Enzymes In Liver Tissue Research Articles

Glycerol tributylate (Triacylglycerol tributanoate) promoted the liver lipid metabolism by cultivating the intestinal flora of grass carp (Ctenopharyngodon idellus).

To investigate the effects of glycerol tributyrin (TB) (Triacylglycerol tributanoate) on the regulation of liver lipid metabolism by intestinal flora of grass carp (Ctenopharyngodon idellus). The compound feed with soybean oil 2.8% + fish oil 1.8%, soybean oil 6.3% + fish oil 1.8%, and soybean oil 6.2% + fish oil 1.8% + TB 0.1% was added to the basal diet as a fat source and fed to the basal (control) group, high lipid (HL) group, and tributyrin (TB) group for 12weeks. We tested the growth performance, fat content, diversity, and abundance of gut flora and other related indexes of grass carp by Soxhlet extraction, liver tissue enzyme activity, oil red O staining, and 16S rRNA high-throughput sequencing. The results showed that the liver fat number and liver fat content of grass carp in the TB group were lower than those in the HL group, while the fattening degree was significantly higher than those in the other two groups; according to the indices such as Shannon, Ace, and Coverage, it was found that the grass carp in the TB group had the highest abundance and diversity of intestinal microflora; at the portal level, Proteobacteria and Fusobacteria were the main dominant flora in the TB group, with the number of unique OUTs accounting for about 59. 9% of the total number measured; at the genus level, the relative abundance of lipase-producing, short-chain fatty acid-associated bacteria, such as Bacillus-Lactobacillus and Bifidobacterium, was significantly lower (p < 0.05). Thus, we conclude that the addition of TB to high-fat diets can alter the structure of the intestinal microbial community and promote hepatic lipid metabolism in grass carp. TB can alleviate fatty liver in grass carp by increasing the relative abundance of short-chain fatty acids in the intestine. Meanwhile, TB inhibits the conversion of primary bile acids to secondary bile acids in the host, which can block intestinal FXR signaling and the hepatic FXR-SHP pathway, thus slowing down fat synthesis and alleviating the accumulation of liver lipids in grass carp.

Effect of Aqueous Turmeric Extract on Lipid Peroxidation and Activity of Antioxidant Enzymes in Liver Tissue of Chick Embryo Treated with silver nanoParticles

Turmeric extract has antioxidant, antibacterial, antifungal, antiviral, and anti-inflammatory effects, and in addition, curcumin present in turmeric extract can be a powerful protective factor against biochemical changes and cellular oxidative damages. In order to investigate the effect of turmeric aqueous extract on lipid peroxidation and the activity of antioxidant enzymes in the liver tissue of chick embryos treated with silver nanoparticles, 45 race Ross 308 fertilized eggs were randomly divided into control groups (single injection of 0.5 ml saline solution) and 4 treated groups. On the 10th day of incubation, treated groups of 1, 2, 3 and 4 received silver nanoparticles (a single injection of 0.5 ml silver nanoparticles, 200 ppm and 60 nm). On the 12th day of incubation, treated groups of 2, 3 and 4 received turmeric aqueous extract with concentrations of 100, 200 and 300 μg/ml (single injection of 0.5 ml turmeric aqueous extract). The injection was done in the amnion sac embryos. On the 20th day of incubation, the concentration of malondialdehyde and the activity of superoxide dismutase, glutathione peroxidase and catalase enzymes in liver tissue were measured by ELISA method. Statistical analysis was carried out by using one-way ANOVA and post-hoc Tukey tests (p&lt;0.05). Compared to treated group 1, the tissue concentration of superoxide dismutase, glutathione peroxidase and catalase in treated groups 2, 3 and 4 significantly increased and the tissue concentration of malondialdehyde decreased significantly (p&lt;0.05). Dose-dependent injection of turmeric aqueous extract dreduces the toxicity caused by silver nanoparticle and reduces oxidative stress and lipid peroxidation in liver tissue of chick embryos.

Therapeutic effect of Bacopa monnieri on Aflatoxin B1-induced oxidative damage in rats

Aflatoxin B1 is the one of most toxic and well-known mycotoxins, which contaminates staple food. Bacopa monnieri popularly known as Brahmi, is a well-documented nootropic drug in Ayurveda. Thus, the present study was designed to evaluate the protective efficacy of brahmi against liver damage induced within 4 weeks by oral doses 200 ìg/kg Aflatoxin B1, to male rats. Resulting in increased lipid peroxidation, decline in reduced glutathione, and antioxidant enzymes in liver tissue, increased serum liver pathology markers in serum. Oral pretreatment with 20 – 40 mg/kg Brahmi for a week showed remarkable protection against the toxic effects of aflatoxin B1.

Antihepatofibrotic effect of Guizhifuling pill on carbon tetrachloride-induced liver fibrosis in mice.

To evaluate the protective effects and the underlying mechanism of Guizhifuling pill (, GZFL) on carbon tetrachloride (CCl)-induced hepatic fibrosis in mice. Male ICR mice by intraperitoneally administered with 20% CCl (mixed 1∶4 in soybean oil) to induce liver fibrosis. Mice that underwent CCl were orally with GZFL. Using hematoxylin and eosin and Masson staining to examine the pathological changes in liver tissue. Serum biochemical parameters, antioxidant enzyme activity and proinflammatory cytokines was assessed. Nuclear factor-kappaB (NF-κB) pathway and nuclear factor-erythroid 2-related factor 2 (Nrf2) family members were evaluated by Western blotting. Our findings indicated that GZFL could effectively suppress the progression of liver fibrosis in mice, which was determined based on the improvement in liver function and reduction of collagen deposition. GZFL treatment also decreased the level of cytokines and increased the activity of antioxidant enzymes in liver tissue. Moreover, GZFL exerted anti-inflammatory and antioxidant effects through regulating the Nrf2-mediated antioxidant system and inhibiting the NF-κB pathway. GZFL may prevent the progression of liver fibrosis by regulating the Nrf2/ heme oxygenase-1 and NF-κB signaling pathways, thereby highlighting its role in the management of liver fibrosis.

Datura stramonium Leaf Extract Exhibits Anti-inflammatory Activity in CCL4-Induced Hepatic Injury Model by Modulating Oxidative Stress Markers and iNOS/Nrf2 Expression.

Background Inflammation is a frequent phenomenon in the pathogenesis of hepatic disorders leading to fibrosis and cirrhosis. Phytopharmaceuticals developed from traditional medicine can provide effective therapeutic alternatives to conventional medications. Datura stramonium (DS) has reported traditional uses in inflammatory diseases. In this study, we have tried to validate its potential as a source of anti-inflammatory agents. Methods Powdered leaf part of DS was extracted using ethyl acetate (EA) to provide the extract (DSL-EA). Lymphocyte and macrophage viability and acute toxicity assays established the safety profile, while nitric oxide (NO) scavenging assay estimated the in vitro anti-inflammatory potential. Noninvasive anti-inflammatory, antidepressant, and antinociceptive activities were monitored using BALB/c mice using low and high doses (150 and 250 mg/kg). Major inflammatory studies were performed on Sprague-Dawley male rats using CCl4-induced liver injury model. Disease induction was initiated by intraperitoneal injections of CCl4 (1 mL/kg of 30% CCl4 in olive oil). The rats were divided into six groups. The anti-inflammatory potential of DSL-EA in low and high doses (150 and 300 mg/kg, respectively) was assessed through hematological, biochemical, liver antioxidant defense, oxidative stress markers, and histological studies as well as the expression of Nrf2 and iNOS. Results DSL-EA exhibited prominent in vitro NO scavenging (IC50: 7.625 ± 0.51 μg/mL) and in vivo anti-inflammatory activity in paw and anal edema models. In CCl4 model, hematological investigations revealed vasotonic effects. Liver functionality was significantly (P < 0.001 − 0.05) improved in DSL-EA-treated rats. The activity level of endogenous antioxidant enzymes in liver tissues was improved in a manner identical to silymarin. The extract reduced the percent concentration of oxidative stress markers in liver tissues. Furthermore, DSL-EA displayed restorative effects on histological parameters (H and E and Masson's trichrome staining). Immunohistochemistry studies showed marked decline in Nrf2 expression, while overexpression of iNOS was also observed in disease control rats. The damage was distinctly reversed by the extract.

Nutritional and Biological evaluation of using Spirulina algae as anew source of protein

Spirulina platensis (SP) alga has been a common dietary substance around the world from ancient times. This study was aimed to using Spirulina as a novel protein source, especially in growth phase. Thirty six male albino rats aged six weeks were divided into six groups according to the protein source as following: The casein groups (C1, C2, and C3) contain (100, 200, and 300 g casein /kg diet) as (10%, 20% &30% casein), respectively. On the corresponding side, the spirulina clusters (SP1, SP2, and SP3) contained (157, 315 and 472 gm algal protein/kg food) respectively. It lasted 28 days. SP has high total antioxidant activity (39.2 %). SP groups recorded significant increases in feed intake, body weight gain, feed efficiency ratio and protein efficiency ratio compared with casein groups. While casein recorded significant increases in apparent digestibility, Co-efficient compared to groups of SP algae. Eating Spirulina has significantly preserved liver and kidney function. As for complete blood picture, the groups of SP3 recorded highest percentage in Hb and RBCs compared with C3 group, other than WBCs, which was lower in SP3. Significant increase in the antioxidant enzymes in liver tissues were observed in SP groups, while Malondialdehyde recorded a significant reduction in the same groups. SP treatment increased GH levels in all groups. On the other side, the results of alpha tumor necrosis factors recorded a significant decrease in groups of SP compared with the groups of casein. In conclusion, Spirulina can be used as a new protein replacement

A highly butyrylcholinesterase selective red-emissive mitochondria-targeted fluorescent indicator imaging in liver tissue of mice

Abstract A long-emitting (λex = 580 nm, λem = 628 nm) mitochondrial targeting butyrylcholinesterase (BChE) selective fluorescent chemosensor (BChE-NBD) has been synthesized. A prominent fluorescence enhancement only for BChE was found in aqueous solution. BChE-NBD has low biological toxicity and has been successfully applied to the detection and imaging of BChE in mitochondria in a variety of cells and not interfered by other analytes (especially acetylcholinesterase). More importantly, imaging study of the distribution of the BChE in mice was performed first time, which confirmed the widespread existence of the enzyme in liver tissue. This making the probe BChE-NBD hopeful to be an effective tool for investigates liver diseases in basic medicine and clinical applications.

Pinus thunbergii PARL leaf protects against alcohol-induced liver disease by enhancing antioxidant defense mechanism in BALB/c mice

Abstract Pinus thunbergii is a black pine that has been widely used in health-promoting foods. This study was conducted to investigate the hepatoprotective effects of the alcohol-aqueous extract of Pinus thunbergii PARL leaves (PTE) in ethanol-induced liver-damaged mice. PTE increased the weight and survival rate of mice while reducing the levels of serum hepatic marker enzymes. PTE also restored the levels of antioxidant enzymes in liver tissues while drastically increasing lipid peroxidation concentrations. Histopathological examination of PTE-treated mice presented relatively less lipid droplets and hepatic tissue damage compared to ethanol-treated mice. Finally, to identify PTE components, Natural Products Application Solution with UNIFI along with an in-house library was processed and results revealed 35 compounds in the extract. These compounds were reported to exhibit significant antioxidant and/or hepatoprotective properties. Our results suggest that PTE improves liver function and can be developed as a food product with hepatoprotective effects.

Ginsenoside Rg1 alleviates ANIT-induced intrahepatic cholestasis in rats via activating farnesoid X receptor and regulating transporters and metabolic enzymes

Ginsenoside Rg1 is an active ingredient extracted from the roots of ginsenoside, and an α-naphthylisothiocyanate (ANIT)-induced rat model of intrahepatic cholestasis was used to investigate the protective effect of Rg1 on cholestasis. 48 SD male rats were randomly divided into 6 groups: control group, model group, UDCA group (ursodeoxycholic acid), low-dose Rg1 group (10 mg/kg), medium-dose Rg1 group (20 mg/kg) and high-dose Rg1 group (40 mg/kg). The model group, the UDCA group and all the Rg1 group were then intragastrically administered with 80 mg/kg ANIT, and the control group were given equal volume of olive oil. Then the pathological changes in liver tissue were observed, the secretion of bile in the bile duct was measured, and the biochemical markers in serum were quantified, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), glutamyl transfer peptidase (GTP) and the content of total bilirubin (TBIL), direct bilirubin (DBIL), total bile acid (TBA). The contents of inflammatory mediators in serum were quantified, including tumor necrosis factor (TNF-α), γ-interferon (IFN-γ) and interleukin-1β (IL-1β). The contents of superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) in liver homogenate were quantified. Expression of farnesoid X receptor (FXR), transporters and metabolic enzymes in liver tissue was monitored. Rg1 treatment improved liver tissue pathological damage, promoted bile secretion and significantly reduced serum levels of the intrahepatic cholestasis markers ALT, AST, ALP, GTP, TBIL, DBIL and TBA. Rg1 increased the activity of SOD and GSH-Px in liver homogenate, while, reducing the serum levels of MDA and inflammatory mediators. Rg1 also regulated the expression of FXR, bile acid transporters and metabolic enzymes. Overall, Rg1 alleviated liver injury by improving secretion of bile and normalizing the activity of enzymes in the serum. The protective mechanism appeared to be related to the activation of FXR and regulation of liver transporters and metabolic enzymes.

Chemoprevention of Colorectal Cancer by Anthocyanidins and Mitigation of Metabolic Shifts Induced by Dysbiosis of the Gut Microbiome

Diets rich in fat, smoking, as well as exposure to environmental pollutants and dysbiosis of gut microbiota, increase the risk of developing colorectal cancer. Much progress has been made in combating colorectal cancer. However, options for chemoprevention from environmental insult and dysbiosis of gut microbiota remain elusive. We investigated the influence of berry-derived anthocyanidins (Anthos), with and without encapsulating them in bovine milk-derived exosomes (ExoAnthos), on the chemoprevention of bacteria-driven colon tumor development. Anthos and ExoAnthos treatment of colon cancer cells showed dose-dependent decreases in cell viability. Calculated selectivity index (SI) values for Anthos and ExoAnthos suggest that both treatments selectively targeted cancer over normal colon cells. In addition, ExoAnthos treatment yielded higher SI values than Anthos. Anthos and ExoAnthos treatment of ApcMin/+ mice inoculated with enterotoxigenic Bacteriodes fragilis (ETBF) bacteria led to significant decreases in colon tumor numbers over mice receiving vehicle treatments. Western blot analysis of normal colon, colon tumor, and liver tissue lysates showed that mice inoculated with ETBF featured increased expression of phase I enzymes in normal colon tissue and decreased expression of phase II enzymes in liver tissue. Treatment with the Anthos and ExoAnthos reverted the modulation of phase I and phase II enzymes, respectively; no significant changes in phase II enzyme expression occurred in colon tumor tissue. Treatment of HCT-116 cells with the ubiquitous carcinogen, benzo[a]pyrene (B[a]P) led to similar modulation of phase I and II enzymes, which was partially mitigated by treatment with Anthos. These results provide a promising outlook on the impact of berry Anthos for prevention and treatment of bacteria- and B[a]P-driven colorectal cancer.

Congo Red Effects on Detoxification and Metabolic Enzymes in Rainbow Trout (Oncorhynchus mykiss Walbaum, 1792)

The aim of this study was to evaluate the activities of the biotransformation enzymes (Glutatyon S-Transferase (GST) and cytochrome P450 (CYP1A1)) and metabolic enzyme (Lactate dehydrogenase-LDH) in the liver of rainbow trout (Oncorhynchus mykiss) after 24 and 48 hour exposure to 0.5, 1.0 and, 2.0 mg l-1 of Congo red (CR). Enzyme activities were determined by using commercial kits with ELISA method. Congo red altered the activities of GST, CYP1A, and LDH enzymes in liver tissue of O. mykiss in a dose-dependent manner. The statistical differences in GST activities among the groups for 24 and 48 h were significant, but, LDH activities were significant for only 24 h. Exposure duration of CR didn‘t affect the biochemical response of rainbow trout. Thus, CR exposure changed the biotransformation and metabolic enzymes, and the changes of these enzymes activities may be used as a potential bioindicator of the CR exposure.

HEPATOPROTECTIVE ROLE OF LOVASTATIN - PREGNANE X RECEPTOR AGONIST IN LITHOCHOLIC ACID INDUCED LIVER CHOLESTASIS DISEASED RATS

Objective: Pregnane X receptor (PXR), member of nuclear receptor family, an integral component of the body defence mechanism against chemical insult are expressed in the liver, gastrointestinal system &amp; lungs. Some studies have shown that the lovastatin is pregnane X receptor (PXR) activation effect.&#x0D; Methods: In the present study the hepatoprotective effect of lovastatin was investigated against lithocholic acid induced liver toxicity. Liver markers in serum and antioxidant enzymes in liver tissue were assessed by using standard procedures.&#x0D; Results: The level of liver marker (such as SGOT &amp; SGPT) and bilirubin were increased significantly (p&lt;0.05) and antioxidant enzyme (i.e. SOD, GSH and CAT) were significantly (p&lt;0.05) decrease in lithocholic acid treated groups as compared to control group. Lovastatin at doses of 0.1, 0.2, 0.3 mg/kg showed significantly (p&lt;0.05) decrease in the levels of liver marker (SGOT &amp; SGPT) and bilirubin as compared to the positive control group in both pre &amp; post treated models. The antioxidant enzymes such as Superoxide dismutase (SOD), Glutathione (GSH) and Catalase (CAT) content in liver tissue were significantly (p&lt;0.05) increase after administration of lovastatin at dose dependent manner in both pre &amp; post treated models.&#x0D; Conclusions: The results of the present study indicates that under the present experimental conditions, lovastatin showed hepatoprotective abilities against lithocholic acid induced hepatotoxicity in albino rat.&#x0D; Keywords: Hepatoprotection, lovastatin, Lithocholic Acid, Pregnane X Receptor

Effects of Isoflavone Supplementation on Lipid Profiles and Antioxidant Enzyme Activities in Growing Rats Fed High Fat Diet.

The purpose of this study was to investigate the effects of isoflavone on serum lipids and antioxidant enzymes activities in growing rats fed high lard diet. Twenty four female Sprague-Dawley rats (body weight 50–60 g) were divided into three groups, control, high fat (HF, lard 200 g/kg diet) and high fat + isoflavone (HFI, lard 200 g/kg diet + isoflavone 310.9 mg/kg diet) for 4 weeks. The results of study indicated that body weight gain was not different by isoflavone diet. Mean intake was significantly lower in HF group and HFI group than control group. Food efficiency ratio was significantly higher in HF group and HFI group than control group. The level of serum triglyceride and total cholesterol were significantly lower in HFI group than control group and HF group. The level of high-density lipoprotein cholesterol, was significantly higher in control group than HF group and HFI group. The level of low-density lipoprotein cholesterol was not significantly different by experimental diets, but atherogenic index (AI) was significantly lower in control group and HFI group than HF group. Contents of total cholesterol and triglyceride in liver tissues were found to be insignificant. The concentration of lipid peroxidation, malondialdehyde was significantly lower in control groups and HFI group than HF group. And antioxidant enzymes in liver tissue were not significantly different by lard and isoflavone supplemented diets. In conclusion, it seems possible that isoflavone supplemented high fat diet may produce positive results on level of serum triglyceride, serum total cholesterol, AI and concentration of malondialdyhyde.

Effect of physiological active compounds on status of prooxidative-antioxidative balance and activity of Krebs cycle enzymes in heart and liver tissues under doxorubicin-induced cardiomyopathy

A study was conducted to determinate the effects of Tiotriasolin, Qudesan and the precursors of ubiquinone synthesis (EPM-Mg: alpha-tocopherol acetate), 4-hydroxybenzoic acid, methionine, Mg2+ ions) on the free radical processes and activity of some Krebs cycle dehydrogenases in rat heart and liver tissues under conditions of doxorubicin-induced cardiomyopathy. Administration of doxorubicin intensified the processes of lipid and protein oxidation and suppressed antioxidant enzymes activity in liver and heart tissues. Administration of metabolic correctional drugs caused a decrease the negative effect of doxorubicin on antioxidant system of heart and liver tissues due to increased activity of catalase and superoxide dismutase and inhibition of free radical processes. Doxorubicin administration caused an increase activity of both dehydrogenases in cardiomyocytes, which can be explained by triggering compensatory mechanisms in organ’s cells. The intake of metabolic drugs decreases the negative effect of anthracycline and approximates the dehydrogenase activity, which is close to the control values. In contrast to heart tissues, doxorubicin administration did not cause significant changes in the activity of energy enzymes in liver tissues, which may be due to the presence in the cells of liver a relatively powerful antioxidant defense system (capable in this experimental conditions effectively counteract doxorubicin-induced free radical processes). Administration of Qudesan and EPM-Mg caused a significant increase of alpha-ketoglutarate dehydrogenase and succinate dehydrogenase activities, which indicates the positive effect of these substances on work of the cell energy system.

Impact of chronic kidney dysfunction on serum Sulfatides and its metabolic pathway in mice.

Serum sulfatides are critical glycosphingolipids that are present in lipoproteins and exert anticoagulant effects. A previous study reported decreased levels of serum sulfatides in hemodialysis patients and suggested an association with cardiovascular disease. However, the mechanism of changes in serum sulfatides in chronic kidney dysfunction has not been well investigated. The current study examined whether a chronic kidney disease (CKD) state could decrease serum sulfatide levels using 5/6 nephrectomy (5/6NCKD) mice, an established CKD murine model, and studied the mechanisms contributing to diminished sulfatides. 5/6NCKD mice and sham operation control mice were sacrificed at the 4th or 12th postoperative week (POW) for measurement of serum sulfatide levels. Hepatic sulfatide content, which is the origin of serum sulfatides, and the expression of sulfatide metabolic enzymes in liver tissue were assessed as well. The 5/6NCKD mice developed CKD and showed increased serum creatinine and indoxyl sulfate. The serum levels and hepatic amounts of sulfatides were significantly decreased in 5/6NCKD mice at both 4 and 12 POW, while the degradative enzymes of sulfatides arylsulfatase A and galactosylceramidase were significantly increased. In a Hepa1-6 murine liver cell line, indoxyl sulfate addition caused intracellular levels of sulfatides to decrease and degradative enzymes of sulfatides to increase in a manner comparable to the changes in 5/6NCKD mice liver tissue. In conclusion, chronic kidney dysfunction causes degradation of sulfatides in the liver to decrease serum sulfatide levels. One explanation of these results is that indoxyl sulfate, a uremic toxin, accelerates the degradation of sulfatides in liver tissue.

The determination of the effect of some 1,3,4 thiadiazole derivatives on biochemical content (Fatty Acids, Sterols, Lipophilic Vitamins) in rat liver.

Thiadiazole derivatives and its metal compounds have antibacterial, antifungal, antitumoral, antiproliferative and antioxidant properties. In the study, the effects caused by thiadiazole ligand and its metal complexes upon the fatty acids and lipophilic vitamins in livers of rats were examined. The fatty acids in liver were specified by GC while the lipophilic vitamins were specified by HPLC. It was observed that the amounts of oleic acids (18:1, n-9) and monounsaturated fatty acids (MUFA) notably increased in the Mn complex group while the amounts of arachidonic acid (20:4, n-6) notably increased in the ligand group, compared to control group. The amounts of vitamin K2, vitamin D3 and α-tocopherol considerably increased in all groups compared to control group. It was noted that the amounts of α-tocopherol were elevated in both the Mn and Cr complex groups compared to control group. However, this elevation was matching with the amount in the same groups. Nevertheless, the amount of retinol was determined to be lower in the Mn complex group compared to other groups. Accordingly, it can be considered that thanks to the utilization of toxic metals such as manganese, cadmium and chrome, unsaturated fatty acids influenced the activities of the enzymes in liver tissue, which are in charge of fatty acid chain elongation.

The devastating effect of exposure to high irradiation dose on liver and the performance of synthesized nano-Hap in relieve the associated symptoms in rats.

Ionizing radiation is one of the environmental factors that may contribute to liver dysfunction through a mechanism involving oxidative stress. This investigation studied the possible therapeutic effects of nano-HAp on hepatotoxicity in rats induced with gamma (γ) radiation. The study was carried out using 3 groups with 10 rats in each. Group 1 comprised the non-irradiated control rats, whereas the rats in groups 2 and 3 received a single dose of 10 Gy γ-radiation. The rats in group 3 were treated with nano-HAp [100 mg·(kg body mass)-1] once a week for 2 weeks starting the day after irradiation. The results showed that the rats exposed to γ-radiation had fragmented DNA, and significantly decreased levels of liver tissue enzymes such as paraoxonase 1, gamma glutamyl, alanine aminotransferase (ALT), and aspartate aminotransferase (AST). Pro-inflammatory factors such as interleukin (IL)-2, IL-6, tumor necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ) in tissue were significantly increased compared with the controls. Also, exposure to γ-radiation significantly decreased the activity of superoxide dismutase and glutathione oxidase and increased lipid peroxidation in liver tissue. These effects were accompanied by severe histopathological changes to the hepatocytes. Intravenous injection of nano-HAp after irradiation has significant therapeutic potential against irradiation-induced liver damage because the treatment with nano-HAp restored antioxidant activity in the liver, antagonized the significant changes in the levels of IL-2, IL-6, TNF-α, IFN-γ, and restored the tissue level of paraoxonase 1, gamma glutamyl, ALT, and AST. Administering nano-HAp seemed to relieve the pathological changes induced by γ-radiation. Based on these results, it could be concluded that nano-HAp may have a therapeutic effect against liver dysfunction induced by γ-radiation through antagonizing the generation of free radicals and enhancing the antioxidant defense mechanisms.

Biochemical and Molecular Investigation of Antioxidant Enzymes in Liver Tissue of Rats Intoxicated with Carbon Tetrachloride and Treated with Aqueous Extract of Fenugreek (Trigonella foenum-graecum L.)

Biochemical and Molecular Investigation of Antioxidant Enzymes in Liver Tissue of Rats Intoxicated with Carbon Tetrachloride and Treated with Aqueous Extract of Fenugreek (Trigonella foenum-graecum L.)

Effect of Jianpi Hewei Qushi Fang on activity and expression of CYP450 enzymes in liver tissue of rats

Effect of Jianpi Hewei Qushi Fang on activity and expression of CYP450 enzymes in liver tissue of rats

Assessment of antioxidant activity of metformin in ethanol induced liver damage in Sprague Dawley rats

Background: Alcoholic liver disease (ALD) is a life style associated and one of the most common causes of chronic liver disease in the world. Chronic and excessive ethanol consumption impairs fatty acid oxidation and thereby stimulates lipogenesis, which leads to steatosis. Manifestation of harmful effects by alcohol occurs by free radical species which react with most of the cell components by changing their structures and functions. The hepatoprotective activity of metformin may be due to its antioxidant effect and enhancing fatty acid oxidation. So the aim of the present study is to evaluate preventive hepatoprotective effect of metformin in terms of hepatic oxidative stress marker enzymes and liver-histopathology scores. Methods: Thirty adult Sprague Dawley rats of either sex, weighing 200-250 g were selected for the study. The study was performed as per CPCSEA guidelines. The rats were randomly divided into 5 groups; n=6. All the treatments were given once a day for 21 days. After day 21, the dissected liver was used to assess oxidative stress marker enzymes malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) spectrophotometrically. The liver damage was assessed by histopathological scoring (HPS). Results: A comparison of The liver tissue MDA, SOD, CAT levels (nmol/g) and HPS value in the various groups on day-22 suggests that a treatment with metformin at low dose displayed a minimal hepatocellular protection when compared to that of the ethanol-treated and vehicle treated groups; however, metformin treatment at moderate and high doses elicited a better hepato protection as compared to low dose metformin treated groups. A dose-dependent hepatoprotection by metformin that high-dose metformin may be a potential therapeutic candidate in attenuating the ALD. Conclusions: Metformin co-administration effectively prevented hepatic damage caused by ethanol in animal model with favourable modification in the oxidative stress marker enzymes in liver tissue and histopathology. It may be effective for preventing liver toxicity in chronic alcoholics. A dose dependent hepatoprotection reveals that metformin may be a potential therapeutic candidate in attenuating the ALD which needs a systematic clinical study.