCL) patients with resolved hepatitis B receiving rituximab-containing chemotherapy compared with HBsAg-negative/HBcAb-negative patients to identify risk factors for HBV reactivation and hepatitis occurrence and to analyze whether HBV reactivation and hepatitis affect the survival of DLBCL patients with resolved hepatitis B.MethodsWe reviewed the clinical data of 278 patients with DLBCL treated with rituximab-containing therapy between January 2004 and May 2008 at Sun Yat-sen University Cancer Center, China. Predictive factors for HBV reactivation, hepatitis development, and survival were examined by univariate analysis using the chi-square or Fisher’s exact test and by multivariate analysis using the Cox regression model.ResultsAmong the 278 patients, 165 were HBsAg-negative. Among these 165 patients, 6 (10.9%) of 55 HBcAb-positive (resolved HBV infection) patients experienced HBV reactivation compared with none (0%) of 110 HBcAb-negative patients (P = 0.001). Patients with resolved hepatitis B had a higher hepatitis occurrence rate than HBsAg-negative/HBcAb-negative patients (21.8% vs. 8.2%, P = 0.013). HBcAb positivity and elevated baseline alanine aminotransferase (ALT) levels were independent risk factors for hepatitis. Among the 55 patients with resolved hepatitis B, patients with elevated baseline serum ALT or aspartate aminotransferase (AST) levels were more likely to develop hepatitis than those with normal serum ALT or AST levels (P = 0.037, P = 0.005, respectively). An elevated baseline AST level was an independent risk factor for hepatitis in these patients. Six patients with HBV reactivation recovered after immediate antiviral therapy, and chemotherapy was continued. HBcAb positivity, HBV reactivation, or hepatitis did not negatively affect the survival of DLBCL patients.ConclusionsDLBCL patients with resolved hepatitis B may have a higher risk of developing HBV reactivation and hepatitis than HBsAg-negative/HBcAb-negative patients. Close monitoring and prompt antiviral therapy are required in these patients.