and cellular infiltration as seen in Figures 1(h) and (i). Histopathology of liver revealed minor changes in non- Bt and Bt group after 1.5 months, but severe changes appeared in Bt group after 3 months. These results were quite in agreement with Kilic & Akay  who found some changes especially in the group feeding on Bt corn MON810 such as infiltration, congestion, border change and granular degeneration. Some feeding studies with GM maize confirmed histopathological changes in the liver of rats such as congestion, cell nucleus border changes and sever granular degeneration. These changes may be due to the insertion of Cry1Ab gene in maize which produces the insecticide in MON810 because this insecticide is a toxin . In the same respect Hammond, et al.  detected infiltration, mononuclear, multifocal and inflammation by microscopic examination in the liver of rats that were fed grain from glyphosate tolerant corn.
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Histopathology of liver in severe P. falciparum malaria Figure 1 displays histopathological changes of the liver in severe P. falciparum malaria. Morphologically, hepa- tocytes and endothelial cells (ECs) in the liver were ge- nerally unaffected in severe P. falciparum malaria. Fatty change and bile duct proliferation were not features of P. falciparum infection. Hyperplastic Kupffer cells, por- tal tract inflammation, sinusoidal congestion and haemo- zoin pigment deposition were important pathological hallmarks related to higher TB levels (Table 3). The total histopathological grading score showed the overall changes and was found to be highest among the group of malaria patients with hyperbilirubinaemia (12/18). Figure 1 (A-C) illustrates a normal portal tract, consis- ting of hepatic vein, hepatic artery, and bile duct, with surrounding hepatocytes. Very few inflammatory cells are noted within the portal tract. Minimal fatty change is sometimes observed (Figure 1C). Liver tissues from mal- aria patient without hyperbilirubinaemia show enlarged sinusoidal area, haemozoin pigment within the hyper- plastic Kupffer cells, and inflammatory cells within the portal tract (Figure 1, D-F). In hyperbilirubinaemia group (Figure 1, G-I), liver tissues show dense inflamma- tory cells infiltration in the portal tract. At higher mag- nification, hyperplastic Kupffer cells are visible and
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AST levels in the blood is influenced by a liver, muscle, heart, brain and kidney condition, because AST contained in those organs. So if there is a damage or inflammation in liver and AST will go into blood circulation and cause the AST level in the blood increases. Based on research that has been done in Rattus norvegicus Wistar strain rats can be conclude that in both male and female treatment group, show that subchronic Ganoderma lucidum PSP treatment had not significantly effect in increasing AST levels in blood. This is appropiate with other study by Zhou X et al (2007) which Fig. 3. Abnormalities on histopathology of liver of the rat models in various treatment group, in 200x magnification; Notes: (A) Cloudy degeneration. (B) Balloning degeneration. (C) Necrosis cell
El-Hadiyah et al. (2011) experiment was used with some modifications to study the sub-acute toxicity of the tested extract fractions.Two groups; six Albino rats weighing 80-140gm each was designed as group one (G1); control group and group two (G2); extract tested group. A twenty four hours single dose of 1000mg/kg of methanol extract of leaves of Capparis spinosa was injected IP to G2 rats for one week. Group one rats were injected with daily dose of 1ml /kg normal saline 0.9% for one week. In the eighth day all treated and control groups rats were anaesthetized via inhalation with Di-ethyl ether and a 3ml orbital blood from each rat was squeezed; 2ml collected in a clot activator blood container and 1ml was collected in an ethylene diamine tetraacetic acid (EDTA) container and immediately the containers transferred to the biochemistry and hematology laboratories at the Modern Medical Center, Khartoum, Sudan to check each of the liver function; total protein, serum albumin, serum globulin, total bilirubin, direct bilirubin, indirect bilirubin, Alkaline phosphate (ALP), Alkaline transaminase (ALT), aspartate aminotransferase (AST) and Gamma-glutamyl transpeptidase (GGT). The anaesthetized rats were sacrificed and the vital liver organ isolated and size minimized with use of blades and kept in 10% formalin in separate well labelled bottles until run for histopathology screening. During the study the groups were checked for any behavioral, neurological and autonomic response. Changes in behavioral response of rats were observed and recorded daily. The observation times was four hours daily divided into four periods; 1 st period which start from zero time (immediately after extract injection) to one hour), 2 nd period started from the end of 1 st hour and lasts for an hour (1 – 2hr.), 3 rd period started from the end of 2 nd hour and lasts for an hour (2 – 3hr.) and 4 th period which started from the end of the 3 rd hour and lasts for an hour (3 – 4hr.).
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50 cHepC patients, 15 with ESRD, having undergone per- cutaneous liver biopsy between December 2011 and June 2013 at a tertiary hospital were included. 25 healthy people w ith similar age and gender were used as controls. Exclu- sion criteria were co-infection with other viruses, chronic hepatitis due to other reasons, decompansated cirrhosis, primary or metastaic liver cancers, malignancies, serious congestive heart failure and pyschiatric disorders.
• The present study is focused on amelioration of HFD+STZ induced metabolic disorder with the administration of M. longifolia hydroethanolic fraction of leaves (MLHEF) through ex vivo and in vivo studies. Chronic HFD administration leads to metabolic changes finally causing the metabolic disorders like obesity, diabetes and cardiovascular diseases. Through ex vivo studies it was depicted that MLHEF exhibits significant glucose uptake inhibition across the intestinal and diaphragm membranes thus it may have potential against met- abolic disease. This was further confirmed through in vivo studies by observing the change in biochemi- cal, metabolic and histopathological parameters like BMI, blood glucose, glycosylated haemoglobin and lipoprotein profile. MLHEF showed significant reduction in elevated blood glucose and lipoprotein levels along with maintaining the BMI and body weight. Histopathological studies supported the MLHEF action as normalisation in liver tissue and WAT was observed MLHEF treated animals as compared diseased control. Thus from this study it can be elucidated that MLHEF exhibits potential action for amelioration of metabolic disorders
in this para-renal space. A single tumor fragment was then placed in para-renal region as showed in Fig. 5. The complete surgical procedure was performed as pre- viously described. Tumor growth was assessed by ultra- sound high resolution US performed at 7 and 14 days after surgery, it allowed detection of the tumors as an ir- regular and inhomogeneous mass, hypoecoic, infiltrating the surrounding tissue, as shown in Figs. 6 and 7 (a-b) respectively. Two weeks after the tumors implantation, rabbits were sacrificed and tumors and other organs, such liver, lung and both kidneys were collected for histopathology analysis (Fig. 8) (Fig. 9 and data not shown). The histological analysis of the tumor after 7 days from tumor tissue implant, revealed the presence of active tumor cells and percentage of 5% of necrotic area. (Fig. 9a, b, c) The histological analysis of the tumor after 14 days from tumor tissue implant, revealed the
The DM in rats was manifested via intraperitoneal administration of STZ-NA. The vital foundation of DM occurs in rats was due to damage of β-cells of Langerhans (Shirwaikar, et al., 2006),which leads to the excessive breakdown of liver glycogen to glucose-6-phosphate along with a reduction in sugar consumption via tissue. The STZ oral administration alone might bring about hyperglycemia via fatal devastation of Langerhans of β-cells. Adjacent to this in a current experimental model combination of STZ-NA exhibit hyperglycaemia and reduce glucose resistance may cause DNA strand breaks which may lead to the progression of type-II diabetes (Lukić, et al., 1998). However, β-cells are still able to release insulin in the presence of sugar, which is likely to be same as to type II DM in human. The oral treatment with extracts exhibited a significant decrease in the elevated FBG levels and increase in serum insulin level. The mechanism behind the restoration in elevated FBG in diabetic rats was due to the enhancement of the activity of plasma insulin via either release from already existing β-cells or from its bound forms.
INTRODUCTION: The liver is the largest glandular organ in the body, and has more functions than any other human organ 1 . Liver is considered to be one of the most vital organs that functions as a centre of metabolism of nutrients such as carbohydrates, proteins, lipids and excretion of waste metabolites. Additionally, it is also managing the metabolism and excretion of drugs and other xenobiotics from the body thereby providing protection against foreign substances by detoxifying and eliminating them. The bile secreted by the liver has, among other things, plays an important role in digestion 2 .
Isoniazid and rifampicin are first line drugs used for the treatment of tuberculosis but their use is associated with potentially serious toxic manifestation in the liver leading to necrosis, cirrhosis and hepatitis causing poor patient compliance. The present study was conducted to evaluate hepatoprotective activity of Fumaria parviflora leaf extract in isoniazid and rifampicin-induced hepatotoxic rats. Acute toxicity was conducted with single oral doses of F. parviflora leaf extracts at 300, 2000 and 5000 mg/kg and rats were observed for changes in body weight, haematological parameters, behavioural changes and signs of toxicity. Hepatoprotective activity of F. parviflora leaf extract (100, 200 and 300 mg/kg, p.o.) was evaluated on isoniazid and rifampicin (50 mg/kg, i.p.) induced hepatotoxic rats using silymarin as a reference drug (100 mg/kg, p.o.). F. parviflora leaf extract was found to be safe up to 5 g/kg. From biochemical and histopathological parameters it was found that pretreatment of rats with F. parviflora leaf extract an hour prior to start isoniazid and rifampicin resulted in a significant decline in the serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and total bilirubin as well as normal histology of liver biopsy specimens. It was concluded that F. parviflora leaf extract has significant hepatoprotective activity at the dose of 200 mg/kg comparable with that of silymarin. The plant extract appeared to have the potential to be used as a dietary supplement to antiTB therapy to protect against the hepatotoxicity of isoniazid and rifampicin.
observed in TAA-treated liver tissues compared to those from the control group. However, ATE 500 mg/k-treated group restored the total GSH contents to near normal levels and exhibited superior effect than positive control treated group. These data suggest that the altered antioxidant enzyme status caused by TAA was significantly ameliorated by ATE treatment. Hydroxyproline, a major constituent of collagen is well studied as a suitable marker to correlate with ECM accumulation causing HSC proliferation and liver fibrosis [40-43] . Therefore, we evaluated the serum
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For quantification of the glycogen content, the glycogen assay from Sigma-Aldrich (MAK016; Steinheim, Ger- many) was used. Liver samples (number of individuals per treatment in Fig. 4) were homogenised with bi-dis- tilled water (10 µL/mg tissue) on ice. Then, the samples were heated to 97 °C for 5 min to inactivate enzymes and centrifuged (Eppendorf 5424R) for 5 min at 13,000 g at 4 °C. Before conducting the assay, the supernatants of the samples were diluted 1:15 with bi-distilled water. For the assay, 96-well plates were used. Glycogen standards (0, 0.4, 0.8, 1.2, 1.6, 1.8, anf 2.0 µg/well) and liver sam- ples were tested in duplicate. Then, 2 µL of a hydrolysis enzyme mix was added per well. In addition to the dupli- cates per sample, each sample was also pipetted without the hydrolysis enzyme mix (sample blank) to determine the background signal caused by glucose in the sample. The plate was incubated for 30 min at room temperature on a shaker. After adding 50 µL of the master reaction mix (containing 46 µL development buffer, 2 µL develop- ment enzyme mix and 2 µL fluorescent peroxidase sub- strate) per well, the plate was covered in aluminium foil and incubated for 30 min on a shaker at room tempera- ture. Measurements were then conducted in a photom- eter (BioTek Instruments ELx800G, USA) at 570 nm.
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Methods: The free radical-scavenging activity of naringenin was evaluated by in vitro cell-free assay systems. In animals, the antioxidant potential of orally administered 50 and 100 mg/kg body weight naringenin for 45 days was assessed by measuring TBARS, lipid hydroperoxides, SOD, catalase, GST, GPx, and glutathione levels in liver homogenates prepared from animals injected intraperitoneally with multiple low dose streptozotocin at 50 mg/kg for five consecutive days. The extent of cellular damage caused by STZ administration was analyzed using H & E staining.
All the animals were sacrificed by spinal dislocation and livers were quickly excised, freed from any adhering tissues, washed and perfused with chilled normal saline, minced and homogenized in ice bath  using homogenizer in chilled 50 mM phosphate buffer (pH 7.4) to obtain 10% liver homogenate for the estimation of (GSH) glutathione  and lipid peroxidation  by using standard methods. A part of the homogenate was taken and mixed with equal volume of 10% trichloroacetic acid (TCA) and centrifuged at 4000 rpm for 15 min at 4 o c and the supernatant i.e., clear solution was collected into another tube and was further used for the determination of parameters like MDA and GSH.
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The present study showed increase in serum TG concentration. The increase was significant (P < 0.05) dependent on dose and oxidation time of the corn oil as shown in Table 1. The present study was in agreement with the results of Shastry (Shastry et al., 2011) and Chako (Chacko and Rajamohan, 2011). Hussain studied that administration of Eruca sativa seed oil have TG decreasing effect on alcoholic injured liver rats, which was inverse to our observation(Hussein et al., 2010). Al-Attar studied increase in serum TG lever in corn oil fed rats (Al-Attar, 2014).
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rate is higher in patients with NASH, while mild degree NAFLD can also lead to fibrosis. NAFLs have mild lobular inflamma- tion without hepatocyte ballooning or fibrosis, although this can progress to definite NASH because of persistent inflam- mation. In this case, there is a risk of poor outcomes and pro- gressive liver damage, with fibrosis being the key to liver dam- age progression. In this analysis, the AST and ALT ratios were correlated with fibrosis progression. Recently, AST and ALT have been focused as markers of definite NASH. Our present study
trichloromethyl free radicals (CCl3 ). This radicals bind to hydrogen atom of cell membrane unsatturated fatty acids and initiates lipid peroxidation of the endoplasmic reticulum membrane and causes a chain reaction. In addition, injury to liver tissues alters their transport function and membrane permeability, leading to leakage of enzymes from the cells. Therefore, the marked release of AST and ALT into the circulation indicates severe damage to hepatic tissue membranes due to CCl 4 intoxication
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After the animals were euthanized, vital organs including liver differential hepatocytes and kidney were removed from the rats and fixed in 10% formalin for at least 48 h, then processed routinely, and the tissues were embedded in paraffin wax. Histological sections were cut at 5 – 6 µm and stained with routines Periodic Acid Schiff (PAS) and Haematoxylin and Eosin (H & E) (Bancroft and Stevens, 1996). Detailed microscopic examinations were carried out by a consultant histopathologist. Photomicrographs of the organs were taken at various magnifications (× 100, × 250, and × 400).
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white crystalline solid is soluble in water and serves as a source of sulfide ions in the synthesis of organic and inorganic compounds. Thioacetamide (TAA) has long been known as a hepatotoxicant since its biotransformation to thioacetamide sulfoxide (TAAS) occurs along the Cytochrome P-450 (CYP)-dependent pathway, which is a toxic reactive metabolite. This reactive metabolite covalently binds to liver macromolecules and dramatically increases the production of reactive oxygen species which then induce acute centrilobular liver necrosis.  The use of a variety of natural and synthetic antioxidants to prevent thioacetamide’s toxicity has been considered and the combinations of thioacetamide with agents capable of blocking its reactive oxygen species mediated toxicity effect has been investigated.  The present study was carried out to investigate the biochemical effect of ethanol extract of Mimosa pudica leaf in thioacetamide-
In summary, our present study for the first time demonstrates that insulin pre-administration has multiple beneficial and side effects in the liver injury of mice exposed to ethanol. As shown in Fig.7, the protective activities of insulin pre-administration in liver against ethanol toxicity is involving in the sup- pressing of acetaldehyde and ROS accumulation through the activation of ALDH and the inhibition of CYP2E1, the increase of Adiponectin, the enhancing of antioxidant system through increasing GSH and activation antioxidative enzymes via Nrf-2 dependent pathway, and the inhibition of inflammatory response through inactivation of inflammatory cells and in- flammatory factors (TNF-α and IL-6) in liver. These above protective abilities inhibited ethanol expo- sure-induced mitochondrial dysfunction and apopto- sis, which can ultimately ameliorated alcoholic liver injury supporting by the improvement of H&E pathological alterations and the inhibition of intra- cytoplasmic enzymes release. However, we also found that insulin pre-administration deteriorated hepatic steatosis in mice exposed to ethanol might be through SRBEP-1c activation. This study gives us a new insight of the biological protective effects of in- sulin on the oxidative stress, apoptosis, mitochondrial dysfunction, and inflammation associated with ALD and also the harmful effects on steatosis associated with ALD. The pathogenesis of ALD is very complex, and the biological actin of insulin is also vary widely, the deeper investigations about the effects and un- derlying mechanisms of insulin and related signal transduction on ALD should be seriously considered in the further researches.
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