curcumin and Carbon-Tetrachloride-Poisoning

The active component in cullilawan oil can be synthesized into curcumin analogue product, which has pharmacological activity. The synthesis process by using conventional and microwave methods can produce different isomer products. Different synthesis products and models of animal are used to provide different hepatoprotective effects. The aim of this study was to use the curcumin analogue synthetic products (AKS-k and AKS-m) from cullilawan oil in male mice (Mus musculus L.) liver damage treatment induced by carbon tetrachloride (CCl4). The in vivo method was employed using biochemical of blood and histopathological images of liver cells as indicators. The results showed that the curcumin analogue synthetic product using microwave methods had better pharmacological effects than the conventional method product in terms of the results of blood biochemical analysis and microscopic images of liver cells.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Cinnamomum; Curcumin; Disease Models, Animal; Liver Function Tests; Male; Mice; Plant Bark; Plant Oils

To investigate the hepatoprotective and antioxidant activity of pentagamavunon-0(PGV-0) against CCl4-induced hepatic injury in rats.. The groups of animals were administered with PGV-0 at the doses 2.5, 5, 10, and 20 mg/kg b.w., p.o. once in a day for 6 days and at day 7 the animals were administrated with carbon tetrachloride (CCl) (20%, 2 mL/kg b.w. in liquid paraffin (i.p.). The effect of PGV-0 on serum transaminase (SGPT), alkaline phosphates (ALP) and total bilirubin were determined in CCl4-induced hepatotoxicity in rats. Further, the effects of PGV-0 on glutathione (GSH) content, catalase (CAT) and NO free radical scavenging activity also were investigated.. The results demonstrated that PGV-0 significantly reduced the activity of SGPT, serum ALP and total bilirubin in CCl4 induced rat hepatotoxicity. PGV-0 has effect on the antioxidant and free radical defense system. It prevented the depletion level of GSH and decrease activity of CAT in CCl4-induced liver injury in rats. PGV-0 also demonstrated the free radical scavenger effects on NO free radical scavenging activity with ES value of 32.32 μM.. All of our findings suggests that PGV-0 could protect the liver cells from CCl4-induced liver damages and the mechanism may through the antioxidative effect of PGV-0 to prevent the accumulation of free radicals and protect the liver damage.

Topics: Analysis of Variance; Animals; Antioxidants; Carbon Tetrachloride Poisoning; Catalase; Chemical and Drug Induced Liver Injury; Curcumin; Glutathione; Male; Nitric Oxide; Rats; Rats, Wistar

Neoangiogenesis and the development of an abnormal angio-architecture in the liver are strongly linked with progressive fibrogenesis. This study aimed to evaluate the ability of curcumin to protect liver fibrosis-associated angiogenesis and capillarization of the sinusoids in experimental rats. Liver fibrosis was induced by intraperitoneal injection of carbon tetrachloride (CCl₄) with or without curcumin for 6 weeks. The results suggest that curcumin treatment markedly attenuated CCl₄-induced liver fibrosis, as assessed by histology and hydroxyproline content, and inhibited hepatic stellate cell activation. Curcumin ameliorated hepatic angiogenesis, as assessed by measuring microvessel density using Von Willebrand factor staining and by examining the expression of the endothelial cell markers CD31 and vascular endothelial growth factor receptor (VEGFR)-2 in the livers. Pathologic remodeling of liver sinusoidal capillarization, as assessed by electron-microscopic analysis of Disse's space and by evaluation of the levels of basement membrane protein expression, was also attenuated by curcumin administration. The intrahepatic gene or protein expression of hypoxia-inducible factor-1α, VEGFR-1, placental growth factor, and cyclooxygenase-2 decreased with treatment with curcumin in fibrotic rats. In conclusion, curcumin ameliorates hepatic angiogenesis and sinusoidal capillarization in CCl₄-induced rat liver fibrosis through suppressing multiple proangiogenic factors.

Topics: Angiogenesis Inhibitors; Animals; Blotting, Western; Capillaries; Carbon Tetrachloride Poisoning; Curcumin; Hepatic Veno-Occlusive Disease; Hydroxyproline; Immunohistochemistry; Liver; Liver Cirrhosis; Male; Microscopy, Electron, Transmission; Rats; Rats, Sprague-Dawley; Real-Time Polymerase Chain Reaction

We investigated whether two naturally-occurring prooxidants, namely, schisandrin B (Sch B) and curcumin, and a synthetic prooxidant, menadione, can invariably elicit cyto/hepatoprotective responses against oxidant-induced injury. Results showed that (-)Sch B (a potent enantiomer of Sch B, 15 μM), curcumin (7.5 μM) and menadione (2 μM) induced a similar extent of reactive oxygen species production in AML12 cells. The relative potencies of cytoprotection in vitro were in a descending order of curcumin>menadione>(-)Sch B, which were parallel to the extent of stimulation in cellular reduced glutathione level. We further examined their hepatoprotection in vivo. Pretreatment with Sch B (800 mg/kg) and curcumin (737 mg/kg), but not menadione (344 mg/kg), protected against CCl(4) toxicity, with the degree of protection afforded by Sch B being much larger than that of curcumin. The attenuated hepatoprotection afforded by curcumin may be attributed to its low bioavailability in vivo. This postulation is supported by the findings that intraperitoneal injections of Sch B (400 mg/kg) and curcumin (368 mg/kg) and the long term, low dose treatment with Sch B (20 mg/kg/d×15) and curcumin (18 mg/kg/d×15) induced glutathione antioxidant response and hepatoprotection to similar extents in vivo. The inability of menadione to induce hepatoprotection may be related to its extensive intestinal metabolism and/or hepatotoxicity. Taken together, prooxidants can invariably induce the glutathione antioxidant response and confer cytoprotection in vitro. Whether or not the prooxidant can produce a similar response in vivo would depend on its bioavailability and potential toxic effect.

Topics: Animals; Antioxidants; Carbon Tetrachloride Poisoning; Cell Line; Curcumin; Cyclooctanes; Female; Glutathione; Lignans; Liver; Mice; Mice, Inbred BALB C; Mice, Inbred ICR; Microsomes, Liver; Polycyclic Compounds; Reactive Oxygen Species; Vitamin E; Vitamin K 3

The present investigation was intended to study the immunostimulant properties of Curcuma longa (turmeric) and Zingiber officinale (ginger) rhizomes on splenic macrophages in carbon tetrachloride intoxicated male albino mice. The study was based on functional parameters like morphology, cell adhesion, phagocytosis, myeloperoxidase release, nitric oxide release and intracellular killing capacity of splenic macrophages. To elucidate the detailed mechanism of boosting of these cell functions, serum levels of TNF-α, and IFN-γ were quantified in different experimental mice groups. Carbon tetrachloride (CCl(4)) intoxication (0.5ml/kg body weight intraperitoneally) was found to affect the functional status of splenic macrophages as evident from these studies. Moreover, CCl(4) intoxicated mice also showed lower levels of cytokines TNF-α and IFN-γ. However, oral administration (singly) of polar fractions of C. longa (50mg/kg b.wt) and Z. officinale (120mg/kg b.wt) rhizomes ameliorated the affects of CCl(4), as evident from an increased functional status as well as the serum levels of these cytokines. Based on this study it can be suggested that, polar fractions of C. longa and Z. officinale rhizomes boost the immune system by altering the cytokine milieu of the immunosuppressed macrophages, thus modulating their functional status. Therefore, it can be inferred that dietary intake of C. longa and Z. officinale potentiates the non-specific host defenses against opportunistic infections.

Topics: Adjuvants, Immunologic; Administration, Oral; Animals; Bacteriolysis; Carbon Tetrachloride Poisoning; Cell Adhesion; Cell Differentiation; Cells, Cultured; Curcuma; Dose-Response Relationship, Immunologic; Drug Evaluation, Preclinical; Immunocompromised Host; Interferon-gamma; Macrophages; Male; Mice; Neutrophil Activation; Nitric Oxide; Phagocytosis; Phytotherapy; Plant Extracts; Plant Roots; Respiratory Burst; Spleen; Staphylococcus aureus; Tumor Necrosis Factor-alpha; Zingiber officinale

Plant-derived polyphenols such as curcumin hold promise as a therapeutic agent in the treatment of chronic liver diseases. However, its development is plagued by poor aqueous solubility resulting in poor bioavailability. To circumvent the suboptimal bioavailability of free curcumin, we have developed a polymeric nanoparticle formulation of curcumin (NanoCurc™) that overcomes this major pitfall of the free compound. In this study, we show that NanoCurc™ results in sustained intrahepatic curcumin levels that can be found in both hepatocytes and non-parenchymal cells. NanoCurc™ markedly inhibits carbon tetrachloride-induced liver injury, production of pro-inflammatory cytokines and fibrosis. It also enhances antioxidant levels in the liver and inhibits pro-fibrogenic transcripts associated with activated myofibroblasts. Finally, we show that NanoCurc™ directly induces stellate cell apoptosis in vitro. Our results suggest that NanoCurc™ might be an effective therapy for patients with chronic liver disease.

Topics: Animals; Biological Availability; Carbon Tetrachloride Poisoning; Cell Line, Transformed; Curcumin; Inflammation Mediators; Male; Mice; Mice, Inbred C57BL; Nanoparticles; Reverse Transcriptase Polymerase Chain Reaction

It has been demonstrated that β-elemene could protect against carbon tetrachloride (CCl(4))-induced liver fibrosis in our laboratory work, and the aim of this paper is to reveal the protective mechanisms of β-elemene. The hepatic fibrosis experimental model was induced by the hypodermical injection of CCl(4) in Wistar male rats. β-elemene was intraperitoneally administered into rats for 8 weeks (0.1 mL/100 g bodyweight per day), and plasma endotoxin content was assayed by biochemistry. The serum TNF-α level was detected using radioactive immunity. CD14 expression in rat livers was measured by immunohistochemistry and Western blot. The results showed that β-elemene can downregulate the levels of plasma endotoxins, serum TNF-α, and hepatic CD14 expression in rats with liver fibrosis. β-elemene plays an important role in downregulating the lipopolysaccharide signal transduction pathway, a significant pathway in hepatic fibrosis development.

Topics: Animals; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; China; Curcuma; Disease Models, Animal; Down-Regulation; Endotoxins; Injections, Intraperitoneal; Lipopolysaccharide Receptors; Liver; Liver Cirrhosis; Male; Plant Preparations; Rats; Rats, Wistar; Sesquiterpenes; Tumor Necrosis Factor-alpha

To investigate the protective effect and possible mechanism of Curcuma comosa hexane extract on CCl(4)-induced liver injury in adult male mice.. Hepatotoxicity was induced by an intraperitoneal injection of CCl(4) and was evaluated after 24 h from the elevations of plasma alanine transaminase (ALT) and aspartate transaminase (AST) activities, and histological analysis of liver injuries. Hexane extract of Curcuma comosa was given at different time points from 1 to 72 h, prior to CCl(4) administration and the protection from liver injury was assessed.. CCl(4)-induced damage to liver cells was resulted in elevations of plasma ALT and AST activities. Pretreatment with Curcuma comosa hexane extract 24 h at a dose of 100, 250, and 500 mg/kg BW resulted in a dose-dependent prevention of the increases in plasma ALT and AST activities as well as time dependent. The protective effect of the extract at a dose of 500 mg/kg BW was seen at 12-24 h. Pretreatment of the extract completely prevented elevation of plasma ALT and AST activities, and centrilobular necrosis. The protective effect of Curcuma comosa was associated with restoration of hepatic glutathione content, and CYP2E1 catalytic activity, and its mRNA and protein levels as well as increase in activity of glutathione-S-transferase (GST).. Curcuma comosa has a potent protective property against CCl(4)-induced hepatic injuries via the activation of detoxifying mechanisms (GST) as well as reduction of the bioactive toxic metabolites. Therefore, Curcuma comosa may be beneficial for prevention of hepatotoxicity.

Topics: Alanine Transaminase; Animals; Antioxidants; Aspartate Aminotransferases; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Curcuma; Cytochrome P-450 CYP2E1; Dose-Response Relationship, Drug; Glutathione; Glutathione Transferase; Liver; Male; Mice; Necrosis; Phytotherapy; Plant Extracts; Rhizome; RNA, Messenger

Curcumin is a phytophenolic compound, which is highly efficacious for treating several inflammatory diseases. The aim of this study was to evaluate the efficacy of curcumin in preventing or reversing liver cirrhosis. A 4-week bile duct ligation (BDL) rat model was used to test the ability of curcumin (100 mg/kg, p.o., daily) to prevent cirrhosis. To reverse cirrhosis, CCl(4) was administered chronically for 3 months, and then it was withdrawn and curcumin administered for 2 months. Alanine aminotransferase, gamma-glutamyl transpeptidase, liver histopathology, bilirubin, glycogen, reduced and oxidized glutathione, and TGF-beta (mRNA and protein) levels were assessed. Curcumin preserved normal values of markers of liver damage in BDL rats. Fibrosis, assessed by measuring hydroxyproline levels and histopathology, increased nearly fivefold after BDL and this effect was partially but significantly prevented by curcumin. BDL increased transforming growth factor-beta (TGF-beta) levels (mRNA and proteins), while curcumin partially suppressed this mediator of fibrosis. Curcumin also partially reversed the fibrosis induced by CCl(4). Curcumin was effective in preventing and reversing cirrhosis, probably by its ability of reducing TGF-beta expression. These data suggest that curcumin might be an effective antifibrotic and fibrolitic drug in the treatment of chronic hepatic diseases.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Cholestasis; Curcumin; Dose-Response Relationship, Drug; Drug Interactions; Liver Cirrhosis, Experimental; Male; Oxidative Stress; Rats; Rats, Wistar; Transforming Growth Factor beta

We previously demonstrated that curcumin, a polyphenolic antioxidant purified from turmeric, up-regulated peroxisome proliferator-activated receptor (PPAR)-gamma gene expression and stimulated its signaling, leading to the inhibition of activation of hepatic stellate cells (HSC) in vitro. The current study evaluates the in vivo role of curcumin in protecting the liver against injury and fibrogenesis caused by carbon tetrachloride (CCl(4)) in rats and further explores the underlying mechanisms. We hypothesize that curcumin might protect the liver from CCl(4)-caused injury and fibrogenesis by attenuating oxidative stress, suppressing inflammation, and inhibiting activation of HSC. This report demonstrates that curcumin significantly protects the liver from injury by reducing the activities of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase, and by improving the histological architecture of the liver. In addition, curcumin attenuates oxidative stress by increasing the content of hepatic glutathione, leading to the reduction in the level of lipid hydroperoxide. Curcumin dramatically suppresses inflammation by reducing levels of inflammatory cytokines, including interferon-gamma, tumor necrosis factor-alpha, and interleukin-6. Furthermore, curcumin inhibits HSC activation by elevating the level of PPARgamma and reducing the abundance of platelet-derived growth factor, transforming growth factor-beta, their receptors, and type I collagen. This study demonstrates that curcumin protects the rat liver from CCl(4)-caused injury and fibrogenesis by suppressing hepatic inflammation, attenuating hepatic oxidative stress and inhibiting HSC activation. These results confirm and extend our prior in vitro observations and provide novel insights into the mechanisms of curcumin in the protection of the liver. Our results suggest that curcumin might be a therapeutic antifibrotic agent for the treatment of hepatic fibrosis.

Topics: Animals; Antioxidants; Carbon Tetrachloride Poisoning; Curcumin; Inflammation; Liver; Liver Cirrhosis; Male; Oxidative Stress; Rats; Rats, Sprague-Dawley

A comparison of crude curcuminoid extract and purified curcumin was made to evaluate hepato- and immunoprotective effect of Curcuma longa (turmeric) Zingiberaceae. Carbon tetrachloride (CCl4) induced cellular hepatic damage was evaluated by transmission electron microscopy, hepatic enzymes and thiobarbituric acid reactive species (TBAR) values. A selective cytolytic effect of CCl4 was observed among immature (PNA+) thymocytes and peripheral helper (CD4+) T lymphocytes in spleen and was paralleled by a significant reduction in CD25, CD71 and Con A receptor expression. Treatment with curcuminoid crude extract at two different doses, showed a significant cellular recovery among hepatocytes, which was reflected in a reduction of hepatic enzymes and TBAR values. A significant restoration of lymphocyte viability and CD25, CD71 and Con A receptor expression in both immature (PNA+) thymocytes and splenic helper (CD4+) T lymphocytes was observed. Turmeric crude extract, at both low and high dose, was found to be more efficient as compared to purified curcumin.

Topics: Animals; Antioxidants; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Curcuma; Curcumin; Cytoprotection; Hepatocytes; Immunity; Immunologic Factors; Liver; Oxidative Stress; Plant Extracts; Rats; Rats, Wistar; T-Lymphocytes

A novel formulation of curcumin in combination with the phospholipids was developed to overcome the limitation of absorption and to investigate the protective effect of curcumin-phospholipid complex on carbon tetrachloride induced acute liver damage in rats. The antioxidant activity of curcumin-phospholipid complex (equivalent of curcumin 100 and 200 mg/kg body weight) and free curcumin (100 and 200 mg/kg body weight) was evaluated by measuring various enzymes in oxidative stress condition. Curcumin-phospholipid complex significantly protected the liver by restoring the enzyme levels of liver glutathione system and that of superoxide dismutase, catalase and thiobarbituric acid reactive substances with respect to carbon tetrachloride treated group (P < 0.05 and <0.01). The complex provided better protection to rat liver than free curcumin at same doses. Serum concentration of curcumin obtained from the complex (equivalent to 1.0 g/kg of curcumin) was higher (Cmax 1.2 microg/ml) than pure curcumin (1.0 g/kg) (Cmax 0.5 microg/ml) and the complex maintained effective concentration of curcumin for a longer period of time in rat serum. The result proved that curcumin-phospholipid complex has better hepatoprotective activity, owe to its superior antioxidant property, than free curcumin at the same dose level.

Topics: Animals; Area Under Curve; Calorimetry, Differential Scanning; Carbon Tetrachloride Poisoning; Catalase; Chemical and Drug Induced Liver Injury; Curcumin; Glutathione; Glutathione Peroxidase; Glutathione Reductase; Glutathione Transferase; Half-Life; Male; Phosphatidylcholines; Rats; Rats, Wistar; Solubility; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances

Curcumin, an anti-inflammatory and antioxidant compound, was evaluated for its ability to suppress acute carbon tetrachloride-induced liver damage. Acute hepatotoxicity was induced by oral administration of CCl4 (4 g/kg, p.o.). Curcumin treatment (200 mg/kg, p.o.) was given before and 2 h after CCl4 administration. Indicators of necrosis (alanine aminotransferase) and cholestasis (gamma-glutamyl transpeptidase and bilirubins) resulted in significant increases after CCl4 intoxication, but these effects were prevented by curcumin treatment. As an indicator of oxidative stress, GSH was oxidized and the GSH/GSSG ratio decreased significantly by CCl4, but was preserved within normal values by curcumin. In addition to its antioxidants properties, curcumin is capable of preventing NF-kappaB activation and therefore to prevent the secretion of proinflammatory cytokines. Therefore, in this study we determined the concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) mRNA, and NF-kappaB activation. CCl4-administered rats depicted significant increases in TNF-alpha, IL-1beta, and IL-6 production, while curcumin remarkably suppressed these mediators of inflammation in liver damage. These results were confirmed by measuring TNF-alpha, and IL-1beta protein production using Western Blot analysis. Accordingly, these proteins were increased by CCl4 and this effect was abolished by curcumin. Administration of CCl4 induced the translocation of NF-kappaB to the nucleus; CCl4 induced NF-kappaB DNA binding activity was blocked by curcumin treatment. These findings suggest that curcumin prevents acute liver damage by at least two mechanisms: acting as an antioxidant and by inhibiting NF-kappaB activation and thus production of proinflammatory cytokines.

Topics: Active Transport, Cell Nucleus; Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Biomarkers; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Cell Nucleus; Cholestasis; Curcumin; Cytokines; Inflammation Mediators; Liver; Male; Necrosis; NF-kappa B; Oxidative Stress; Rats; Rats, Wistar

We investigated the effects of curcumin, a major antioxidant constituent of turmeric, on hepatic cytochrome P450 (CYP) activity in rats. Wistar rats received curcumin-containing diets (0.05, 0.5 and 5 g/kg diet) with or without injection of carbon tetrachloride (CCl(4)). The hepatic CYP content and activities of six CYP isozymes remained unchanged by curcumin treatment, except for the group treated with the extremely high dose (5 g/kg). This suggested that daily dose of curcumin does not cause CYP-mediated interaction with co-administered drugs. Chronic CCl(4) injection drastically decreased CYP activity, especially CYP2E1 activity, which is involved in the bioactivation of CCl(4), thereby producing reactive free radicals. Treatment with curcumin at 0.5 g/kg alleviated the CCl(4)-induced inactivation of CYPs 1A, 2B, 2C and 3A isozymes, except for CYP2E1. The lack of effect of curcumin on CYP2E1 damage might be related to suicidal radical production by CYP2E1 on the same enzyme. It is speculated that curcumin inhibited CCl(4)-induced secondary hepatic CYPs damage through its antioxidant properties. Our results demonstrated that CYP isozyme inactivation in rat liver caused by CCl(4) was inhibited by curcumin. Dietary intake of curcumin may protect against CCl(4)-induced hepatic CYP inactivation via its antioxidant properties, without inducing hepatic CYPs.

Topics: Animals; Antioxidants; Body Weight; Carbon Tetrachloride Poisoning; Curcumin; Cytochrome P-450 Enzyme System; Dose-Response Relationship, Drug; Enzyme Activation; Liver; Male; Organ Size; Rats; Rats, Wistar

To observe the prophylactic effect of curcumin on hepatic fibrosis and the number, location, apoptosis of activated hepatic stellate cells (HSCs) in the livers and to discuss the relationship between the prophylactic effects and activated HSC.. A rat model of hepatic fibrosis was established by intraperitoneal injection of carbon tetrachloride. Curcumin doses of 5 mg, 10 mg, 20 mg per 100 gram per 100g of body weight were given to three groups of the model rats. No curcumin was given to one group of the model rats and it served as the control. After eight weeks, all rats were sacrificed and their left liver lobes were examined histopathologically with H.E and Masson stainings. Grades of hepatic fibrosis were evaluated according to the SSS system. Activated HSC was detected by the alpha-SMA immunohistochemistry staining. HSC apoptosis was detected by double-stainings of terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) and desmin immunohistochemistry staining.. Degrees (SSS system scores) of hepatic fibrosis in the curcumin groups were all less severe in comparison with those of the control group. Activated HSCs in the livers of the rats of the control group increased significantly compared with that of the treatment groups, and also fewer apoptotic HSCs were detected in the control group. On the contrary, fewer activated HSCs and more apoptotic HSCs were detected in the curcumin groups compared with those of the control group. The degrees of the effects were curcumin dose-dependent.. Curcumin can prevent hepatic fibrosis. It can inhibit activation and proliferation of HSCs and induce HSCs apoptosis, which may be the mechanism(s) contributing to the prophylactic effects of curcumin on hepatic fibrosis.

Topics: Animals; Apoptosis; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Curcumin; Enzyme Inhibitors; Hepatocytes; Liver Cirrhosis, Experimental; Rats; Rats, Sprague-Dawley

Topics: Angiotensin II; Animals; Carbon Tetrachloride; Carbon Tetrachloride Poisoning; Curcuma; Drugs, Chinese Herbal; Liver Cirrhosis, Experimental; Male; Phytotherapy; Rats; Rats, Sprague-Dawley; Receptor, Angiotensin, Type 1

To Study the protective effect of curcumin on three models of experimental liver injury in mice.. The experimental models of live injury were induced by carbon tetrachloride (CCl4), D-galactosamine (D-Gal N), and Bacillus Calmette-Guerin (BCG) Plus lipolysaccharides (LPS), respectively, in mice. The serum ALT, AST, NO and liver MDA were measured to evaluate the protective effect of curcumin on experimental injury in mice.. Curcumin (50 mg.kg-1, 100 mg.kg-1, 150 mg.kg-1), like biophenyldicarboxylate, were shown to significantly inhibit the increase of serum ALT, AST, NO and liver molondialdehyde (MDA) content induced by CCl4, D-Gal N, BCG + LPS.. Curcumin showed protective effect against liver injury induced by CCl4, D-Gal N, BCG plus LPS.

Topics: Alanine Transaminase; Animals; Aspartate Aminotransferases; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Curcumin; Galactosamine; Lipopolysaccharides; Liver; Liver Diseases; Male; Malondialdehyde; Mice; Nitric Oxide; Protective Agents

The protective effect of tumeric extract (TE) in diet on CCl4-treated rats was studied. Rats were divided into 5 groups: (1) untreated, (2) CCl4 treated, (3) pre-TE for 2 weeks followed by CCl4, (4) TE + CCl4 given concurrently and (5) 5% TE as positive control. The serum levels of bilirubin, cholesterol, aspartate aminotransferase, (AST), alanine amino transferase (AST), (ALT) and alkaline phosphatase were estimated after 1, 2 and 3 months. CCl4 caused a maximum increase (2-3-fold in all the above parameters. As compared to CCl4 group, a short pre-treatment of TE showed reduction in cholesterol, bilirubin, AST, ALT and alkaline phosphatase activity whereas concurrent treatment of TE + CCl4 reduced to a greater extent the levels of all parameters except ALT. To conclude, concurrent treatment of TE gave significant protection against CCl4 though the values did not reach the normal levels.

Topics: Animals; Bilirubin; Carbon Tetrachloride Poisoning; Chemical and Drug Induced Liver Injury; Curcuma; Male; Plant Extracts; Rats; Rats, Wistar