Rat Hepatic Tissue Research Articles

Cadmium-induced hematological, renal, and hepatic toxicity: The amelioration by spirulina platensis

Background: spirulina platensis (SP) is known as a valuable additional food and therapeutic agent. Objective: We investigate the protective effect of SP on cadmium (Cd)-induced hematological, renal and hepatic toxicity in rats. Materials and Methods: The rats were divided into four groups. Group 1: received saline orally. Group 2: treated with SP orally for 28 days. Groups 3: treated with CdCl2for 28 days. Group 4: treated with CdCl2and SP for 28 days. Renal and hepatic damages were evaluated by investigating the renal and hepatic functions, oxidative markers, and histopathological changes. Results: There was a statistically significant (P ≤ 0.05) increase in Cd concentration in the liver and kidneys of G3 and a significant decrease with the administration of SP in G4. In rat hepatic and renal tissues, superoxide dismutase and catalase were significantly reduced while malondialdehyde (MDA) was significantly increased and significant decrease in RBC count, hemoglobin concentration, and hematocrit in Group 3 when compared to G1 and G2 (P ≤ 0.05), with improvements of these parameters in G4 when compared to G3. A significant increase was observed in plasma MDA level in Group 3 compared to control group and SP-treated group, and it was significantly decreased in G4 compared to G3. Conclusion: It can be concise that accumulation of Cd in liver and kidneys of rats is associated with remarkable alterations enzymatic activities of the antioxidant system. Our data suggested that lipid peroxidation was associated with Cd toxicity in both liver and kidney tissues. The oxidative damage in kidney and liver of rats induced by Cd is protected by SP.

Iron-induced pro-oxidant and pro-lipogenic responses in relation to impaired synthesis and accretion of long-chain polyunsaturated fatty acids in rat hepatic and extrahepatic tissues.

Iron is involved in processes involving oxygen transfer and utilization. Excess iron is linked to cardiovascular diseases and some types of cancer. Iron overload is associated with oxidative stress development, and may have important interactions with lipid metabolism in the liver favoring the development and progression of non-alcoholic fatty liver disease. The aim of the study described here was to assess the effect of high intake of iron on oxidative stress-related parameters, lipid metabolism, and levels of long-chain polyunsaturated fatty acids (LCPUFAs) in liver and other tissues of the rat. Male Wistar rats (21d old) were fed an iron-rich diet (200mg iron/kg diet, IRD) versus a control diet (50mg iron/kg diet; CD) for 21d. Samples of erythrocytes, liver, adipose tissue, brain, heart, and testicles were evaluated for fatty acid composition and hepatic biochemical and oxidative stress parameters, Δ-6 and Δ-5 desaturase activities, SREBP-1c and PPAR-α mRNA expression and DNA-binding capacity, and lipolytic, lipogenic, and antioxidant enzymatic activities. The IRD caused liver steatosis and increased activity of plasma transaminases, with higher oxidative stress status in plasma and liver. Liver Δ-6 and Δ-5 desaturase exhibited decreased activity, but enhanced expression in response to the IRD compared with the CD, with lower levels of ω-3 and ω-6 LCPUFAs and higher expression and DNA binding of SREBP-1c, whereas expression and DNA-binding activity of PPAR-α were diminished. IRD induced oxidative stress and a reduction in the desaturation capacity of the liver, with LCPUFA depletion in the different tissues studied, thus promoting a pro-steatotic condition in the liver.

Effect of Litchi chinensis on adipose and hepatic tissues in rats with obesity and non-alcoholic fatty liver disease (NAFLD)

Abstract The use of lychee extract as a supplemental therapeutic to ameliorate diabetes, obesity and its complications, such as non-alcoholic fatty liver disease, has been investigated to determine whether lychee can act as a functional food during the development of obesity. Objective: to evaluate the effect of the pulp of Litchi chinensis dietary on adipose and hepatic tissues associated with the development of obesity and fatty liver in Wistar rats. Methodology: four groups of rats were used control group (C), Metabolic syndrome (MS) Lychee-Sucrose (Lch-Suc) and Lychee without sucrose (Lch). The dose of pulp of lychee was 40% p/v for 5 weeks. However, very little is known about the hypertrophy of hepatic tissues during the development of obesity and fatty liver in Wistar rats. Methodology: The following four groups of rats were used: control (C), metabolic syndrome (MS), Lychee-Sucrose (Lch-Suc) and Lychee without sucrose (Lch). The dosage of lychee pulp was 40% p/v for 5 weeks. Results: We observed differences in the abdominal fat weights between the C and MS groups. In the Lch group, the adipose tissue weight, triglycerides (36%) and cholesterol (11%) were significantly lower than those in the MS group. The MS, Lch-Suc and Lch groups showed macrovesicular steatosis, which was not found in the C group. Finally, the number of small adipocytes (areas 2 ) was higher in the Lch group than in the MS group and the Lch-Suc group. Conclusion: Lychee pulp in drinking water affected the cellular dynamics of adipose tissue, reducing the hypertrophy of adipocytes and exerting an effect that countered the accumulation of fat in the liver tissue of Wistar rats.

Effect of Ligustri Lucidi Fructus on hepatic COX activity in normal rats and preliminary investigation of its DNA methylation mechanism

The study aims to investigate the effect of Ligustri Lucidi Fructus on cytochrome c oxidase(COX) activity in rat hepatic tissues and explore its possible mechanism of DNA methylation. Male SD rats received aqueous extract of Ligustri Lucidi Fructus (2.0，6.0 g•kg⁻¹) by intragastric administration for 30 d. After the rats were sacrificed, hepatic tissues of rats were taken to detect COX activity, protein concentration of COX4I1, TET1 and DNMT3A protein levels, mRNA expression levels of Cox4i1, Dnmt3a and Tet1, and determine the DNA methylation frequency of Cox4i1.Results showed that both low and high doses of Ligustri Lucidi Fructus could significantly increase COX activity and concentration of COX4I1(P<0.05), with a decreasing tendency of both TET1 protein and DNMT3a protein expression； however, mRNA expression levels of Cox4i1, Dnmt3a and Tet1 were not significantly changed by Ligustri Lucidi Fructus. In addition, DNA methylation frequency of Cox4i1 in high dose group showed a declining tendency as compared with the blank control group, but without significant difference.These results indicated that Ligustri Lucidi Fructus had promotive effect on hepatic COX activity in rats, which may be achieved by increasing protein content of COX4I1. Moreover, a decreased tendency of DNMT3A protein could be one of the reasons for the lower trend of Cox4i1 methylation rate. In addition, Ligustri Lucidi Fructus may regulate the expression levels of DNMT3A and TET1 in the same direction and its mechanism is not clear.

Therapeutic effect of green tea extract on alcohol induced hepatic mitochondrial DNA damage in albino wistar rats

The present study principally sought to investigate the effect of green tea extract (GTE) supplementation on hepatic mitochondrial DNA (mtDNA) damage in alcohol receiving rats. MtDNA was isolated from hepatic tissues of albino wistar rats after alcohol treatment with and without GTE supplementation. Entire displacement loop (D-loop) of mtDNA was screened by PCR-Sanger’s sequencing method. In addition, mtDNA deletions and antioxidant activity were measured in hepatic tissue of all rats. Results showed increased frequency of D-loop mutations in alcoholic rats (ALC). DNA mfold analysis predicted higher free energy for 15507C and 16116C alleles compared to their corresponding wild alleles which represents less stable secondary structures with negative impact on overall mtDNA function. Interestingly, D-loop mutations observed in ALC rats were successfully restored on GTE supplementation. MtDNA deletions were observed in ALC rats, but intact native mtDNA was found in ALC+GTE group suggesting alcohol induced oxidative damage of mtDNA and ameliorative effect of GTE. Furthermore, markedly decreased activities of glutathione peroxidise, superoxide dismutase, catalase and glutathione content were identified in ALC rats; however, GTE supplementation significantly (P<0.05) restored these levels close to normal. In conclusion, green tea could be used as an effective nutraceutical against alcohol induced mitochondrial DNA damage.

Short-term effects of troxerutin (vitamin P4) on muscle fatigue and gene expression of Bcl-2 and Bax in the hepatic tissue of rats.

In the current study, the effects of troxerutin (TRX) on muscle fatigue and gene expression of Bcl-2 and Bax in the hepatic tissue of rats was investigated. Forty male Wistar rats were randomly divided into 4 groups and designated as control and TRX treatment at 75 (TRX75), 150 (TRX150), and 300 mg/kg per day (TRX300). The treated groups and control group received TRX and water orally for 7 days. After an exhaustive swimming test on the 7th day, all animals were euthanized immediately and several biochemical parameters related to fatigue and gene expression of Bcl-2 and Bax in the hepatic tissue were measured. Our results showed that the exhaustion swimming time in the TRX300 groups significantly increased 1.2-fold compared with the control group (P < 0.001). TRX300 significantly reduced ALT (P < 0.05) activity and increased liver SOD activity compared with the control group (P < 0.01). Additionally, TRX significantly reduced the liver mRNA expressions of Bax (P < 0.001) and increased the Bcl-2/Bax ratio (P < 0.001) compared with the control group. Based on our data, TRX possesses anti-apoptotic and hepatoprotective action following exhaustive swimming exercise.

Protective effects of Fraxinus xanthoxyloides (Wall.) leaves against CCl4 induced hepatic toxicity in rat.

BackgroundLeaves and root bark of Fraxinus xanthoxyloides Wall. (Oleaceae) are used locally for the treatment of jaundice, malaria and pneumonia. Decoction of stem, twigs and bark is used in pain, internal injuries, rheumatism and in bone fracture. In this investigation we have evaluated the methanol extract of leaves for its hepatoprotective potential against CCl4 induced hepatic injuries in rat.MethodsPowder of F. xanthoxyloides leaves was extracted with methanol (FXM) and subjected for the determination of polyphenolics through HPLC-DAD analysis. Sprague–Dawley (Rattus novergicus) male rats were divided into eight groups (six rats in each). Group I: non-treated control; Group II: vehicle treated (DMSO plus olive oil) while Group III- VI treated with 1 ml/kg body weight (bw) of CCl4 (30 % in olive oil) for 30 days (15 dosages) to induce the hepatic injuries. Group IV: treated with silymarin (100 mg/kg bw); Group V and VI with FXM (200, 400 mg/kg bw) on alternate days with CCl4 treatment. Group VII and VIII was administered with FXM (200, 400 mg/kg bw) alone (15 dosages). After 30 days the serum was evaluated for liver function enzymes and biochemical markers, liver samples for antioxidant enzymes, biochemical markers, comet assay and for histopathology.ResultsHPLC-DAD analysis of FXM revealed the existence of rutin and caffeic acid. In CCl4 treated rats the level of alanine transaminase (ALT), aspartate transaminase (AST), total bilirubin was significantly increased while the albumin concentration in serum was decreased as compared to control group. The level of hepatic antioxidant enzymes, catalase (CAT), peroxidase (POD), superoxide dismutase (SOD), glutathione-S-transferase (GST) and glutathione reductase (GSR) was significantly decreased against the control group. Further, significant decrease in GSH while increase in lipid peroxides (TBARS), H2O2, DNA damages and comet length was induced with CCl4 in hepatic tissues of rat. In contrast, co-administration of FXM and silymarin restored the biochemical and histopathological status of the liver.ConclusionResults of present investigation revealed that F. xanthoxyloides leaves possibly protect the liver against CCl4 induced injuries like silymarin by its antioxidant constituents.

Targeted multimodal nano-reporters for pre-procedural MRI and intra-operative image-guidance.

Multimodal-imaging probes offer a novel approach, which can provide detail diagnostic information for the planning of image-guided therapies in clinical practice. Here we report targeted multimodal Nd3+-doped upconversion nanoparticle (UCNP) imaging reporters, integrating both magnetic resonance imaging (MRI) and real-time upconversion luminescence imaging (UCL) capabilities within a single platform. Nd3+-doped UCNPs were synthesized as a core-shell structure showing a bright visible emission upon excitation at the near infrared (minimizing biological overheating and increasing tissue penetration depth) as well as providing strong MRI T2 contrast (high r2/r1 ratio). Transcatheter intra-arterial infusion of Nd3+-doped UCNPs conjugated with anti-CD44-monoclonal antibody allowed for high performance invivo multimodal UCL and MR imaging of hepatocellular carcinoma (HCC) in an orthotopic rat model. The resulted invivo multimodal imaging of Nd3+ doped core-shell UCNPs combined with transcatheter intra-arterial targeting approaches successfully discriminated liver tumors from normal hepatic tissues in rats for surgical resection applications. The demonstrated multimodal UCL and MRI imaging capabilities of our multimodal UCNPs reporters suggest strong potential for invivo visualization of tumors and precise surgical guidance to fill the gap between pre-procedural imaging and intraoperative reality.

Pequi (Caryocar brasiliense Camb.) almond oil attenuates carbon tetrachloride-induced acute hepatic injury in rats: Antioxidant and anti-inflammatory effects

Carbon tetrachloride (CCl4) is a potent hepatotoxin, capable of generating free radicals that lead to oxidative stress and the inflammation process. Pequi almond oil (PAO) has been reported to possess unsaturated fatty acid and antioxidant compounds related to beneficial effects on oxidation and inflammatory conditions. The present study was undertaken to evaluate the hepatoprotective effects of handmade and coldpressed PAO on CCl4-induced acute liver injury. The possible mechanisms underlying the effect on liver injury enzymes, histopathological parameters, lipid profile, lipid peroxidation, and antioxidant and detoxification defense systems, as well as inflammatory parameters, were determined. Rats treated with PAO (3 or 6 mL/kg) for 21 days before CCl4 induction (3 mL/kg, 70%) showed significantly decreased levels of alanine aminotransferase and aspartate aminotransferase, milder hepatic lesions and higher levels of serum high-density lipoprotein compared to CCl4 group. Moreover, PAO enhanced antioxidant capacity by increasing hepatic glutathione peroxidase and glutathione reductase enzyme activities, as well as reducing circulating concentrations of leptin and inflammatory mediators such as interleukin-6, leukotrienes -4 and -5 and the tumor necrosis factor receptor. In summary, PAO, especially cold-pressed oil, attenuated the CCl4-induced alterations in serum and hepatic tissue in rats due to its antioxidant and anti-inflammatory properties.

Promising anti-oxidative therapeutic potentials of edible freshwater snail Bellamya bengalensis extract against arsenic-induced rat hepatic tissue and DNA damage

Epidemiological data suggest that arsenic ultimately results in cancer in different parts of the body. Several synthetic therapeutic agents manifest inadequate potency with severe side effects against arsenic toxicity. The flesh of B. bengalensis , has long been used as an ethno-medicine in case of arthritis, blood-impurities, impaired immune system, conjunctivitis and liver anomalies. This potent organism might be a natural choice against arsenic and several other toxicities. Our earlier studies on arsenic-exposed human can correlate carcinogenesis with DNA-damage. In an attempt to investigate the possible protective and therapeutic effect against arsenic induced hepatotoxicity, the extract of B. bengalensis was tested in arsenic intoxicated rat model. The time- and dose-dependent effect of arsenic toxicity was also tested in B. bengalensis . Sodium-meta-arsenite NaAsO 2 (0.6 ppm/100g bw/day for 28 days, as earlier reported) was treated alone or in combination with the B. bengalensis water extract (BBE, 100 mg/100g bw) to rat and compared with vehicle treated control. In a separate experiment, the B. bengalensis was exposed to high concentration of NaAsO 2 contaminated water (5 to 20 ppm for 1 to 9 days) in laboratory condition and their DNA quality was evaluated in relation to its possible oxidative threat. Any concentration of arsenic was incapable to initiate a significant DNA damage in B. bengalensis . Lipid peroxidation was increased in arsenic exposed B. bengalensis after longer duration of its exposure. Increase in reduced antioxidant like non-protein-soluble thiol (NPSH) is concordant with the decrease in lipid peroxidation and DNA stability in this organism. In rat experiment, the BBE supplementation strongly prevented arsenic-induced oxidative, necrotic and apoptotic damages to liver tissue/DNA by strengthening antioxidant systems, which has been shown in hepatic DNA-fragmentation, comet-assay, histo-architecture (hematoxylin/eosin), alkaline-phosphatase, serum-glutamate-pyruvate-transaminase and lactate-dehydrogenase (tissue-degeneration-marker) results. Only arsenic exposure decreased hepatic superoxide-dismutase (SOD) in-vivo and in-vitro (H 2 O 2 /arsenite redox-stress to dialyzed and concentrated, 6-8kd cutoff-Millipore liver cytosolic SOD), catalase, xanthine-oxidase, lactoperoxidase activities and the level of NPSH with a concomitant increase in malondialdehyde resulting in mutagenic DNA-breakage and apoptotic liver damage which has been decisively restrained in B. bengalensis extract. The present investigation offers strong evidence on the hepato-protective and medicinal efficiencies of BBE against oxidative stress induced by arsenic.

Loss of Raf kinase inhibitor protein is associated with malignant progression in hepatic fibrosis

Raf kinase inhibitory protein (RKIP), besides regulating important intracellular signaling cascades, was described to be associated with progression, metastasis and prognosis in several human neoplasms. But its role in hepatic fibrogenesis remains unclear. In the present study, we found that the absence of RKIP expression significantly enhanced the proliferation of HSC-T6 cells. Reduced RKIP expression promoted the activation of HSCs and the accumulation of collagen, as evidenced by the increases in the levels of collagen I and α-smooth muscle actin. Moreover, down-regulating RKIP expression led to severe histopathological changes and collagen accumulation in hepatic tissues of rats with liver fibrosis. Furthermore, the absence of RKIP promoted the activation of ERK/MAPK pathway in vitro and in vivo. Our findings clearly demonstrate an inverse correlation between RKIP level and the degree of the liver injury and fibrosis. Loss of RKIP may be associated with malignant progression in hepatic fibrosis.

Effects of Qizhi Jiangtang capsule on protein expressions of InsR, PI3K, GLUT2 and p-JNK in hepatic tissues of rats with type 2 diabetes

To observe the hypoglycemic effect of Qizhi Jiangtang capsule in rats with type 2 diabetes, and investigate the preliminary mechanism of its hypoglycemic effect, type 2 diabetes rat models were established by high glucose and high fat combined with small dose of streptozotocin (STZ). After continuous administration for 6 weeks, blood glucose, and glycosylated serum protein (GSP) levels were detected in all of the animals; immunohistochemistry assay was used to detect the number of islet β cells; Western blot assay was used to detect the protein expression levels of insulin receptor (InsR), phosphoinositide-3 kinases (PI3K), glucose transporter-2 (GLUT2) and phosphorylated Jun N-terminal kinases (p-JNK)in hepatic tissues. The results showed that Qizhi Jiangtang capsule could reduce the blood sugar and GSP levels in serum in animals with type 2 diabetes mellitus, increase the level of insulin in serum and number of islet β cells, increase the protein expression levels of InsR, PI3K and GLUT2, and reduce the level of p-JNK protein expression. In conclusion, Qizhi Jiangtang capsule has relatively stable hypoglycemic effect, and the mechanism may be associated with increasing the number of islet β cells and level of insulin in serum, up-regulating the protein expression levels of InsR, PI3K and GLUT2, down-regulating the level of p-JNK protein expression in hepatic tissues, and reducing the level of insulin in hepatic tissues.

Acetaminophen Induces Mitochondrial Permeability Transition in Rats Without Causing Necrotic Liver Damage

Mitochondrial Permeability Transition (MPT) is reported as the mechanism of acetaminophen induced hepatic damage, however, rat models are resistant to acetaminophen induced toxicity. The occurrence and degree of mitochondrial permeability transition after treatment with 400 mg kgG1 of acetaminophen in albino Wistar rats were assessed. Animals were randomly distributed into seven groups; control, 12, 24, 36, 48, 60 and 72 h based on varying time (in hour) post acetaminophen prior to sacrifice after treatment. Mitochondrial Membrane Permeability Transition (MMPT) pore opening and mitochondrial cytochrome c release were estimated. Opening of MMPT pore and cytochrome c release were observed in 12, 24, 36 and 72 h, when compared with the control group. Liver function and histological results indicated no liver damage. It is concluded that toxic dose of acetaminophen induced mitochondrial permeability transition in rat hepatic tissues without leading to necrotic damage suggesting that rat hepatic tissues evade damage by mechanisms downstream of MPT.

Hepatoprotective effect of grape seed proanthocyanidins on Cadmium-induced hepatic injury in rats: Possible involvement of mitochondrial dysfunction, inflammation and apoptosis.

The present study was undertaken to evaluate the possible ameliorative role of grape seed proanthocyanidins (GSP) against Cadmium (Cd) induced hepatic inflammation, apoptosis and hepatic mitochondrial toxicity in rats. Male Wistar rats were distributed in four experimental groups: control, GSP, Cd and Cd + GSP. Exposure to a hepatotoxic dose of Cd (5 mg/kg BW) caused liver damage, coupled with enhanced reactive oxygen species (ROS) generation, increased inflammation and apoptosis in liver with increased DNA damage in hepatocytes of rats. Mitochondria were isolated from the hepatic tissues of rats from each group. Our results showed significant decrease in the tri-carboxylic acid cycle enzymes, increased mitochondrial swelling, inhibition of cytochrome c oxidase activity and complex I–III, II–III and IV mediated electron transfer, decreased mitochondrial ATPases, a reduction in calcium content and mitochondrial oxygen consumption in Cd treated rats. All these molecular changes caused by Cd were alleviated by the pre-supplementation with GSP (100 mg/kg BW). The ultra structural changes in the liver also support our findings. From our results, it is clearly indicated that the free radical scavenging, metal chelating and antioxidant potentials of GSP might be the possible reason, responsible for the rescue action against Cd induced mitochondrial damage in the liver of rats.

Biochemical and morphological alterations caused by silver nanoparticles in Wistar rats

This study evaluated the biochemical effect of the oral administration of silver nanoparticles on some biochemical parameters and tissue morphology. Wistar rats of both sexes with an average weight of 160 ± 5 g were randomly assigned into four groups. Animals in Group 1 served as the control and received 0.5 mL of distilled water (drug vehicle). Those in Groups 2, 3, and 4 were administered with 10, 50, and 100 mg/kg body weight silver nanoparticles, respectively. The animals were sacrificed under slight anesthesia 24 hours after the last treatment. Silver nanoparticle exposure in rats elevated the level of rat serum total cholesterol, triacylglyceride, free glycerol, low density lipoprotein-cholesterol, and bilirubin ( p < 0.05) when compared with the control. The level of high density lipoprotein-cholesterol was depleted by nanoparticle exposure, whereas the atherogenic index rose. The levels of albumin, urea, creatinine, as well as activities of aspartate transaminase and alkaline phosphatase were decreased by the nanoparticles, whereas the total protein and alanine transaminase were inconsistently altered relative to the control. Furthermore, the nanoparticle treatment caused morphological lesions in rat cardiac, renal, and hepatic tissues relative to the control. We show evidence that silver nanoparticle potentiated biochemical changes predisposing to liver injury and cardiovascular disorder in rat.

Quercetin protection against ciprofloxacin induced liver damage in rats

Ciprofloxacin is a common, broad spectrum antibacterial agent; however, evidence is accumulating that ciprofloxacin may cause liver damage. Quercetin is a free radical scavenger and antioxidant. We investigated histological changes in hepatic tissue of rats caused by ciprofloxacin and the effects of quercetin on these changes using histochemical and biochemical methods. We divided 28 adult female Wistar albino rats into four equal groups: control, quercetin treated, ciprofloxacin treated, and ciprofloxacin + quercetin treated. At the end of the experiment, liver samples were processed for light microscopic examination and biochemical measurements. Sections were prepared and stained with hematoxylin and eosin, and a histopathologic damage score was calculated. The sections from the control group appeared normal. Hemorrhage, inflammatory cell infiltration and intracellular vacuolization were observed in the ciprofloxacin group. The histopathological findings were reduced in the group treated with quercetin. Significant differences were found between the control and ciprofloxacin groups, and between the ciprofloxacin and ciprofloxacin + quercetin groups. Quercetin administration reduced liver injury caused by ciprofloxacin in rats. We suggest that quercetin may be useful for preventing ciprofloxacin induced liver damage.

Effect of Acetaminofen Versus Lornoxicam Admistration on Oxidative Stress in Rat Hepatic and Renal Tissues

Background and aim : The aim of study was to assess the oxidative status in rat hepatic and renal tissues after intraperitoneal administration of acetaminophen (AP) versus lornoxicam (L). Materials and Methods : For this purpose 18 Wistar Albino rats were randomly divided into 3 groups; each group consists of 6 rats. Group Control (Group C) remain untreated, comprises healthy rats. Group AP received AP (100 mg kg -1 ) and Group L received L (1.3 mg kg -1 ) intraperitoneally. Oxidative status was evaluated by MDA, SOD, GST and CAT in hepatic and renal tissues. Furthermore histopathalogical evaluation was performed in both tissues. Results : The lornoxicam received rats (Group L) showed significantly increased level of MDA and GST [(p=0.015), (p=0.048) respectively],decreased level of SOD (p=0.02)in liver tissue. Renal tissue MDA, SOD and GST activity and CAT levels were similar in groups [(p=0.168), (p=0.270), (p=0.686) respectively]. Histopathalogically Group AP and Group L more damaged than in Group C. Hepatic injury was moderate level in two groups. Minimal injury was observed in group AP. Renal injury in group L more than the Group AP. Conclusion : The results suggest that hepatotoxic effects of lornoxicam more than the AP while no remarkable difference nephrotoxicity.

Antioxidant and DNA Damage Protective Effects of Asparagus racemosus in Human Colon and Mice Muscle Cells

Introduction: The present study was designed to investigate the in vitro antioxidant and macromolecule damage protective effects of Asparagus racemosus water (AWE) and methanolic (AME) fractions of roots. Methods: The in vitro antioxidant activity of AWE/AME was estimated by free radical scavenging assays. The DNA damage of HT29 and C2C12 cells was analyzed by comet assay. The plasmid DNA damage and protein oxidation were carried out by agarose gel electrophoresis and SDS-PAGE analysis respectively, where as lipid peroxidation was performed by TBARS assay. Results: Both the extracts showed scavenging activity with IC 50 values of 417.4 ± 19.5 / 298 ± 13.5, 381 ± 18.2 / 235 ± 11.9, 54.8 ± 2.95 / 31.6 ± 1.52, 28.9 ± 1.73 / 19.7 ± 1.55 µg/mL for DPPH, metal chelating, ABTS and Nitric oxide scavenging activities respectively. Similarly the methanolic extract showed more potent reducing power and total antioxidant activities over water fraction. The AME showed 56.8% and 41.2% protection against H 2 O 2 (Hydrogen peroxide) induced DNA damage of HT29 human colon cells and C2C12 murine myoblasts. The extract also showed protection against H 2 O 2 induced plasmid DNA damge, AAPH induced protein oxidation of bovine serum albumin (BSA) and lipid peroxidation of rat hepatic tissue. Conclusion: Over all this study showed remarkable antioxidant and macromolecule damage protective effects of A.racemosus. The observed biological properties may be attributed to the high content phenols and flavonoids in the methanolic extract A. racemosus over water extract.

Influence of vitamin D3on ultramicrostructural changes of hepatic tissue in rats with experimental hepatic injury

Influence of vitamin D₃on ultramicrostructural changes of hepatic tissue in rats with experimental hepatic injury

Effect of co-administration of Angelicae gigantis radix and Lithospermi radix on rat hepatic injury induced by carbon tetrachloride.

Background:Co-administration of Angelicae gigantis radix (AGR) and Lithospermi radix (LR) has been commonly applied to patients to treat cardiac and hepatic disorders. Individual bioactivities of these herbal medicines have been widely investigated, but the hepatoprotective effects of co-treatment of AGR and LR have yet to be clarified.Objective:The present study investigated the protective effects of extracts of AGR and LR on carbon tetrachloride (CCl4) induced hepatic injury.Materials and Methods:In this study, we measured the hepatoprotective activity of individual and co-treatment of the two herbal medicines on hepatic injury induced by CCl4 by measuring different biochemical parameters such as serum aspartate aminotransaminase (AST) and serum alanine aminotransaminase (ALT). Microarray technology also used to compare ontological difference with individual and co-treatment of these two.Results:Combined treatment with AGR and LR (AGR + LR) decreased AST and ALT level in serum which demonstrate hepatoprotective effect of the therapy. When the effect of AGR and LR according to treatment conditions was measured, co-treatment showed the most prominent effect on hepatic injury by CCl4 rather than individual treatment condition. We further defined gene set that could be the molecular target of herbal effect on hepatic injury by CCl4 using bioinformatical analysis of interaction network. Highly recovered genes by treating AGR + LR play significant roles in response to hepatic injury induced by CCl4.Conclusion:Combined treatment with AGR and LR showed synergistic protective effects on the CCl4-induced rat hepatic tissue injury.