Activities Of Hepatic Marker Enzymes Research Articles

Alcohol promotes liver fibrosis in high fat diet induced diabetic rats.

Type 2 diabetes (T2DM) and alcoholism are considered to be lifestyle-associated independent risk factors in fatty liver diseases (FLD) mediated cirrhosis and hepatocellular carcinoma (HCC). A combined effect of both these conditions may exacerbate the pathological changes and a pre-clinical exploration of this is expected to provide a mechanical detail of the pathophysiology. The present study aims to understand the effect of alcohol on pre- diabetic and type 2 diabetic female Wistar rats. In this experimental study, 12 Wistar rats (180-220 g) were randomly assigned into three groups: Normal (fed normal rat chow), alcohol (20 %) fed diabetic (HFD+STZ), and pre-diabetic rats (HFD alone). After, two months of the experimental period, blood and liver tissues were collected lipid metabolic alteration, liver injury, and fibrosis were determined following biochemical and histological methods. Data were analyzed using one-way ANOVA and Dunnett's Post Hoc test. Significant dyslipidemia was observed in the liver tissues of diabetic and pre-diabetic rats following alcohol ingestion. A significant (p<0.05) increase in lipid peroxidation status, and hepatic marker enzyme activities (p<0.0001) were observed in diabetic animals. In corroborating with these observations, hematoxylin and eosin staining of hepatic tissue revealed the presence of sinusoidal dilation along with heavily damaged hepatocytes and inflammatory cell infiltration. Further, significantly (p<0.001) increased hepatic hydroxyproline content and extended picrosirius red stained areas of collagen in liver tissue indicated initiation of fibrosis in alcohol-fed diabetic rats. Overall, the results indicate that alcohol consumption in T2DM conditions is more deleterious than pre diabetic conditions in progressing to hepatic fibrosis.

Evaluation of Liver and Kidney Function Markers of Mature Albino Male Rats Fed with Maize-Plantain Pudding Delicacy Cooked in Metallic Plates and Edible Plant Leaves

Traditional maize-plantain puddings are usually cooked in diverse containers such as aluminium plates, cast iron plates and all types of edible plant leaves. This paper therefore, evaluates biochemical markers of liver and kidney function of mature albino male rats fed with maize-plantain pudding delicacy cooked in aluminium and cast iron plates and edible Zingiber officinale (ginger) and Musa paradisiaca (plantain) leaves using appropriate standard methods. Data obtained reveal that the activities of hepatic marker enzymes; alanine transaminase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) in the serum and liver were significantly lower in rats given the pudding extracts when compared with the control. No significant differences were observed in urea and creatinine levels in the serum and kidney of rats given pudding extracts as compared to control. In conclusion, this study has proved that maize-plantain pudding organized using ginger leaves, plantain leaves and cast iron plate are beneficial in the maintenance and improvement of liver and kidney function when compared with aluminium plate. However, in this efficacy maize-plantain pudding cooked using ginger leaves was found to be more effective than the pudding cooked using plantain leaves and cast iron plate.&#x0D;

Isolation of Brucella Melitensis and Evaluation of Serum Biochemical Changes in Camels: A Pilot Study to Prevent Human Brucellosis

Brucellosis is an infectious disease of livestock animals, which is reflected as one of the most severe public health issues worldwide. The main aim of this study is to isolate the B.melitensis and to examine the biochemical parameters in the serum of brucella infected and healthy camels. A total of 200 blood samples were collected from the camels of Shahaniya Governorate, Qatar. The Brucella isolation was done using different bacterial growth techniques. The status of blood metabolites and hepatic marker enzyme activities, kidney function markers, and mineral contents were estimated in the serum samples. Our findings revealed the probability of B.melitensis growth with 93-98%. The 34-50% of other species such as S.paucimobilis, A.lwoffii, A.salmonicida, and O.ureolytica were also noted in the serum of camels. In biochemical studies, the decreased status of glucose, total protein, albumin, and globulin in the serum of brucella-affected camels. The activities of AST, ALT, ALP, LDH, and GGT were up-regulated in the serum of brucella-infected camels. The levels BUN, creatinine, urea, creatine kinase, and bilirubin were also increased in the serum of brucella-affected camels. The calcium, magnesium, phosphorus, and iron were decreased in the brucella-infected camels. Here, we found the 93-98% probability of B.melitensis growth in the blood samples of camels. Furthermore, Brucella infection adversely altered the blood metabolites, liver function marker enzyme activities, kidney function markers, and mineral contents in the serum of camels.

Phytochemistry and Hepatoprotective Activity of Chloroform Extract of NKC Ingredient in Santalum album Against D-Galactosamine Induced Hepatotoxicity in Rats

Objective: Nilavembu Kudineer Chooranam is the combination of nine plant materials. The nine components are Nilavempu (Andrographis paniculata), Vettiver (Vetiveria zizanioides), Vilamiccamver (plectranthus vettiveroides), Santanam (Santalum album), Peyputtal (Trichosanthes dioica), Koraikkilanku (Cyperus rotandus), Cukku (Zingeber officinale), Milaku (Piper nigrum), Parpatakam (Mollugo cerviana). All these plants are used conventionally in the treatment of fever, inflammation, arthralgia, arthritis, gastric ulcer, jaundice, and general weaknes&#x0D; Methods: About 500gm of dried fine powder of Santalum album were soaked in the extractor and macerated for 30 hrs with petroleum ether. On the 22ndday after overnight fast the blood was collected from retro- orbital After the separation of serum from the blood assay of ALT, AST, ALP, γGT and bilirubin were done using standard methods and enzyme assay tests.&#x0D; Results: The preliminary phytochemical analysis of the Chloroform extract of Santalum album reveals the presence of alkaloid, flavonoid, phenol, coumarin, and tannin. The pretreatment of chloroform extract of Santalum album at a dose of 200mg and 400mg/kg (group IV and V) appeared to significantly prevent the galactosamine toxicity as revealed by the hepatic cells which were preserved in cytoplasms.&#x0D; Conclusion: Our findings demonstrated that chloroform extract of Santalum album at both doses possesses hepatoprotective and antioxidant activity, which is evidenced by lowered serum hepatic marker enzyme activities. Among the two dosages tested, 400 mg/kg/body weight showed more promising hepatoprotective and antioxidant activity, and is comparable to the standard drug Silymarin.&#x0D; Keywords: Nilavembu Kudineer Chooranam, Chloroform extract of Santalum album, preliminary phytochemical analysis, Hepatoprotective activity, D-Galactosamine induced hepatotoxicity in rats.

Carnosine decreased oxidation and glycation products in serum and liver of high-fat diet and low-dose streptozotocin-induced diabetic rats.

High-fat diet (HFD) and low-dose streptozotocin (STZ)-treated rats provide useful animal model for type II diabetes mellitus. Oxidative stress and advanced glycation end products (AGEs) play a role in the development of diabetic complications. Carnosine (CAR) has anti-oxidant and anti-glycating properties. We investigated the effects of CAR on oxidation and glycation products in HFD+STZ rats. Rats were fed with HFD (60% of total calories from fat) for 4weeks, and then a single dose of STZ (40mg/kg; i.p.) was applied. Rats with blood glucose levels above 200mg/dl were fed with HFD until the end of the 12th week. CAR (250mg/kg body weight; i.p.; five times a week) was administered to the rats for the last fourweeks. CAR significantly decreased serum triglyceride (TG) (57.7%), cholesterol (35.6%) levels and hepatic marker enzyme activities of HFD+STZ rats. It significantly reduced serum reactive oxygen species (ROS) (23.7%), AGEs (13.4%) and advanced oxidized protein products (AOPP) (35.9%) and hepatic TG (59%), ROS (26%), malondialdehyde (MDA) (11.5%), protein carbonyl (PC) (19.2%) and AGE (20.2%) levels. Liver steatosis and hepatocyte ballooning were also significantly reduced. However, CAR treatment did not alter serum glucose and blood glycated haemoglobin and hepatic anti-oxidant enzyme activities/mRNA expressions in HFD+STZ rats. Our results indicate that CAR decreased accumulation of oxidation and glycation products, such as MDA, AGE, AOPP and PC in the serum and liver and ameliorated hepatic dysfunction in HFD+STZ rats. This effect may be related to its anti-oxidative, anti-glycating, and anti-lipogenic potential.

Protective effects of dieckol on N-nitrosodiethylamine induced hepatocarcinogenesis in rats.

Dieckol (DEK) is a naturally occuring phlorotannins found in marine brown algae Ecklonia cava which is attributed with various pharmacological properties. This study was aimed to investigate the protective role of DEK on N-Nitrosdiethylamine (NDEA) induced rat hepatocarcinogenesis. In this investigation 0.01% NDEA in drinking water for 15 weeks to induce hepatocellular carcinoma (HCC). DEK was administered orally (10, 20 and 40mg/kg body weight) for 15 weeks with 0.01% NDEA through drinking water. Hepatocarcinogesis was measured by the increased activities of serum liver marker enzymes namely aspartate trasaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT), lactate dehydrogenase (LDH), α-fetoprotein (AFP) and total bilirubin along with increased elevation of cytochrome p450, lipid peroxidation markers, thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (HP), protein carbonyl content (PCC) and conjugated dienes (CD). The effect of NDEA was indicated by significant decreased activities of enzymatic antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR) and non-enzymatic antioxidants like reduced glutathione, vitamin C and vitamin E. The oral administration of DEK at a dose of 40mg/kg body weight significantly reversed the activities of hepatic marker enzymes, dercreased lipid peroxidative markers, increased antioxidant cascade and decreased NDEA concentration in liver. DEK at a dose of 40mg/kg body weight was highly effective when compared to other two doses (10 and 20mg/kg body weight). All these changes were accompanied by histopathological observations in liver. The obtained results clearly demonstrated that DEK prevents lipid peroxidation, hepatic cell damage and promote the enzymatic and non-enzymatic antioxidant defense system in NDEA-induced hepatocarcinogenesis which might be due to activities like scavenging of oxy radicals by Dieckol.

Assessment of In Vivo Antidiabetic Properties of Umbelliferone and Lupeol Constituents of Banana (Musa sp. var. Nanjangud Rasa Bale) Flower in Hyperglycaemic Rodent Model.

Banana is an extensively cultivated plant worldwide, mainly for its fruit, while its ancillary product, the banana flower is consumed as a vegetable and is highly recommended for diabetics in the traditional Indian medicine system. This study is based on an investigation of the in vivo antihyperglycaemic activity of Umbelliferone (C1) and Lupeol (C2) isolated from the ethanol extract of banana flower (EF) in alloxan induced diabetic rat model. Diabetic rats which were administered with C1, C2 and EF (100 and 200 mg/kg b. wt.) for 4 weeks showed deterioration in fasting hyperglycaemia and reversal of abnormalities in serum/urine protein, urea and creatinine, when compared to the diabetic control group of rats. The diabetic group of rats fed with EF, C1 and C2 (100 mg/kg b. wt.) once daily, for a period of 28 days resulted in a significant reduction of diabetic symptoms viz., polyphagia, polydipsia, polyuria and urine sugar together with an improved body weight. HbA1c extent was reduced whereas levels of insulin and Hb were increased. Both the extract and compounds wielded positive impacts in diabetic rats by reversal of altered activities of hepatic marker enzymes viz., aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP); glycolytic enzyme (hexokinase); shunt enzyme (glucose-6-phosphate dehydrogenase); gluconeogenic enzymes (glucose-6-phosphatase, fructose-1,6-bisphosphatase, lactate dehydrogenase) and pyruvate kinase. The characteristic diabetic complications such as hypercholesterolemia and hypertriacylglycerolemia also significantly reverted to normal in the serum/liver of diabetic rats. Besides these, the treatment increased the activities of enzymatic and non-enzymatic antioxidants in the serum and liver. The histological observations revealed a marked regeneration of the β-cells in the drug treated diabetic rats. In conclusion, the present study illustrates that EF, C1 and C2 enhances the glycolytic activities, besides increasing the hepatic glucose utilization in diabetic rats by stimulating insulin secretion from the remnant β-cells along with potential enzymatic and non-enzymatic antioxidant activities.

Prevention of cardiac dysfunction, kidney fibrosis and lipid metabolic alterations in l-NAME hypertensive rats by sinapic acid—Role of HMG-CoA reductase

The present study was designed to evaluate the effect of sinapic acid, a bioactive phenolic acid on high blood pressure associated cardiac dysfunction, kidney fibrosis and lipid alterations in Nω-nitro-l-arginine methyl ester hydrochloride (l-NAME) induced hypertensive rats. Sinapic acid was administered to rats orally at a dosage of 40mg/kg everyday for a period of 4 weeks. Sinapic acid treatment significantly decreased mean arterial pressure, left ventricular end diastolic pressure, organ weights (liver and kidney), lipid peroxidation products in tissues (liver and kidney), activities of hepatic marker enzymes and the levels of renal function markers in serum of l-NAME rats. Sinapic acid treatment also significantly increased the level of plasma nitric oxide metabolites, and enzymatic and non-enzymatic antioxidants in tissues of l-NAME rats. Tissue damage was assessed by histopathological examination. Alterations in plasma angiotensin-converting enzyme activity, level of plasma lipoproteins and tissue lipids were corrected by sinapic acid treatment in l-NAME rats. Sinapic acid treatment significantly decreased the activity of 3-hydroxy-3-methylglutaryl-Coenzyme A (HMG-CoA) reductase in plasma and liver, whereas the activity of lecithin cholesterol acyl transferase was significantly increased in the plasma of hypertensive rats. Docking result showed the interaction between sinapic acid and HMG-CoA reductase. Sinapic acid has shown best ligand binding energy of −5.5kcal/M. Moreover, in chick embryo model, sinapic acid improved vessel density on chorioallantoic membrane. These results of the present study concludes that sinapic acid acts as a protective agent against hypertension associated cardiac dysfunction, kidney fibrosis and lipid alterations.

Prophylactic effects of pomegranate (Punica granatum) juice on sodium fluoride induced oxidative damage in liver and erythrocytes of rats

The objective of this study was to investigate the protective effects of pomegranate (Punica granatum) juice (PGJ) on oxidative damages in liver tissue and erythrocytes of rats intoxicated by sodium fluoride (NaF). Rats were randomly divided into two groups: group I received standard diet and group II received orally 1 mL of PGJ. After 5 weeks of pretreatment, each group was divided again into two subgroups and treated for another 3 weeks as follows: group I was subdivided into a control group and a group that was treated with 100 ppm of NaF (in drinking water); group II was subdivided into one group that was treated daily with both 100 ppm NaF and PGJ (1 mL orally) and one that received daily 1 mL of pomegranate juice. Exposure to NaF decreased hematological parameters, changed the total protein, albumin, bilirubin levels, and increased the activities of hepatic marker enzymes. We also noted an increase in lipid peroxidation contents, accompanied by a decrease of reduced glutathione levels. Antioxidant enzyme activities in both tissues were modified in the NaF group compared with the control group. However, the administration of PGJ juice caused an amelioration of the previous parameters. Our results indicated the potential effects of NaF to induce oxidative damage in tissues and the ability of PGJ to attenuate NaF-induced oxidative injury.

Potential role of interleukin 28B-gene polymorphism and natural immune enhancer treatment response in chronic HCV patients

HCV infection is a major health problem in Egypt. Studies using safe natural products Blue green® tablet showed its antiviral effect. Polymorphisms in the interleukin-28B (IL28B) gene are associated with outcomes from infection with HCV. The rationale of the present study is to evaluate the potential role of interleukin 28B gene polymorphism (IL28B) and natural immuneenhancer treatment response in chronic HCV patients. This study included 100 chronic HCV patients. Patients were classified into two groups: Group I, fifty patients with cirrhosis and advanced liver disease. Patients were unfit INF/ Ribavirin: Group II, fifty patients who refused INF/Ribavirin. Patients were treated with combination of natural products of Blue green® tablet (4 tablets daily which equivalent to 100 mg AFA/30 kg BW), vitamin D, tea spoon field paste of black seeds, olive oil and honey. Alanine Aminotransferase (AST), Aspartate Aminotransferase (ALT), complete blood count (CBC) were measured in the two groups. Detection of HCV-RNA level by quantitative PCR was done before &amp; after 3, 6, 12 and 18 months of treatment. Genomic DNA extracted from all the 100 patient’s blood samples was analyzed for the rs12979860 SNPof IL28B using a real-time polymerase chain technique incorporating SYBR Green. The results showed that, the activities of hepatic marker enzymes (AST and ALT), complete blood pictures (Hb, WBCs and Platelets), HCV RNA PCR, IL 28-B gene polymorphism were non-significantly (p&gt;0.05) differences when compared untreated patients (Group I) and treated patients (Group )were CC genotype before treatment was 8 (34%) &amp; was 13 (26%) after treatment, CT genotype before treatment was 26 (52%) &amp; was 28 (56%) after treatment, TT genotype before treatment was 7 (14%) &amp; was 9 (18%) after treatment. Also, there were non-significant (p&gt;0.05) differences between responder &amp; non-responder in treated patients. In conclusion, the treatmentwith natural immune enhancer in chronic HCV patients showed no significance correlation with IL 28 gene polymorphism

Hepatoprotective potentials of the methanolic leaf extract of Jatropha curcas (LINN) on cadmium induced toxicity in rabbit

This study was carried out to investigate the possible hepatoprotective potentials of methanolic leaf extract of Jatropha curcas Linn on cadmium induced hepatotoxicity and oxidative stress in rabbits. Sixteen matured rabbits were used for the study; they were divided into four groups and treated as follows: Group I (control) was treated with normal saline (0.85% w/v NaCl) at 2 ml/kg body weight per day. Group II were treated with only cadmium chloride at 1.25 mg/kg body weight per day. Groups III and IV were pre-treated with 300 mg/kg body weight per day of Jatropha curcas extract and vitamin E respectively, one hour later, cadmium chloride was administered to them at 1.25 mg/kg body weight. All the animals were treated orally for 10 days. The animals were sacrificed on day 11, blood, liver and kidneys were removed and preserved for biochemical analyses. The liver samples were digested with mixture of concentrated trioxonitrate (V) acid (HNO3) and hydrochloric acid (HCl) (1:4 v/v). Cadmium concentrations in the liver were determined by atomic absorption spectroscopy (AAS). The concentrations of total plasma protein, albumin, uric acid and the activities of hepatic marker enzymes; alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma glutamyltransferase (GGT) were determined in the plasma and liver homogenates by standard procedures. The result of phytochemical screening revealed that flavonoids, tannins, terpenoids steroids, phlobatanins and saponins were present in the extract. The analysis by atomic absorption spectroscopy of the liver revealed that there were traces of cadmium (0.01 μg/g) in the liver of animals pre-treated with vitamin E and Jatropha curcas extract while the concentration of cadmium in the liver of only cadmium group was 0.14 µg/g. Additionally, the activities of hepatic marker enzymes (AST, ALT, GGT) were elevated in cadmium only treated group but pretreatment with methanolic extract of Jatropha curcas reduced significantly (p<0.05) the activities of these enzymes. The total protein and uric acid concentrations were also significantly reduced in cadmium treated group when compared with the extract pre-treated group. Comparison of the activities of hepatic marker enzymes (ALT, AST and GGT) in vitamin E and Jatropha curcas extract pre-treated groups revealed that ALT, AST and GGT activities were not significantly different in these groups. Also, albumin and uric acid concentrations were not significantly different between the groups. The results of biochemical studies of blood samples and liver homogenates revealed significant increase in the levels of maker enzymes reflecting liver injury caused by cadmium while pre-treatment with Jatropha curcas extract reduced the activities of the enzymes. Oral administration of methanolic extract of Jatropha curcas at 300 mg/kg body weight in this study was able to reduce the hepatotoxic effects of cadmium toxicity at 1.25 mg/kg body weight. This suggests that methanolic leaf extract of Jatropha curcas might possess hepatoprotective effect. The results of this investigation has further confirmed the inherent therapeutic properties of Jatropha curcas and also justified its uses in traditional medicine to cure various ailments in

Effect of ursolic acid and Rosiglitazone combination on hepatic lipid accumulation in high fat diet-fed C57BL/6J mice

This study investigated the combined effect of ursolic acid (UA) and Rosiglitazone (RSG) on lipid regulatory genes in high fat diet (HFD)-fed mice. Male C57BL/6J mice were fed either normal diet or HFD for 10 weeks, after which animals in each dietary group were divided into following six groups, (normal diet, normal diet plus UA and RSG, HFD alone, HFD plus UA, HFD plus RSG, and HFD plus UA and RSG), for the next 5 weeks. UA (5mg/kg BW) and RSG (4mg/kg BW) were administered as suspensions directly into the stomach using a gastric tube. At the end of the study (106th day), their liver was analyzed for lipid content. RT-PCR and western blotting methods were used to analyze lipid regulatory genes. HFD-fed mice showed increased activities of hepatic marker enzymes (aspartate aminotransferase and alanine aminotransferase) in plasma and an increased concentration of total cholesterol, triglyceride and free fatty acid in liver. These results were confirmed by upregulated mRNA expression of lipogenic genes such as sterol-regulatory-element-binding protein-1c, fatty acid synthase and acetyl-CoA carboxylase and downregulated mRNA expression of fatty acid oxidative genes such as carnitine palmitoyltransferase-1, acetyl-CoA carboxylase and peroxisome proliferator activated receptor-α in HFD-fed mice. Combined treatment (UA/RSG) significantly reduced the hepatic marker enzyme activities and decreased the lipid accumulation in liver. Furthermore, combination treatment (UA/RSG) down-regulated lipogenic genes and upregulated fatty acid oxidative genes in HFD-fed mice. This study suggests that UA in combination with RSG reduced lipid accumulation in liver.

Daytime food restriction influences the circadian rhythms of circulatory hepatic marker enzymes activity in rats

The objective of this study was to evaluate the effects of daytime food restriction on the circadian patterns of glucose and hepatic marker enzyme activities such as aspartate aminotransferase, alanine aminotransferase and alkaline phosphatase rhythms in rats. Adult male Wistar rats (180–200 g) restricted of food from 08:00 to 16:00 h in LD (12:12 h) condition. Blood samples were collected after every 4 h from each group of experimental and control rats throughout the 24 h period continuously. Daytime restricted feeding was found to alter acrophase, amplitude and mesor values of glucose, AST, ALT and ALP rhythms as compared to control rats in after 21 days. Altered circadian pattern of these biochemical variables in daytime food restricted may be due to modulation of circadian timing patterns in peripheral tissues and reflection/feedback of these changes through the master circadian clock, suprachiasmatic nuclei.

Valproic acid prevents the deregulation of lipid metabolism and renal renin–angiotensin system in l-NAME induced nitric oxide deficient hypertensive rats

The present study was aimed to investigate the antihyperlipidemic and renoprotective potential of valproic acid against Nω-nitro-l arginine methyl ester hydrochloride (l-NAME) induced hypertension in male albino Wistar rats. In hypertensive rats, mean arterial pressure (MAP), kidney weight, levels of oxidative stress markers in tissues were increased. Dyslipidemia was also observed in hypertensive rats. Moreover, enzymatic and nonenzymatic antioxidant network also deregulated in tissues. Valproic acid (VPA) supplementation daily for four weeks brought back all the above parameters to near normal level and showed no toxicity which was established using serum hepatic marker enzyme activities and renal function markers. Moreover the up regulated expression of renin–angiotensin system (RAS) components were also attenuated by VPA treatment. All the above outcomes were confirmed by the histopathological examination. These results suggest that VPA has enough potential to attenuate hypertension, dyslipidemia and renal damage in nitric oxide deficiency induced hypertension.

Effect of carnosine alone or combined with α-tocopherol on hepatic steatosis and oxidative stress in fructose-induced insulin-resistant rats

A diet high in fructose (HFr) induces insulin resistance in animals. Free radicals are involved in the pathogenesis of HFr-induced insulin resistance. Carnosine (CAR) is a dipeptide with antioxidant properties. We investigated the effect of CAR alone or in combination with α-tocopherol (CAR + TOC) on HFr-induced insulin-resistant rats. Rats fed with HFr containing 60% fructose received CAR (2 g/L in drinking water) with/without TOC (200 mg/kg, i.m. twice a week) for 8 weeks. Insulin resistance, serum lipids, inflammation markers, hepatic lipids, lipid peroxides, and glutathione (GSH) levels together with glutathione peroxidase (GSH-Px) and superoxide dismutase 1 (CuZnSOD; SOD1) activities and their protein expressions were measured. Hepatic histopathological examinations were performed. HFr was observed to cause insulin resistance, inflammation and hypertriglyceridemia, and increased triglyceride and lipid peroxide levels in the liver. GSH-Px activity and expression decreased, but GSH levels and SOD1 activity and expression did not alter in HFr rats. Hepatic marker enzyme activities in serum increased and marked macro- and microvesicular steatosis were seen in the liver. CAR treatment did not alter insulin resistance and hypertriglyceridemia, but it decreased steatosis and lipid peroxidation without any change in the antioxidant system of the liver. However, CAR + TOC treatment decreased insulin resistance, inflammation, hepatic steatosis, and lipid peroxidation and increased GSH-Px activity and expression in the liver. Our results may indicate that CAR + TOC treatment is more effective to decrease HFr-induced insulin resistance, inflammation, hepatic steatosis, and dysfunction and pro-oxidant status in rats than CAR alone.

Modulatory effect of sesamol on DOCA-salt-induced oxidative stress in uninephrectomized hypertensive rats

The present study was undertaken to investigate the antihypertensive and antioxidant effects of sesamol on uninephrectomized deoxycorticosterone acetate (DOCA)-salt-induced hypertensive rats. Hypertension was induced in surgically single-kidney-removed (left) adult male albino Wistar rats, weighing 180–200 g, by injecting DOCA (25 mg/kg BW) subcutaneously twice a week for 6 weeks, with saline instead of tap water for drinking. Rats were treated with three different doses of sesamol (50, 100 and 200 mg/kg BW) post-orally by gavage daily for 6 weeks. Hypertension was revealed by increased systolic and diastolic blood pressure and the toxicity of DOCA-salt was determined using hepatic marker enzymes, aspartate aminotransferase, alanine aminotransferase, alkaline phospatase and gamma-glutamyl transpeptidase; and, lipid peroxidative markers, thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes were assayed. The activities of enzymatic antioxidants, superoxide dismutase, catalase and glutathione peroxidase and the levels of non-enzymatic antioxidants (vitamin C, vitamin E and reduced glutathione) were evaluated in erythrocytes, plasma and tissues. Post-oral administration of sesamol at the dosage of 50 mg/kg BW remarkably decreased systolic and diastolic blood pressure, hepatic marker enzyme activities and lipid peroxidation products and also enhanced the antioxidant activity. The biochemical observations were also supported by histopathological examinations of the rat liver, kidney and heart sections. These results suggest that sesamol possesses antihypertensive and antioxidant effects.

Effect of morin, a flavonoid against DOCA-salt hypertensive rats: a dose dependent study

ObjectiveTo determine the protective effect of morin, a flavonoid against deoxycorticosterone acetate (DOCA)-salt induced hypertension in male Wistar rats. MethodsHypertension was induced in uninephrectomized rats by weekly twice subcutaneous injection of DOCA (25 mg/kg bw) and 1% NaCl in the drinking water for six consecutive weeks. Effect of morin against DOCA-salt induced hypertension was evaluated by measuring blood pressure and performing biochemical estimations and histopathological examination of renal tissues. ResultsDOCA-salt hypertensive rats showed considerably increased systolic and diastolic blood pressure, serum hepatic marker enzyme activities such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT) and renal function markers (urea, uric acid and creatinine) in plasma. Oral administration of morin (25, 50 and 75 mg/kg bw) brought back all the above parameters to near normal level. Histopathology of kidney also confirmed the biochemical findings of this study. The effect at a dose of 50 mg/kg bw of morin was more pronounced than that of the other two doses (25 and 75 mg/kg bw). ConclusionsThese findings indicate that morin exhibits strong antihypertensive effect against DOCA-salt induced hypertension.

Protective effect of zinc against cadmium hepatotoxicity depends on this bioelement intake and level of cadmium exposure: A study in a rat model

It was estimated, in a rat model of moderate and relatively high chronic human exposure to cadmium (Cd), whether enhanced zinc (Zn) consumption may prevent Cd-induced liver injury and if the possible protective effect of this bioelement depends on its intake. For this purpose, the structure and function of the liver of the rats that received Zn (30 and 60 mg/l) or/and Cd (5 and 50 mg/l) for 6 months were evaluated. The treatment with Cd led to, dependent on the exposure level, pathological changes in the liver, including enhanced apoptosis and induction of inflammatory and necrotic processes. Moreover, the serum activities of hepatic marker enzymes (alanine transaminase and aspartate transaminase) and the concentration of proinflammatory cytokine – tumor necrosis factor α were increased. The supplementation with 30 and 60 mg Zn/l (enhancing daily Zn intake by 79% and 151%, respectively) partially or totally prevented from some of the Cd-induced changes in the liver structure and function; however, it provided no protection from necrosis, and the administration of 60 mg Zn/l during the higher Cd exposure even intensified this process. At both levels of Cd treatment, the use of 30 mg Zn/l was more effective in preventing liver injury than that of 60 mg Zn/l. The hepatoprotective impact of Zn may be explained, at least partly, by its antioxidative, antiapoptotic and anti-inflammatory action, ability to stimulate regenerative processes in the liver tissue, and indirect action resulting in a decrease in the liver pool of the non-metallothionein-bound Cd 2+ ions able to exert toxic action. The results provide strong evidence that enhanced Zn consumption may be beneficial in protection from Cd hepatotoxicity; however, its excessive intake at relatively high exposure to Cd may intensify liver injury.

Hepatoprotective role of naringin on nickel-induced toxicity in male Wistar rats

Aim of the present study was planned to determine the protective role of naringin in attenuating the toxicity induced by nickel sulfate in rat liver. In this investigation nickel sulfate (20 mg/kg body weight) was administered intraperitoneally for 20 days to induce toxicity. Naringin was administered orally (20, 40 and 80 mg/kg body weight) for 20 days with intraperitoneal administration of nickel sulfate. Liver injury was measured by the increased activities of serum hepatic enzymes namely aspartate transaminase, alanine transaminase, alkaline phosphatase, gamma glutamyl transferase, lactate dehydrogenase and total bilirubin along with increased elevation of lipid peroxidation markers, thiobarbituric reactive acid substances, lipid hydroperoxides, protein carbonyl content and conjugated dienes. The toxic effect of nickel was also indicated by significantly decreased activities of enzymatic antioxidants like superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase and glucose-6-phosphate dehydrogenase and non-enzymatic antioxidants like reduced glutathione, total sulfhydryl groups, vitamin C and vitamin E levels were significantly decreased. Naringin administered at a dose of 80 mg/kg body weight significantly reversed the activities of hepatic marker enzymes, decreasing lipid peroxidative markers, increasing the antioxidant cascade and decreasing the nickel concentration in the liver. The effect at a dose of 80 mg/kg body weight was more pronounced than that of other two doses (20 and 40 mg/kg body weight). All these changes were supported by histopathological observations. These results clearly demonstrate that naringin has the potential in alleviating the toxic effects of nickel in rat liver.

Effect of chrysin on hepatoprotective and antioxidant status in d-galactosamine-induced hepatitis in rats

Chrysin is a natural, biologically active compound present in many plants and possesses potent anti-inflammatory, anticancer and antioxidation properties. This work was designed to investigate the effect of chrysin, on the hepatoprotective efficacy in d-galactosamine-intoxication rats. d-galactosamine-induced toxicity was manifested by the elevation of serum hepatic marker enzyme activities (aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase) and the lipid peroxidation process and by decreasing the antioxidant capacity of the plasma, erythrocyte and tissues. Treatment with chrysin (25, 50 and 100 mg/kg body weight) decreased hepatic marker enzyme activities and lipid peroxidation products such as thiobarbituric acid reactive substances, lipid hydroperoxides and conjugated dienes, increased the activities of free-radical scavenging enzymes superoxide dismutase, catalase and glutathione peroxidase and the levels of non-enzymatic antioxidants reduced glutathione, vitamin C and vitamin E. These findings demonstrate that chrysin acts as a hepatoprotective and antioxidant agent against d-galactosamine-induced hepatotoxicity.